mmk1  (Alomone Labs)


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    Structured Review

    Alomone Labs mmk1
    Mmk1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 90/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mmk1/product/Alomone Labs
    Average 90 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    mmk1 - by Bioz Stars, 2022-11
    90/100 stars

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  • 94
    Alomone Labs primary antibodies against kca 3 1
    Effects of a 24 h treatment with various signaling pathway inhibitors on IL-10 and IL-8 expression and effects of the 24 h treatment with the <t>ERK1/2</t> inhibitor, SCH772984 and JNK inhibitor, SP600125 on IL-10 and IL-8 secretion in THP-1-derived M 2 macrophages. ( A , D ): Real-time PCR examination of IL-10 ( A ) and IL-8 ( D ) expression in SCH772964 (1 μM)-, SP600125 (10 μM)-, PD169316 (10 μM)-, LY294002 (10 μM)-, AZD5363 (2 μM)-, everolimus (10 nM)-, LY364947 (10 μM)-, ciclosporin A (CsA, 1 μM)-, T-5224 (10 μM)-, and Bay11-7082 (10 μM)-treated THP-1-derived M 2 macrophages for 24 h. Relative mRNA expression in the vehicle control is expressed as 1.0 (n = 4 for each). ( B , C , E , F ): Quantitative detection of IL-10 ( B , C ) and/or IL-8 ( E , F ) secretion by an ELISA assay in SCH772964 ( B , E )- and SP600125 ( C , F )-treated THP-1-derived M 2 macrophages. Relative cytokine secretion in the vehicle control is expressed as 1.0 (n = 4 for each). **: p
    Primary Antibodies Against Kca 3 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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    98
    Cell Signaling Technology Inc phospho p44 42 mapk erk1 2 thr202 tyr204 antibody
    ( A ) Expression of P-ERK 1/2 in neonatal rat cardiomyocytes. Total proteins were extracted from neonatal rat ventricular cardiomyocytes. Cells were treated with 1 µM Norepinephrine (NE) for 4–24 h or pre-treated with either U0126 <t>(P-ERK1/2</t> inhibitor) or metoprolol tartrate (β1-blocker) for 1 h followed by treatment with NE for 24 h. Proteins were separated on an 8% SDS-polyacrylamide gel, transferred to a nitrocellulose membrane, and probed with anti-P-ERK, anti-total-ERK antibodies overnight and then incubated with HRP-conjugated goat anti-rabbit secondary antibody. Lanes were loaded with 30 μg of proteins. NE: cardiomyocytes treated with 1 µM norepinephrine, 24 h + U0126: Cardiomyocytes pre-treated with U0126 for 1 h followed by treatment with NE for 24 h. 24 h + β1-blocker: Cardiomyocytes pre-treated with metoprolol tartrate (β1-blocker) for 1 h followed by treatment with NE for 24 h. ( B ) Graph showing the total protein expression of P-ERK normalized to total-ERK. * p
    Phospho P44 42 Mapk Erk1 2 Thr202 Tyr204 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Alomone Labs cd90 2 antibody anti mouse
    Adeno-associated virus (AAV)-mediated deletion of Per2 in glial cells of adult mice leads to a depression resistant behavior. (A) Fluorescent imaging of whole brains 3 weeks after no injection (left), intravenous (i.v.) injection of the engineered AAV-PHP.eB, which can pass the blood-brain barrier (BBB), containing the general CAG driver (second from left) or the glial Gfap driver (middle). The second to last brain is from an animal with i.v. injected AAