rabbit anti kcnj10  (Alomone Labs)


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    Alomone Labs rabbit anti kcnj10
    Primers
    Rabbit Anti Kcnj10, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 96 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti kcnj10 - by Bioz Stars, 2023-02
    96/100 stars

    Images

    1) Product Images from "Loss of KCNJ10 protein expression abolishes endocochlear potential and causes deafness in Pendred syndrome mouse model"

    Article Title: Loss of KCNJ10 protein expression abolishes endocochlear potential and causes deafness in Pendred syndrome mouse model

    Journal: BMC Medicine

    doi: 10.1186/1741-7015-2-30

    Primers
    Figure Legend Snippet: Primers

    Techniques Used:

    Quantification of KCNJ10 and KCNQ1 mRNA expression in stria vascularis and spiral ganglia of Slc26a4 +/+ and Slc26a4 -/- mice. a: Electropherogram of total RNA isolated from stria vascularis microdissected from one mouse. The amount of total RNA was obtained from the total integral ( shaded ) and the amount of 18S rRNA was obtained from the integral of the 18S peak. Sharp peaks representing 18S and 28S rRNA demonstrate the high quality of RNA. Insert: Genotype of Slc26a4 -/- mice was verified by the observation of one or few very large rhomboedric otoconia in the utricular macula ( arrow ). A, crista ampullaris; U, utricular macula. Scale bar: 100 μm. b: Example of real-time RT-PCR data used for quantification of 18S, KCNJ10, KCNQ1 and KCNQ4. Known quantities of 18S rRNA were used to calibrate the threshold. SV, stria vascularis; SG, spiral ganglia. c: Quantification of KCNJ10 and KCNQ1 mRNA in young Slc26a4 +/+ and young and old Slc26a4 -/- mice.
    Figure Legend Snippet: Quantification of KCNJ10 and KCNQ1 mRNA expression in stria vascularis and spiral ganglia of Slc26a4 +/+ and Slc26a4 -/- mice. a: Electropherogram of total RNA isolated from stria vascularis microdissected from one mouse. The amount of total RNA was obtained from the total integral ( shaded ) and the amount of 18S rRNA was obtained from the integral of the 18S peak. Sharp peaks representing 18S and 28S rRNA demonstrate the high quality of RNA. Insert: Genotype of Slc26a4 -/- mice was verified by the observation of one or few very large rhomboedric otoconia in the utricular macula ( arrow ). A, crista ampullaris; U, utricular macula. Scale bar: 100 μm. b: Example of real-time RT-PCR data used for quantification of 18S, KCNJ10, KCNQ1 and KCNQ4. Known quantities of 18S rRNA were used to calibrate the threshold. SV, stria vascularis; SG, spiral ganglia. c: Quantification of KCNJ10 and KCNQ1 mRNA in young Slc26a4 +/+ and young and old Slc26a4 -/- mice.

    Techniques Used: Expressing, Isolation, Quantitative RT-PCR

    Protein localization of KCNJ10 in the cochlea of Slc26a4 +/+ and Slc26a4 -/- mice. a: Overview of cochlea; bar = 100 μm. Compare to Fig. 1a to note the enlarged scala media and the distended Reissner's membrane. b-c: Detail of lateral wall and spiral ganglia ( insert ); main bar: 10 μm, insert: 5 μm. Expression of KCNJ10 in Slc26a4 -/- mice was absent in stria vascularis but unchanged in spiral ganglion cells. RM, Reissner's membrane, SV, stria vascularis; SP, spiral prominence; SL, spiral ligament; LIM, spiral limbus; SG, spiral ganglion.
    Figure Legend Snippet: Protein localization of KCNJ10 in the cochlea of Slc26a4 +/+ and Slc26a4 -/- mice. a: Overview of cochlea; bar = 100 μm. Compare to Fig. 1a to note the enlarged scala media and the distended Reissner's membrane. b-c: Detail of lateral wall and spiral ganglia ( insert ); main bar: 10 μm, insert: 5 μm. Expression of KCNJ10 in Slc26a4 -/- mice was absent in stria vascularis but unchanged in spiral ganglion cells. RM, Reissner's membrane, SV, stria vascularis; SP, spiral prominence; SL, spiral ligament; LIM, spiral limbus; SG, spiral ganglion.

    Techniques Used: Expressing

    Model for the loss of KCNJ10 in the absence of pendrin expression in stria vascularis. Cys, cysteine, Glu, glutamate, Gly, glycine, CA, carbonic anhydrase, GST, glutathione-S-transferase, GSH, glutathione.
    Figure Legend Snippet: Model for the loss of KCNJ10 in the absence of pendrin expression in stria vascularis. Cys, cysteine, Glu, glutamate, Gly, glycine, CA, carbonic anhydrase, GST, glutathione-S-transferase, GSH, glutathione.

    Techniques Used: Expressing

    rabbit anti kcnj10  (Alomone Labs)


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  • 96

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    Alomone Labs rabbit anti kcnj10
    Primers
    Rabbit Anti Kcnj10, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti kcnj10/product/Alomone Labs
    Average 96 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti kcnj10 - by Bioz Stars, 2023-02
    96/100 stars

    Images

    1) Product Images from "Loss of KCNJ10 protein expression abolishes endocochlear potential and causes deafness in Pendred syndrome mouse model"

    Article Title: Loss of KCNJ10 protein expression abolishes endocochlear potential and causes deafness in Pendred syndrome mouse model

    Journal: BMC Medicine

    doi: 10.1186/1741-7015-2-30

    Primers
    Figure Legend Snippet: Primers

    Techniques Used:

    Quantification of KCNJ10 and KCNQ1 mRNA expression in stria vascularis and spiral ganglia of Slc26a4 +/+ and Slc26a4 -/- mice. a: Electropherogram of total RNA isolated from stria vascularis microdissected from one mouse. The amount of total RNA was obtained from the total integral ( shaded ) and the amount of 18S rRNA was obtained from the integral of the 18S peak. Sharp peaks representing 18S and 28S rRNA demonstrate the high quality of RNA. Insert: Genotype of Slc26a4 -/- mice was verified by the observation of one or few very large rhomboedric otoconia in the utricular macula ( arrow ). A, crista ampullaris; U, utricular macula. Scale bar: 100 μm. b: Example of real-time RT-PCR data used for quantification of 18S, KCNJ10, KCNQ1 and KCNQ4. Known quantities of 18S rRNA were used to calibrate the threshold. SV, stria vascularis; SG, spiral ganglia. c: Quantification of KCNJ10 and KCNQ1 mRNA in young Slc26a4 +/+ and young and old Slc26a4 -/- mice.
    Figure Legend Snippet: Quantification of KCNJ10 and KCNQ1 mRNA expression in stria vascularis and spiral ganglia of Slc26a4 +/+ and Slc26a4 -/- mice. a: Electropherogram of total RNA isolated from stria vascularis microdissected from one mouse. The amount of total RNA was obtained from the total integral ( shaded ) and the amount of 18S rRNA was obtained from the integral of the 18S peak. Sharp peaks representing 18S and 28S rRNA demonstrate the high quality of RNA. Insert: Genotype of Slc26a4 -/- mice was verified by the observation of one or few very large rhomboedric otoconia in the utricular macula ( arrow ). A, crista ampullaris; U, utricular macula. Scale bar: 100 μm. b: Example of real-time RT-PCR data used for quantification of 18S, KCNJ10, KCNQ1 and KCNQ4. Known quantities of 18S rRNA were used to calibrate the threshold. SV, stria vascularis; SG, spiral ganglia. c: Quantification of KCNJ10 and KCNQ1 mRNA in young Slc26a4 +/+ and young and old Slc26a4 -/- mice.

    Techniques Used: Expressing, Isolation, Quantitative RT-PCR

    Protein localization of KCNJ10 in the cochlea of Slc26a4 +/+ and Slc26a4 -/- mice. a: Overview of cochlea; bar = 100 μm. Compare to Fig. 1a to note the enlarged scala media and the distended Reissner's membrane. b-c: Detail of lateral wall and spiral ganglia ( insert ); main bar: 10 μm, insert: 5 μm. Expression of KCNJ10 in Slc26a4 -/- mice was absent in stria vascularis but unchanged in spiral ganglion cells. RM, Reissner's membrane, SV, stria vascularis; SP, spiral prominence; SL, spiral ligament; LIM, spiral limbus; SG, spiral ganglion.
    Figure Legend Snippet: Protein localization of KCNJ10 in the cochlea of Slc26a4 +/+ and Slc26a4 -/- mice. a: Overview of cochlea; bar = 100 μm. Compare to Fig. 1a to note the enlarged scala media and the distended Reissner's membrane. b-c: Detail of lateral wall and spiral ganglia ( insert ); main bar: 10 μm, insert: 5 μm. Expression of KCNJ10 in Slc26a4 -/- mice was absent in stria vascularis but unchanged in spiral ganglion cells. RM, Reissner's membrane, SV, stria vascularis; SP, spiral prominence; SL, spiral ligament; LIM, spiral limbus; SG, spiral ganglion.

    Techniques Used: Expressing

    Model for the loss of KCNJ10 in the absence of pendrin expression in stria vascularis. Cys, cysteine, Glu, glutamate, Gly, glycine, CA, carbonic anhydrase, GST, glutathione-S-transferase, GSH, glutathione.
    Figure Legend Snippet: Model for the loss of KCNJ10 in the absence of pendrin expression in stria vascularis. Cys, cysteine, Glu, glutamate, Gly, glycine, CA, carbonic anhydrase, GST, glutathione-S-transferase, GSH, glutathione.

    Techniques Used: Expressing

    anti kir4 1  (Alomone Labs)


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    Alomone Labs anti kir4 1
    Immunohistochemical detection of <t>Kir4.1,</t> aquaporin-4, and anti-glial fibrillary acidic protein in the retina. In the normal eyes, Kir4.1 ( A ) and aquaporin-4 (AQP4; I ) were enriched in the endfoot membranes facing the vitreous body (arrowheads) and retinal blood vessels (arrows). Staining for AQP4 ( K - P ) maintained the same pattern during the different stages of endotoxin-induced uveitis (EIU), and only a slight reduction in immunostaining was seen in the inner plexiform at 1-7 day after lipopolysaccharide (LPS) injection. Kir4.1 ( C - H ) immunoreactivity decreased significantly from one day after LPS injection, had almost disappeared at 3-7 day after injection, and had partially recovered by 14 days. Anti-glial fibrillary acidic protein (GFAP; Q - X ) was predominantly found in astrocytes in the retinas of the untreated controls. Seven days and 14 days after intravitreal LPS injection, GFAP ( W - X ) immunoreactivity was significantly increased in Müller cells. In the retinas of sham-treated eyes, the immunostaining for Kir4.1 ( A - H ) was unchanged at 3 day after phosphate-buffered saline (PBS) treatment ( B ). AQP4 immunoreactivity was unchanged at one day after PBS treatment ( J ). GFAP immunoreactivity was mildly increased at 7 day after PBS treatment ( R ). GCL indicates ganglion cell layer; INL indicates inner nuclear layer; IPL indicates inner plexiform layer; ONL indicates outer nuclear layer; OPL indicates outer plexiform layer. Scale bar represents 20 μm.
    Anti Kir4 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    96/100 stars

    Images

    1) Product Images from "Differential expression of Kir4.1 and aquaporin 4 in the retina from endotoxin-induced uveitis rat"

    Article Title: Differential expression of Kir4.1 and aquaporin 4 in the retina from endotoxin-induced uveitis rat

    Journal: Molecular Vision

    doi:

    Immunohistochemical detection of Kir4.1, aquaporin-4, and anti-glial fibrillary acidic protein in the retina. In the normal eyes, Kir4.1 ( A ) and aquaporin-4 (AQP4; I ) were enriched in the endfoot membranes facing the vitreous body (arrowheads) and retinal blood vessels (arrows). Staining for AQP4 ( K - P ) maintained the same pattern during the different stages of endotoxin-induced uveitis (EIU), and only a slight reduction in immunostaining was seen in the inner plexiform at 1-7 day after lipopolysaccharide (LPS) injection. Kir4.1 ( C - H ) immunoreactivity decreased significantly from one day after LPS injection, had almost disappeared at 3-7 day after injection, and had partially recovered by 14 days. Anti-glial fibrillary acidic protein (GFAP; Q - X ) was predominantly found in astrocytes in the retinas of the untreated controls. Seven days and 14 days after intravitreal LPS injection, GFAP ( W - X ) immunoreactivity was significantly increased in Müller cells. In the retinas of sham-treated eyes, the immunostaining for Kir4.1 ( A - H ) was unchanged at 3 day after phosphate-buffered saline (PBS) treatment ( B ). AQP4 immunoreactivity was unchanged at one day after PBS treatment ( J ). GFAP immunoreactivity was mildly increased at 7 day after PBS treatment ( R ). GCL indicates ganglion cell layer; INL indicates inner nuclear layer; IPL indicates inner plexiform layer; ONL indicates outer nuclear layer; OPL indicates outer plexiform layer. Scale bar represents 20 μm.
    Figure Legend Snippet: Immunohistochemical detection of Kir4.1, aquaporin-4, and anti-glial fibrillary acidic protein in the retina. In the normal eyes, Kir4.1 ( A ) and aquaporin-4 (AQP4; I ) were enriched in the endfoot membranes facing the vitreous body (arrowheads) and retinal blood vessels (arrows). Staining for AQP4 ( K - P ) maintained the same pattern during the different stages of endotoxin-induced uveitis (EIU), and only a slight reduction in immunostaining was seen in the inner plexiform at 1-7 day after lipopolysaccharide (LPS) injection. Kir4.1 ( C - H ) immunoreactivity decreased significantly from one day after LPS injection, had almost disappeared at 3-7 day after injection, and had partially recovered by 14 days. Anti-glial fibrillary acidic protein (GFAP; Q - X ) was predominantly found in astrocytes in the retinas of the untreated controls. Seven days and 14 days after intravitreal LPS injection, GFAP ( W - X ) immunoreactivity was significantly increased in Müller cells. In the retinas of sham-treated eyes, the immunostaining for Kir4.1 ( A - H ) was unchanged at 3 day after phosphate-buffered saline (PBS) treatment ( B ). AQP4 immunoreactivity was unchanged at one day after PBS treatment ( J ). GFAP immunoreactivity was mildly increased at 7 day after PBS treatment ( R ). GCL indicates ganglion cell layer; INL indicates inner nuclear layer; IPL indicates inner plexiform layer; ONL indicates outer nuclear layer; OPL indicates outer plexiform layer. Scale bar represents 20 μm.

    Techniques Used: Immunohistochemical staining, Staining, Immunostaining, Injection

    Time course of Kir4.1 and aquaporin-4 mRNA expression in lipopolysaccharide- or phosphate-buffered saline-treated rats. A : Total RNA (1 μg) was used for reverse transcriptase polymerase chain reaction (RT-PCR). A 330-bp product for aquaporin-4 (AQP4), a 225-bp product for Kir4.1, and a 240-bp product for β-actin were separated on a 2.0% agarose gel. B , C : The relative levels of Kir4.1 and AQP4 mRNA expression were quantified. Compared with the control, there was a significant decline in Kir4.1 in lipopolysaccharide (LPS)-treated animals, whereas there was no change in AQP4 after LPS injection (means±SEM, n=4; asterisk (*) indicates p<0.05, double asterisks (**) signifies p<0.001 versus control). C indicates control; P indicates phosphate-buffered saline; L represents lipopolysaccharide.
    Figure Legend Snippet: Time course of Kir4.1 and aquaporin-4 mRNA expression in lipopolysaccharide- or phosphate-buffered saline-treated rats. A : Total RNA (1 μg) was used for reverse transcriptase polymerase chain reaction (RT-PCR). A 330-bp product for aquaporin-4 (AQP4), a 225-bp product for Kir4.1, and a 240-bp product for β-actin were separated on a 2.0% agarose gel. B , C : The relative levels of Kir4.1 and AQP4 mRNA expression were quantified. Compared with the control, there was a significant decline in Kir4.1 in lipopolysaccharide (LPS)-treated animals, whereas there was no change in AQP4 after LPS injection (means±SEM, n=4; asterisk (*) indicates p<0.05, double asterisks (**) signifies p<0.001 versus control). C indicates control; P indicates phosphate-buffered saline; L represents lipopolysaccharide.

    Techniques Used: Expressing, Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction, Agarose Gel Electrophoresis, Injection

    Time courses of Kir4.1 and aquaporin-4 protein expression in retinas from lipopolysaccharide- or phosphate-buffered saline-treated rats. A : Equal amounts of protein (30 μg) were subjected to immunoblotting analysis. A band at about 200 kDa represents Kir4.1 in its tetrameric form; aquaporin-4 (AQP4) consists of two bands, representing its M1 and M23 forms. B , C : The relative levels of Kir4.1 and AQP4 protein expression were quantified. Compared with that of the control, the expression of Kir4.1 was significantly reduced after LPS injection. In contrast, there was only a slight, statistically insignificant decline in AQP4 expression from 1 day to 7 day after LPS injection. (means±SEM, n=5; double asterisks (**) p<0.001 versus control). C indicates control; P indicates phosphate-buffered saline; L indicates lipopolysaccharide.
    Figure Legend Snippet: Time courses of Kir4.1 and aquaporin-4 protein expression in retinas from lipopolysaccharide- or phosphate-buffered saline-treated rats. A : Equal amounts of protein (30 μg) were subjected to immunoblotting analysis. A band at about 200 kDa represents Kir4.1 in its tetrameric form; aquaporin-4 (AQP4) consists of two bands, representing its M1 and M23 forms. B , C : The relative levels of Kir4.1 and AQP4 protein expression were quantified. Compared with that of the control, the expression of Kir4.1 was significantly reduced after LPS injection. In contrast, there was only a slight, statistically insignificant decline in AQP4 expression from 1 day to 7 day after LPS injection. (means±SEM, n=5; double asterisks (**) p<0.001 versus control). C indicates control; P indicates phosphate-buffered saline; L indicates lipopolysaccharide.

    Techniques Used: Expressing, Western Blot, Injection

    anti kir4 1  (Alomone Labs)


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    Alomone Labs anti kir4 1
    Primer pairs used for PCR experiments.
    Anti Kir4 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti kir4 1/product/Alomone Labs
    Average 96 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti kir4 1 - by Bioz Stars, 2023-02
    96/100 stars

    Images

    1) Product Images from "Müller Cell Reactivity in Response to Photoreceptor Degeneration in Rats with Defective Polycystin-2"

    Article Title: Müller Cell Reactivity in Response to Photoreceptor Degeneration in Rats with Defective Polycystin-2

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0061631

    Primer pairs used for PCR experiments.
    Figure Legend Snippet: Primer pairs used for PCR experiments.

    Techniques Used:

    kir4 1  (Alomone Labs)


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    Alomone Labs kir4 1
    Impaired astrocytes were subsequently recovered in the LPS-injected SNpc. ( A - D ) LPS (5 μg/2 μl) was injected into the SNpc. Sections obtained at the indicated times after LPS injection were labeled with antibodies specific for GFAP ( A ), S100β ( B ), EAAT1 ( C ), and Kir 4.1 ( D ), and visualized with peroxidase-conjugated secondary antibodies. Lower panels (SNpc and SNr) are higher magnification images of boxed areas (SNpc and SNr) in upper panels. Arrows indicate GFAP + ( A ), S100β + ( B ) EAAT1 + ( C ) and <t>Kir4.1</t> + ( D ) cells. Contralateral (Contra) sides of LPS-injected animals and PBS-injected animals were used as controls. Asterisks (*) indicate injection sites. Scale bars, 1 mm (upper panels in A ), 200 μm (upper panels in C - E ), 50 μm (lower panels in A ), 20 μm (lower panels in C - E ). ( E - H ) GFAP-, S100β-, EAAT1-, and Kir 4.1-negative areas in every sixth brain section were quantified using Axiovision image analysis software, as described in “Materials and Methods”. Values are means ± SEMs of at least three samples (*p < 0.01; **p < 0.001; Student’s t -test). Three or more animals were used for each time point. All data presented in this study are representative of at least three independent experiments unless indicated.
    Kir4 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Repair of astrocytes, blood vessels, and myelin in the injured brain: possible roles of blood monocytes"

    Article Title: Repair of astrocytes, blood vessels, and myelin in the injured brain: possible roles of blood monocytes

    Journal: Molecular Brain

    doi: 10.1186/1756-6606-6-28

    Impaired astrocytes were subsequently recovered in the LPS-injected SNpc. ( A - D ) LPS (5 μg/2 μl) was injected into the SNpc. Sections obtained at the indicated times after LPS injection were labeled with antibodies specific for GFAP ( A ), S100β ( B ), EAAT1 ( C ), and Kir 4.1 ( D ), and visualized with peroxidase-conjugated secondary antibodies. Lower panels (SNpc and SNr) are higher magnification images of boxed areas (SNpc and SNr) in upper panels. Arrows indicate GFAP + ( A ), S100β + ( B ) EAAT1 + ( C ) and Kir4.1 + ( D ) cells. Contralateral (Contra) sides of LPS-injected animals and PBS-injected animals were used as controls. Asterisks (*) indicate injection sites. Scale bars, 1 mm (upper panels in A ), 200 μm (upper panels in C - E ), 50 μm (lower panels in A ), 20 μm (lower panels in C - E ). ( E - H ) GFAP-, S100β-, EAAT1-, and Kir 4.1-negative areas in every sixth brain section were quantified using Axiovision image analysis software, as described in “Materials and Methods”. Values are means ± SEMs of at least three samples (*p < 0.01; **p < 0.001; Student’s t -test). Three or more animals were used for each time point. All data presented in this study are representative of at least three independent experiments unless indicated.
    Figure Legend Snippet: Impaired astrocytes were subsequently recovered in the LPS-injected SNpc. ( A - D ) LPS (5 μg/2 μl) was injected into the SNpc. Sections obtained at the indicated times after LPS injection were labeled with antibodies specific for GFAP ( A ), S100β ( B ), EAAT1 ( C ), and Kir 4.1 ( D ), and visualized with peroxidase-conjugated secondary antibodies. Lower panels (SNpc and SNr) are higher magnification images of boxed areas (SNpc and SNr) in upper panels. Arrows indicate GFAP + ( A ), S100β + ( B ) EAAT1 + ( C ) and Kir4.1 + ( D ) cells. Contralateral (Contra) sides of LPS-injected animals and PBS-injected animals were used as controls. Asterisks (*) indicate injection sites. Scale bars, 1 mm (upper panels in A ), 200 μm (upper panels in C - E ), 50 μm (lower panels in A ), 20 μm (lower panels in C - E ). ( E - H ) GFAP-, S100β-, EAAT1-, and Kir 4.1-negative areas in every sixth brain section were quantified using Axiovision image analysis software, as described in “Materials and Methods”. Values are means ± SEMs of at least three samples (*p < 0.01; **p < 0.001; Student’s t -test). Three or more animals were used for each time point. All data presented in this study are representative of at least three independent experiments unless indicated.

    Techniques Used: Injection, Labeling, Software

    Primary antibodies used in immunohistochemistry
    Figure Legend Snippet: Primary antibodies used in immunohistochemistry

    Techniques Used:

    apc 035  (Alomone Labs)


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    Alomone Labs apc 035
    Apc 035, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    kir4 1  (Alomone Labs)


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    Alomone Labs kir4 1
    The slices were derived from control and detached retina of C57BL/6 mice 24 h after surgery. A,G: Retinal sections were probed with antibodies against GFAP (green) and for nuclei (Dapi, blue). Note the upregulation of GFAP after RD. B,H: Sections were also stained with antibodies against <t>Kir4.1</t> (green). RD induced a mislocation of Kir4.1 along Müller cells (filled arrowhead) while the staining at the ILM (open arrowhead) and around blood vessels (arrow) remain unchanged. C,I: AQP4 staining (green) at the ILM (open arrowhead), around blood vessels (arrow) and at the OPL (filled arrowhead) was reduced in detached retina. D,J: Retinal sections were probed with a pan specific antibody against all forms of dystrophins (green). Dystrophin-Dp71 staining is localized at the ILM (open arrowhead) and around blood vessels (arrow), as previously reported . RD induced a reduction of Dp71 staining. E,K: 24 h after surgery Immunoreactivity for Utrophin (green) at the ILM (open arrowhead) was upregulated after RD. In control retina utrophin was localized at the ILM, around blood vessels and in the OPL. F,L: Sections were stained with antibodies against β-dystroglycan (β-DG). In control retina, β-DG is localized at the ILM (open arrowhead), around blood vessels (arrow) and at the OPL (filled arrowhead). RD induced a reduction of the staining in the ILM while the staining at the OPL (filled arrowhead) and around blood vessels (arrow) remain unchanged. ONL, outer nuclear layer; OPL, outer plexiform layer; INL, inner nuclear layer; IPL, inner plexiform layer; GCL, ganglion cell layer; ILM, inner limiting membrane. Scale bar = 30 µm.
    Kir4 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 1 article reviews
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    Images

    1) Product Images from "Functional Implication of Dp71 in Osmoregulation and Vascular Permeability of the Retina"

    Article Title: Functional Implication of Dp71 in Osmoregulation and Vascular Permeability of the Retina

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0007329

    The slices were derived from control and detached retina of C57BL/6 mice 24 h after surgery. A,G: Retinal sections were probed with antibodies against GFAP (green) and for nuclei (Dapi, blue). Note the upregulation of GFAP after RD. B,H: Sections were also stained with antibodies against Kir4.1 (green). RD induced a mislocation of Kir4.1 along Müller cells (filled arrowhead) while the staining at the ILM (open arrowhead) and around blood vessels (arrow) remain unchanged. C,I: AQP4 staining (green) at the ILM (open arrowhead), around blood vessels (arrow) and at the OPL (filled arrowhead) was reduced in detached retina. D,J: Retinal sections were probed with a pan specific antibody against all forms of dystrophins (green). Dystrophin-Dp71 staining is localized at the ILM (open arrowhead) and around blood vessels (arrow), as previously reported . RD induced a reduction of Dp71 staining. E,K: 24 h after surgery Immunoreactivity for Utrophin (green) at the ILM (open arrowhead) was upregulated after RD. In control retina utrophin was localized at the ILM, around blood vessels and in the OPL. F,L: Sections were stained with antibodies against β-dystroglycan (β-DG). In control retina, β-DG is localized at the ILM (open arrowhead), around blood vessels (arrow) and at the OPL (filled arrowhead). RD induced a reduction of the staining in the ILM while the staining at the OPL (filled arrowhead) and around blood vessels (arrow) remain unchanged. ONL, outer nuclear layer; OPL, outer plexiform layer; INL, inner nuclear layer; IPL, inner plexiform layer; GCL, ganglion cell layer; ILM, inner limiting membrane. Scale bar = 30 µm.
    Figure Legend Snippet: The slices were derived from control and detached retina of C57BL/6 mice 24 h after surgery. A,G: Retinal sections were probed with antibodies against GFAP (green) and for nuclei (Dapi, blue). Note the upregulation of GFAP after RD. B,H: Sections were also stained with antibodies against Kir4.1 (green). RD induced a mislocation of Kir4.1 along Müller cells (filled arrowhead) while the staining at the ILM (open arrowhead) and around blood vessels (arrow) remain unchanged. C,I: AQP4 staining (green) at the ILM (open arrowhead), around blood vessels (arrow) and at the OPL (filled arrowhead) was reduced in detached retina. D,J: Retinal sections were probed with a pan specific antibody against all forms of dystrophins (green). Dystrophin-Dp71 staining is localized at the ILM (open arrowhead) and around blood vessels (arrow), as previously reported . RD induced a reduction of Dp71 staining. E,K: 24 h after surgery Immunoreactivity for Utrophin (green) at the ILM (open arrowhead) was upregulated after RD. In control retina utrophin was localized at the ILM, around blood vessels and in the OPL. F,L: Sections were stained with antibodies against β-dystroglycan (β-DG). In control retina, β-DG is localized at the ILM (open arrowhead), around blood vessels (arrow) and at the OPL (filled arrowhead). RD induced a reduction of the staining in the ILM while the staining at the OPL (filled arrowhead) and around blood vessels (arrow) remain unchanged. ONL, outer nuclear layer; OPL, outer plexiform layer; INL, inner nuclear layer; IPL, inner plexiform layer; GCL, ganglion cell layer; ILM, inner limiting membrane. Scale bar = 30 µm.

    Techniques Used: Derivative Assay, Staining

    A: 24 h after surgery, proteins of control and detached retina from C57BL/6 mice were extracted and Western blotting was performed. Representative photograph of immunoblots reacted with anti-GFAP, anti-Kir4.1, anti-AQP4, anti utrophins, anti β-dystroglycan (β-DG) and β-Actin antibodies. Numbers on the left refer to the relative electrophoretic mobility of prestained molecular mass standards in kiloDaltons. B: The relative protein level is expressed in arbitrary units. Each value represents the ratio of the specific band stain intensity normalized to β-Actin expression (TotalLab TL120, Nonlinear Inc, Durham NC, USA). In detached retina, GFAP expression level was significantly upregulated while AQP4 expression was downregulated. There was no significant difference in Kir4.1, utrophin and β-DG protein expression level after retinal detachment. All experiments were repeated at least three times, and the bars represent means + SE for triplicate data points; n = 4. *p<0.05; ***p<0.001 significant differences versus control.
    Figure Legend Snippet: A: 24 h after surgery, proteins of control and detached retina from C57BL/6 mice were extracted and Western blotting was performed. Representative photograph of immunoblots reacted with anti-GFAP, anti-Kir4.1, anti-AQP4, anti utrophins, anti β-dystroglycan (β-DG) and β-Actin antibodies. Numbers on the left refer to the relative electrophoretic mobility of prestained molecular mass standards in kiloDaltons. B: The relative protein level is expressed in arbitrary units. Each value represents the ratio of the specific band stain intensity normalized to β-Actin expression (TotalLab TL120, Nonlinear Inc, Durham NC, USA). In detached retina, GFAP expression level was significantly upregulated while AQP4 expression was downregulated. There was no significant difference in Kir4.1, utrophin and β-DG protein expression level after retinal detachment. All experiments were repeated at least three times, and the bars represent means + SE for triplicate data points; n = 4. *p<0.05; ***p<0.001 significant differences versus control.

    Techniques Used: Western Blot, Staining, Expressing

    anti kir4 1  (Alomone Labs)


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    Alomone Labs anti kir4 1
    ( A ) Inwardly rectifying potassium channels <t>Kir4.1</t> (green) are localized in the area of the photoreceptors and in outer nuclear layer (red arrowhead), but not in Müller cell processes such as stalks or endfeet. This is different from most of vertebrates where Kir4.1 channels were found in Müller cells . ( B ) Glial Müller cell specific marker vimentin, V (green); photoreceptor specific alpha-1 subunit of transducin, Gαt1 (red); nucleus-specific marker, DAPI (blue). Vimentin staining is observed in endfeet, somata, stalks and in distal processes (yellow arrowhead points somata, white arrow shows stalk). DAPI staining (blue) shows nuclei of retinal cells. Alpha-1 subunit of transducin (Gαt1, red) is a marker of the second messenger G-protein cascade and it is found mostly in photoreceptors. ( C ) ATP-dependent K + channel, Kir6.1 (black), is localized in stalks (white arrow) and in endfeet, while ( D ) two pore domain acid sensitive K + channels, TASK-1 (black) are found in whole Müller cell compartments: in endfeet (black arrowhead), stalks (white arrow), somata (yellow arrowhead) and in distal processes (white arrowhead). Scale bar = 20 µm. ILM-inner limiting membrane, GCL-ganglion cell layer, IPL-inner plexiform layer, INL-inner nuclear layer, ONL-outer nuclear layer, IS- inner segments of photoreceptors.
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    Images

    1) Product Images from "Unidirectional Photoreceptor-to-Müller Glia Coupling and Unique K + Channel Expression in Caiman Retina"

    Article Title: Unidirectional Photoreceptor-to-Müller Glia Coupling and Unique K + Channel Expression in Caiman Retina

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0097155

    ( A ) Inwardly rectifying potassium channels Kir4.1 (green) are localized in the area of the photoreceptors and in outer nuclear layer (red arrowhead), but not in Müller cell processes such as stalks or endfeet. This is different from most of vertebrates where Kir4.1 channels were found in Müller cells . ( B ) Glial Müller cell specific marker vimentin, V (green); photoreceptor specific alpha-1 subunit of transducin, Gαt1 (red); nucleus-specific marker, DAPI (blue). Vimentin staining is observed in endfeet, somata, stalks and in distal processes (yellow arrowhead points somata, white arrow shows stalk). DAPI staining (blue) shows nuclei of retinal cells. Alpha-1 subunit of transducin (Gαt1, red) is a marker of the second messenger G-protein cascade and it is found mostly in photoreceptors. ( C ) ATP-dependent K + channel, Kir6.1 (black), is localized in stalks (white arrow) and in endfeet, while ( D ) two pore domain acid sensitive K + channels, TASK-1 (black) are found in whole Müller cell compartments: in endfeet (black arrowhead), stalks (white arrow), somata (yellow arrowhead) and in distal processes (white arrowhead). Scale bar = 20 µm. ILM-inner limiting membrane, GCL-ganglion cell layer, IPL-inner plexiform layer, INL-inner nuclear layer, ONL-outer nuclear layer, IS- inner segments of photoreceptors.
    Figure Legend Snippet: ( A ) Inwardly rectifying potassium channels Kir4.1 (green) are localized in the area of the photoreceptors and in outer nuclear layer (red arrowhead), but not in Müller cell processes such as stalks or endfeet. This is different from most of vertebrates where Kir4.1 channels were found in Müller cells . ( B ) Glial Müller cell specific marker vimentin, V (green); photoreceptor specific alpha-1 subunit of transducin, Gαt1 (red); nucleus-specific marker, DAPI (blue). Vimentin staining is observed in endfeet, somata, stalks and in distal processes (yellow arrowhead points somata, white arrow shows stalk). DAPI staining (blue) shows nuclei of retinal cells. Alpha-1 subunit of transducin (Gαt1, red) is a marker of the second messenger G-protein cascade and it is found mostly in photoreceptors. ( C ) ATP-dependent K + channel, Kir6.1 (black), is localized in stalks (white arrow) and in endfeet, while ( D ) two pore domain acid sensitive K + channels, TASK-1 (black) are found in whole Müller cell compartments: in endfeet (black arrowhead), stalks (white arrow), somata (yellow arrowhead) and in distal processes (white arrowhead). Scale bar = 20 µm. ILM-inner limiting membrane, GCL-ganglion cell layer, IPL-inner plexiform layer, INL-inner nuclear layer, ONL-outer nuclear layer, IS- inner segments of photoreceptors.

    Techniques Used: Marker, Staining

    kir4 1  (Alomone Labs)


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    Alomone Labs kir4 1
    Primer sequences for RT-PCR and/or qPCR
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    Images

    1) Product Images from "Spatial and temporal correlation in progressive degeneration of neurons and astrocytes in contusion-induced spinal cord injury"

    Article Title: Spatial and temporal correlation in progressive degeneration of neurons and astrocytes in contusion-induced spinal cord injury

    Journal: Journal of Neuroinflammation

    doi: 10.1186/1742-2094-9-100

    Primer sequences for RT-PCR and/or qPCR
    Figure Legend Snippet: Primer sequences for RT-PCR and/or qPCR

    Techniques Used:

    Loss of astrocytes and reduced expression of GLT-1 and Kir4.1 in injured spinal cords. (A, D) Sections from intact and P1 areas at the indicated times after injury were stained with NeuN/GFAP (A), and GLT-1 or Kir4.1 ( D ) antibodies. Right panels in ( A ) and lower panels in ( D ) are higher magnification images of indicated regions in the left and upper panels, respectively. (B, C) Spinal cord tissues (2 mm in length around the contusion center) were obtained at the indicated times after SCI, and total RNA was prepared and analyzed by RT-PCR ( B ) or q-PCR ( C ) as described in Materials and Methods. Values in ( C ) are means ± SEMs of five animals. ( D ) The white arrow represents neuronal cell body-like morphology. Data shown are representative of three independent experiments. Scale bars: 200 μm (left panels in A and upper panels in D), 10 μm (right panels in A), and 50 μm (lower panels in D).
    Figure Legend Snippet: Loss of astrocytes and reduced expression of GLT-1 and Kir4.1 in injured spinal cords. (A, D) Sections from intact and P1 areas at the indicated times after injury were stained with NeuN/GFAP (A), and GLT-1 or Kir4.1 ( D ) antibodies. Right panels in ( A ) and lower panels in ( D ) are higher magnification images of indicated regions in the left and upper panels, respectively. (B, C) Spinal cord tissues (2 mm in length around the contusion center) were obtained at the indicated times after SCI, and total RNA was prepared and analyzed by RT-PCR ( B ) or q-PCR ( C ) as described in Materials and Methods. Values in ( C ) are means ± SEMs of five animals. ( D ) The white arrow represents neuronal cell body-like morphology. Data shown are representative of three independent experiments. Scale bars: 200 μm (left panels in A and upper panels in D), 10 μm (right panels in A), and 50 μm (lower panels in D).

    Techniques Used: Expressing, Staining, Reverse Transcription Polymerase Chain Reaction

    anti kcnj10  (Alomone Labs)


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    Alomone Labs anti kcnj10
    A , Bdp1 protein expression in the cochlea at postnatal day 5. Bdp1 shows expression in the stria vascularis (red arrow), Reissner's membrane (red arrowhead), basilar membrane (black arrowhead), and spiral ligament (black arrow). B–D , Bdp1, <t>Kcnj10</t> and laminin expression in the stria vascularis. Our immunohistochemistry detected Bdp1 protein in the proximity of blood vessels (example of the same blood vessel in adjacent sections is indicated with an arrow in B, C, D). We used Kcnj10 as a marker of intermediate cells (C) and laminin as a marker of the basal lamina surrounding blood vessels (D) in the stria vascularis in the sections shown in A. The expression pattern suggests that Bdp1 is expressed in endothelial cells of the stria vascularis. Scale bars: A: 50 µm; B–D: 10 µm. sv: stria vascularis.
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    1) Product Images from "Linkage Study and Exome Sequencing Identify a BDP1 Mutation Associated with Hereditary Hearing Loss"

    Article Title: Linkage Study and Exome Sequencing Identify a BDP1 Mutation Associated with Hereditary Hearing Loss

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0080323

    A , Bdp1 protein expression in the cochlea at postnatal day 5. Bdp1 shows expression in the stria vascularis (red arrow), Reissner's membrane (red arrowhead), basilar membrane (black arrowhead), and spiral ligament (black arrow). B–D , Bdp1, Kcnj10 and laminin expression in the stria vascularis. Our immunohistochemistry detected Bdp1 protein in the proximity of blood vessels (example of the same blood vessel in adjacent sections is indicated with an arrow in B, C, D). We used Kcnj10 as a marker of intermediate cells (C) and laminin as a marker of the basal lamina surrounding blood vessels (D) in the stria vascularis in the sections shown in A. The expression pattern suggests that Bdp1 is expressed in endothelial cells of the stria vascularis. Scale bars: A: 50 µm; B–D: 10 µm. sv: stria vascularis.
    Figure Legend Snippet: A , Bdp1 protein expression in the cochlea at postnatal day 5. Bdp1 shows expression in the stria vascularis (red arrow), Reissner's membrane (red arrowhead), basilar membrane (black arrowhead), and spiral ligament (black arrow). B–D , Bdp1, Kcnj10 and laminin expression in the stria vascularis. Our immunohistochemistry detected Bdp1 protein in the proximity of blood vessels (example of the same blood vessel in adjacent sections is indicated with an arrow in B, C, D). We used Kcnj10 as a marker of intermediate cells (C) and laminin as a marker of the basal lamina surrounding blood vessels (D) in the stria vascularis in the sections shown in A. The expression pattern suggests that Bdp1 is expressed in endothelial cells of the stria vascularis. Scale bars: A: 50 µm; B–D: 10 µm. sv: stria vascularis.

    Techniques Used: Expressing, Immunohistochemistry, Marker

    anti kir4 1  (Alomone Labs)


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    Alomone Labs anti kir4 1
    Anti Kir4 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Alomone Labs rabbit anti kcnj10
    Primers
    Rabbit Anti Kcnj10, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Alomone Labs anti kir4 1
    Immunohistochemical detection of <t>Kir4.1,</t> aquaporin-4, and anti-glial fibrillary acidic protein in the retina. In the normal eyes, Kir4.1 ( A ) and aquaporin-4 (AQP4; I ) were enriched in the endfoot membranes facing the vitreous body (arrowheads) and retinal blood vessels (arrows). Staining for AQP4 ( K - P ) maintained the same pattern during the different stages of endotoxin-induced uveitis (EIU), and only a slight reduction in immunostaining was seen in the inner plexiform at 1-7 day after lipopolysaccharide (LPS) injection. Kir4.1 ( C - H ) immunoreactivity decreased significantly from one day after LPS injection, had almost disappeared at 3-7 day after injection, and had partially recovered by 14 days. Anti-glial fibrillary acidic protein (GFAP; Q - X ) was predominantly found in astrocytes in the retinas of the untreated controls. Seven days and 14 days after intravitreal LPS injection, GFAP ( W - X ) immunoreactivity was significantly increased in Müller cells. In the retinas of sham-treated eyes, the immunostaining for Kir4.1 ( A - H ) was unchanged at 3 day after phosphate-buffered saline (PBS) treatment ( B ). AQP4 immunoreactivity was unchanged at one day after PBS treatment ( J ). GFAP immunoreactivity was mildly increased at 7 day after PBS treatment ( R ). GCL indicates ganglion cell layer; INL indicates inner nuclear layer; IPL indicates inner plexiform layer; ONL indicates outer nuclear layer; OPL indicates outer plexiform layer. Scale bar represents 20 μm.
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    Impaired astrocytes were subsequently recovered in the LPS-injected SNpc. ( A - D ) LPS (5 μg/2 μl) was injected into the SNpc. Sections obtained at the indicated times after LPS injection were labeled with antibodies specific for GFAP ( A ), S100β ( B ), EAAT1 ( C ), and Kir 4.1 ( D ), and visualized with peroxidase-conjugated secondary antibodies. Lower panels (SNpc and SNr) are higher magnification images of boxed areas (SNpc and SNr) in upper panels. Arrows indicate GFAP + ( A ), S100β + ( B ) EAAT1 + ( C ) and <t>Kir4.1</t> + ( D ) cells. Contralateral (Contra) sides of LPS-injected animals and PBS-injected animals were used as controls. Asterisks (*) indicate injection sites. Scale bars, 1 mm (upper panels in A ), 200 μm (upper panels in C - E ), 50 μm (lower panels in A ), 20 μm (lower panels in C - E ). ( E - H ) GFAP-, S100β-, EAAT1-, and Kir 4.1-negative areas in every sixth brain section were quantified using Axiovision image analysis software, as described in “Materials and Methods”. Values are means ± SEMs of at least three samples (*p < 0.01; **p < 0.001; Student’s t -test). Three or more animals were used for each time point. All data presented in this study are representative of at least three independent experiments unless indicated.
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    Alomone Labs apc 035
    Impaired astrocytes were subsequently recovered in the LPS-injected SNpc. ( A - D ) LPS (5 μg/2 μl) was injected into the SNpc. Sections obtained at the indicated times after LPS injection were labeled with antibodies specific for GFAP ( A ), S100β ( B ), EAAT1 ( C ), and Kir 4.1 ( D ), and visualized with peroxidase-conjugated secondary antibodies. Lower panels (SNpc and SNr) are higher magnification images of boxed areas (SNpc and SNr) in upper panels. Arrows indicate GFAP + ( A ), S100β + ( B ) EAAT1 + ( C ) and <t>Kir4.1</t> + ( D ) cells. Contralateral (Contra) sides of LPS-injected animals and PBS-injected animals were used as controls. Asterisks (*) indicate injection sites. Scale bars, 1 mm (upper panels in A ), 200 μm (upper panels in C - E ), 50 μm (lower panels in A ), 20 μm (lower panels in C - E ). ( E - H ) GFAP-, S100β-, EAAT1-, and Kir 4.1-negative areas in every sixth brain section were quantified using Axiovision image analysis software, as described in “Materials and Methods”. Values are means ± SEMs of at least three samples (*p < 0.01; **p < 0.001; Student’s t -test). Three or more animals were used for each time point. All data presented in this study are representative of at least three independent experiments unless indicated.
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    Alomone Labs anti kcnj10
    A , Bdp1 protein expression in the cochlea at postnatal day 5. Bdp1 shows expression in the stria vascularis (red arrow), Reissner's membrane (red arrowhead), basilar membrane (black arrowhead), and spiral ligament (black arrow). B–D , Bdp1, <t>Kcnj10</t> and laminin expression in the stria vascularis. Our immunohistochemistry detected Bdp1 protein in the proximity of blood vessels (example of the same blood vessel in adjacent sections is indicated with an arrow in B, C, D). We used Kcnj10 as a marker of intermediate cells (C) and laminin as a marker of the basal lamina surrounding blood vessels (D) in the stria vascularis in the sections shown in A. The expression pattern suggests that Bdp1 is expressed in endothelial cells of the stria vascularis. Scale bars: A: 50 µm; B–D: 10 µm. sv: stria vascularis.
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    Image Search Results


    Primers

    Journal: BMC Medicine

    Article Title: Loss of KCNJ10 protein expression abolishes endocochlear potential and causes deafness in Pendred syndrome mouse model

    doi: 10.1186/1741-7015-2-30

    Figure Lengend Snippet: Primers

    Article Snippet: Slides were incubated overnight at 4°C with primary antibodies in PBS-TX with 1–3% BSA [rabbit anti-pendrin, 1:500 (h766–780); rat anti-ZO-1, 1:100 (Chemicon, Temecula, CA); goat anti-KCNQ1, 1:200 (C20, Santa Cruz Biotechnology, Santa Cruz, CA), rabbit anti-KCNE1, 1:200 (Alomone, Jerusalem, Israel); rabbit anti-KCNJ10, 1:300 (Alomone); rabbit anti-SLC12A2, 1:100 (Chemicon); and rabbit anti-connexin 26, 1:100 (Zymed, San Francisco, CA)].

    Techniques:

    Quantification of KCNJ10 and KCNQ1 mRNA expression in stria vascularis and spiral ganglia of Slc26a4 +/+ and Slc26a4 -/- mice. a: Electropherogram of total RNA isolated from stria vascularis microdissected from one mouse. The amount of total RNA was obtained from the total integral ( shaded ) and the amount of 18S rRNA was obtained from the integral of the 18S peak. Sharp peaks representing 18S and 28S rRNA demonstrate the high quality of RNA. Insert: Genotype of Slc26a4 -/- mice was verified by the observation of one or few very large rhomboedric otoconia in the utricular macula ( arrow ). A, crista ampullaris; U, utricular macula. Scale bar: 100 μm. b: Example of real-time RT-PCR data used for quantification of 18S, KCNJ10, KCNQ1 and KCNQ4. Known quantities of 18S rRNA were used to calibrate the threshold. SV, stria vascularis; SG, spiral ganglia. c: Quantification of KCNJ10 and KCNQ1 mRNA in young Slc26a4 +/+ and young and old Slc26a4 -/- mice.

    Journal: BMC Medicine

    Article Title: Loss of KCNJ10 protein expression abolishes endocochlear potential and causes deafness in Pendred syndrome mouse model

    doi: 10.1186/1741-7015-2-30

    Figure Lengend Snippet: Quantification of KCNJ10 and KCNQ1 mRNA expression in stria vascularis and spiral ganglia of Slc26a4 +/+ and Slc26a4 -/- mice. a: Electropherogram of total RNA isolated from stria vascularis microdissected from one mouse. The amount of total RNA was obtained from the total integral ( shaded ) and the amount of 18S rRNA was obtained from the integral of the 18S peak. Sharp peaks representing 18S and 28S rRNA demonstrate the high quality of RNA. Insert: Genotype of Slc26a4 -/- mice was verified by the observation of one or few very large rhomboedric otoconia in the utricular macula ( arrow ). A, crista ampullaris; U, utricular macula. Scale bar: 100 μm. b: Example of real-time RT-PCR data used for quantification of 18S, KCNJ10, KCNQ1 and KCNQ4. Known quantities of 18S rRNA were used to calibrate the threshold. SV, stria vascularis; SG, spiral ganglia. c: Quantification of KCNJ10 and KCNQ1 mRNA in young Slc26a4 +/+ and young and old Slc26a4 -/- mice.

    Article Snippet: Slides were incubated overnight at 4°C with primary antibodies in PBS-TX with 1–3% BSA [rabbit anti-pendrin, 1:500 (h766–780); rat anti-ZO-1, 1:100 (Chemicon, Temecula, CA); goat anti-KCNQ1, 1:200 (C20, Santa Cruz Biotechnology, Santa Cruz, CA), rabbit anti-KCNE1, 1:200 (Alomone, Jerusalem, Israel); rabbit anti-KCNJ10, 1:300 (Alomone); rabbit anti-SLC12A2, 1:100 (Chemicon); and rabbit anti-connexin 26, 1:100 (Zymed, San Francisco, CA)].

    Techniques: Expressing, Isolation, Quantitative RT-PCR

    Protein localization of KCNJ10 in the cochlea of Slc26a4 +/+ and Slc26a4 -/- mice. a: Overview of cochlea; bar = 100 μm. Compare to Fig. 1a to note the enlarged scala media and the distended Reissner's membrane. b-c: Detail of lateral wall and spiral ganglia ( insert ); main bar: 10 μm, insert: 5 μm. Expression of KCNJ10 in Slc26a4 -/- mice was absent in stria vascularis but unchanged in spiral ganglion cells. RM, Reissner's membrane, SV, stria vascularis; SP, spiral prominence; SL, spiral ligament; LIM, spiral limbus; SG, spiral ganglion.

    Journal: BMC Medicine

    Article Title: Loss of KCNJ10 protein expression abolishes endocochlear potential and causes deafness in Pendred syndrome mouse model

    doi: 10.1186/1741-7015-2-30

    Figure Lengend Snippet: Protein localization of KCNJ10 in the cochlea of Slc26a4 +/+ and Slc26a4 -/- mice. a: Overview of cochlea; bar = 100 μm. Compare to Fig. 1a to note the enlarged scala media and the distended Reissner's membrane. b-c: Detail of lateral wall and spiral ganglia ( insert ); main bar: 10 μm, insert: 5 μm. Expression of KCNJ10 in Slc26a4 -/- mice was absent in stria vascularis but unchanged in spiral ganglion cells. RM, Reissner's membrane, SV, stria vascularis; SP, spiral prominence; SL, spiral ligament; LIM, spiral limbus; SG, spiral ganglion.

    Article Snippet: Slides were incubated overnight at 4°C with primary antibodies in PBS-TX with 1–3% BSA [rabbit anti-pendrin, 1:500 (h766–780); rat anti-ZO-1, 1:100 (Chemicon, Temecula, CA); goat anti-KCNQ1, 1:200 (C20, Santa Cruz Biotechnology, Santa Cruz, CA), rabbit anti-KCNE1, 1:200 (Alomone, Jerusalem, Israel); rabbit anti-KCNJ10, 1:300 (Alomone); rabbit anti-SLC12A2, 1:100 (Chemicon); and rabbit anti-connexin 26, 1:100 (Zymed, San Francisco, CA)].

    Techniques: Expressing

    Model for the loss of KCNJ10 in the absence of pendrin expression in stria vascularis. Cys, cysteine, Glu, glutamate, Gly, glycine, CA, carbonic anhydrase, GST, glutathione-S-transferase, GSH, glutathione.

    Journal: BMC Medicine

    Article Title: Loss of KCNJ10 protein expression abolishes endocochlear potential and causes deafness in Pendred syndrome mouse model

    doi: 10.1186/1741-7015-2-30

    Figure Lengend Snippet: Model for the loss of KCNJ10 in the absence of pendrin expression in stria vascularis. Cys, cysteine, Glu, glutamate, Gly, glycine, CA, carbonic anhydrase, GST, glutathione-S-transferase, GSH, glutathione.

    Article Snippet: Slides were incubated overnight at 4°C with primary antibodies in PBS-TX with 1–3% BSA [rabbit anti-pendrin, 1:500 (h766–780); rat anti-ZO-1, 1:100 (Chemicon, Temecula, CA); goat anti-KCNQ1, 1:200 (C20, Santa Cruz Biotechnology, Santa Cruz, CA), rabbit anti-KCNE1, 1:200 (Alomone, Jerusalem, Israel); rabbit anti-KCNJ10, 1:300 (Alomone); rabbit anti-SLC12A2, 1:100 (Chemicon); and rabbit anti-connexin 26, 1:100 (Zymed, San Francisco, CA)].

    Techniques: Expressing

    Immunohistochemical detection of Kir4.1, aquaporin-4, and anti-glial fibrillary acidic protein in the retina. In the normal eyes, Kir4.1 ( A ) and aquaporin-4 (AQP4; I ) were enriched in the endfoot membranes facing the vitreous body (arrowheads) and retinal blood vessels (arrows). Staining for AQP4 ( K - P ) maintained the same pattern during the different stages of endotoxin-induced uveitis (EIU), and only a slight reduction in immunostaining was seen in the inner plexiform at 1-7 day after lipopolysaccharide (LPS) injection. Kir4.1 ( C - H ) immunoreactivity decreased significantly from one day after LPS injection, had almost disappeared at 3-7 day after injection, and had partially recovered by 14 days. Anti-glial fibrillary acidic protein (GFAP; Q - X ) was predominantly found in astrocytes in the retinas of the untreated controls. Seven days and 14 days after intravitreal LPS injection, GFAP ( W - X ) immunoreactivity was significantly increased in Müller cells. In the retinas of sham-treated eyes, the immunostaining for Kir4.1 ( A - H ) was unchanged at 3 day after phosphate-buffered saline (PBS) treatment ( B ). AQP4 immunoreactivity was unchanged at one day after PBS treatment ( J ). GFAP immunoreactivity was mildly increased at 7 day after PBS treatment ( R ). GCL indicates ganglion cell layer; INL indicates inner nuclear layer; IPL indicates inner plexiform layer; ONL indicates outer nuclear layer; OPL indicates outer plexiform layer. Scale bar represents 20 μm.

    Journal: Molecular Vision

    Article Title: Differential expression of Kir4.1 and aquaporin 4 in the retina from endotoxin-induced uveitis rat

    doi:

    Figure Lengend Snippet: Immunohistochemical detection of Kir4.1, aquaporin-4, and anti-glial fibrillary acidic protein in the retina. In the normal eyes, Kir4.1 ( A ) and aquaporin-4 (AQP4; I ) were enriched in the endfoot membranes facing the vitreous body (arrowheads) and retinal blood vessels (arrows). Staining for AQP4 ( K - P ) maintained the same pattern during the different stages of endotoxin-induced uveitis (EIU), and only a slight reduction in immunostaining was seen in the inner plexiform at 1-7 day after lipopolysaccharide (LPS) injection. Kir4.1 ( C - H ) immunoreactivity decreased significantly from one day after LPS injection, had almost disappeared at 3-7 day after injection, and had partially recovered by 14 days. Anti-glial fibrillary acidic protein (GFAP; Q - X ) was predominantly found in astrocytes in the retinas of the untreated controls. Seven days and 14 days after intravitreal LPS injection, GFAP ( W - X ) immunoreactivity was significantly increased in Müller cells. In the retinas of sham-treated eyes, the immunostaining for Kir4.1 ( A - H ) was unchanged at 3 day after phosphate-buffered saline (PBS) treatment ( B ). AQP4 immunoreactivity was unchanged at one day after PBS treatment ( J ). GFAP immunoreactivity was mildly increased at 7 day after PBS treatment ( R ). GCL indicates ganglion cell layer; INL indicates inner nuclear layer; IPL indicates inner plexiform layer; ONL indicates outer nuclear layer; OPL indicates outer plexiform layer. Scale bar represents 20 μm.

    Article Snippet: The primary antibodies were rabbit anti-Kir4.1 (1:200; Alomone Laboratories, Jerusalem, Israel), rabbit anti-AQP4 (1:250, Chemicon, Temecula, CA), and mouse anti-glial fibrillary acidic protein (GFAP; 1:1000, Transduction Laboratories, Lexington, KY).

    Techniques: Immunohistochemical staining, Staining, Immunostaining, Injection

    Time course of Kir4.1 and aquaporin-4 mRNA expression in lipopolysaccharide- or phosphate-buffered saline-treated rats. A : Total RNA (1 μg) was used for reverse transcriptase polymerase chain reaction (RT-PCR). A 330-bp product for aquaporin-4 (AQP4), a 225-bp product for Kir4.1, and a 240-bp product for β-actin were separated on a 2.0% agarose gel. B , C : The relative levels of Kir4.1 and AQP4 mRNA expression were quantified. Compared with the control, there was a significant decline in Kir4.1 in lipopolysaccharide (LPS)-treated animals, whereas there was no change in AQP4 after LPS injection (means±SEM, n=4; asterisk (*) indicates p<0.05, double asterisks (**) signifies p<0.001 versus control). C indicates control; P indicates phosphate-buffered saline; L represents lipopolysaccharide.

    Journal: Molecular Vision

    Article Title: Differential expression of Kir4.1 and aquaporin 4 in the retina from endotoxin-induced uveitis rat

    doi:

    Figure Lengend Snippet: Time course of Kir4.1 and aquaporin-4 mRNA expression in lipopolysaccharide- or phosphate-buffered saline-treated rats. A : Total RNA (1 μg) was used for reverse transcriptase polymerase chain reaction (RT-PCR). A 330-bp product for aquaporin-4 (AQP4), a 225-bp product for Kir4.1, and a 240-bp product for β-actin were separated on a 2.0% agarose gel. B , C : The relative levels of Kir4.1 and AQP4 mRNA expression were quantified. Compared with the control, there was a significant decline in Kir4.1 in lipopolysaccharide (LPS)-treated animals, whereas there was no change in AQP4 after LPS injection (means±SEM, n=4; asterisk (*) indicates p<0.05, double asterisks (**) signifies p<0.001 versus control). C indicates control; P indicates phosphate-buffered saline; L represents lipopolysaccharide.

    Article Snippet: The primary antibodies were rabbit anti-Kir4.1 (1:200; Alomone Laboratories, Jerusalem, Israel), rabbit anti-AQP4 (1:250, Chemicon, Temecula, CA), and mouse anti-glial fibrillary acidic protein (GFAP; 1:1000, Transduction Laboratories, Lexington, KY).

    Techniques: Expressing, Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction, Agarose Gel Electrophoresis, Injection

    Time courses of Kir4.1 and aquaporin-4 protein expression in retinas from lipopolysaccharide- or phosphate-buffered saline-treated rats. A : Equal amounts of protein (30 μg) were subjected to immunoblotting analysis. A band at about 200 kDa represents Kir4.1 in its tetrameric form; aquaporin-4 (AQP4) consists of two bands, representing its M1 and M23 forms. B , C : The relative levels of Kir4.1 and AQP4 protein expression were quantified. Compared with that of the control, the expression of Kir4.1 was significantly reduced after LPS injection. In contrast, there was only a slight, statistically insignificant decline in AQP4 expression from 1 day to 7 day after LPS injection. (means±SEM, n=5; double asterisks (**) p<0.001 versus control). C indicates control; P indicates phosphate-buffered saline; L indicates lipopolysaccharide.

    Journal: Molecular Vision

    Article Title: Differential expression of Kir4.1 and aquaporin 4 in the retina from endotoxin-induced uveitis rat

    doi:

    Figure Lengend Snippet: Time courses of Kir4.1 and aquaporin-4 protein expression in retinas from lipopolysaccharide- or phosphate-buffered saline-treated rats. A : Equal amounts of protein (30 μg) were subjected to immunoblotting analysis. A band at about 200 kDa represents Kir4.1 in its tetrameric form; aquaporin-4 (AQP4) consists of two bands, representing its M1 and M23 forms. B , C : The relative levels of Kir4.1 and AQP4 protein expression were quantified. Compared with that of the control, the expression of Kir4.1 was significantly reduced after LPS injection. In contrast, there was only a slight, statistically insignificant decline in AQP4 expression from 1 day to 7 day after LPS injection. (means±SEM, n=5; double asterisks (**) p<0.001 versus control). C indicates control; P indicates phosphate-buffered saline; L indicates lipopolysaccharide.

    Article Snippet: The primary antibodies were rabbit anti-Kir4.1 (1:200; Alomone Laboratories, Jerusalem, Israel), rabbit anti-AQP4 (1:250, Chemicon, Temecula, CA), and mouse anti-glial fibrillary acidic protein (GFAP; 1:1000, Transduction Laboratories, Lexington, KY).

    Techniques: Expressing, Western Blot, Injection

    Impaired astrocytes were subsequently recovered in the LPS-injected SNpc. ( A - D ) LPS (5 μg/2 μl) was injected into the SNpc. Sections obtained at the indicated times after LPS injection were labeled with antibodies specific for GFAP ( A ), S100β ( B ), EAAT1 ( C ), and Kir 4.1 ( D ), and visualized with peroxidase-conjugated secondary antibodies. Lower panels (SNpc and SNr) are higher magnification images of boxed areas (SNpc and SNr) in upper panels. Arrows indicate GFAP + ( A ), S100β + ( B ) EAAT1 + ( C ) and Kir4.1 + ( D ) cells. Contralateral (Contra) sides of LPS-injected animals and PBS-injected animals were used as controls. Asterisks (*) indicate injection sites. Scale bars, 1 mm (upper panels in A ), 200 μm (upper panels in C - E ), 50 μm (lower panels in A ), 20 μm (lower panels in C - E ). ( E - H ) GFAP-, S100β-, EAAT1-, and Kir 4.1-negative areas in every sixth brain section were quantified using Axiovision image analysis software, as described in “Materials and Methods”. Values are means ± SEMs of at least three samples (*p < 0.01; **p < 0.001; Student’s t -test). Three or more animals were used for each time point. All data presented in this study are representative of at least three independent experiments unless indicated.

    Journal: Molecular Brain

    Article Title: Repair of astrocytes, blood vessels, and myelin in the injured brain: possible roles of blood monocytes

    doi: 10.1186/1756-6606-6-28

    Figure Lengend Snippet: Impaired astrocytes were subsequently recovered in the LPS-injected SNpc. ( A - D ) LPS (5 μg/2 μl) was injected into the SNpc. Sections obtained at the indicated times after LPS injection were labeled with antibodies specific for GFAP ( A ), S100β ( B ), EAAT1 ( C ), and Kir 4.1 ( D ), and visualized with peroxidase-conjugated secondary antibodies. Lower panels (SNpc and SNr) are higher magnification images of boxed areas (SNpc and SNr) in upper panels. Arrows indicate GFAP + ( A ), S100β + ( B ) EAAT1 + ( C ) and Kir4.1 + ( D ) cells. Contralateral (Contra) sides of LPS-injected animals and PBS-injected animals were used as controls. Asterisks (*) indicate injection sites. Scale bars, 1 mm (upper panels in A ), 200 μm (upper panels in C - E ), 50 μm (lower panels in A ), 20 μm (lower panels in C - E ). ( E - H ) GFAP-, S100β-, EAAT1-, and Kir 4.1-negative areas in every sixth brain section were quantified using Axiovision image analysis software, as described in “Materials and Methods”. Values are means ± SEMs of at least three samples (*p < 0.01; **p < 0.001; Student’s t -test). Three or more animals were used for each time point. All data presented in this study are representative of at least three independent experiments unless indicated.

    Article Snippet: Kir4.1 , rabbit , 1:800 , apc-035 , Alomone.

    Techniques: Injection, Labeling, Software

    Primary antibodies used in immunohistochemistry

    Journal: Molecular Brain

    Article Title: Repair of astrocytes, blood vessels, and myelin in the injured brain: possible roles of blood monocytes

    doi: 10.1186/1756-6606-6-28

    Figure Lengend Snippet: Primary antibodies used in immunohistochemistry

    Article Snippet: Kir4.1 , rabbit , 1:800 , apc-035 , Alomone.

    Techniques:

    A , Bdp1 protein expression in the cochlea at postnatal day 5. Bdp1 shows expression in the stria vascularis (red arrow), Reissner's membrane (red arrowhead), basilar membrane (black arrowhead), and spiral ligament (black arrow). B–D , Bdp1, Kcnj10 and laminin expression in the stria vascularis. Our immunohistochemistry detected Bdp1 protein in the proximity of blood vessels (example of the same blood vessel in adjacent sections is indicated with an arrow in B, C, D). We used Kcnj10 as a marker of intermediate cells (C) and laminin as a marker of the basal lamina surrounding blood vessels (D) in the stria vascularis in the sections shown in A. The expression pattern suggests that Bdp1 is expressed in endothelial cells of the stria vascularis. Scale bars: A: 50 µm; B–D: 10 µm. sv: stria vascularis.

    Journal: PLoS ONE

    Article Title: Linkage Study and Exome Sequencing Identify a BDP1 Mutation Associated with Hereditary Hearing Loss

    doi: 10.1371/journal.pone.0080323

    Figure Lengend Snippet: A , Bdp1 protein expression in the cochlea at postnatal day 5. Bdp1 shows expression in the stria vascularis (red arrow), Reissner's membrane (red arrowhead), basilar membrane (black arrowhead), and spiral ligament (black arrow). B–D , Bdp1, Kcnj10 and laminin expression in the stria vascularis. Our immunohistochemistry detected Bdp1 protein in the proximity of blood vessels (example of the same blood vessel in adjacent sections is indicated with an arrow in B, C, D). We used Kcnj10 as a marker of intermediate cells (C) and laminin as a marker of the basal lamina surrounding blood vessels (D) in the stria vascularis in the sections shown in A. The expression pattern suggests that Bdp1 is expressed in endothelial cells of the stria vascularis. Scale bars: A: 50 µm; B–D: 10 µm. sv: stria vascularis.

    Article Snippet: The primary antibodies were anti-Bdp1 (Abcam: Ab74415; 1∶50), anti-Lama1 (laminin, alpha 1; Abcam, Cambridge, Uk, cat.no ab11575; 1∶100), anti-Kcnj10 (Alomone Labs, Jerusalem, Israel, cat.no APC-035; 1∶300), while the secondary antibodies used were Epitomics (Burlingame, CA, USA) anti-mouse IgG (3021–1; 1∶500) and Jackson ImmunoResearch (West Grove, PA, USA) biotin conjugated donkey anti-rabbit (711–065–152; 1∶100).

    Techniques: Expressing, Immunohistochemistry, Marker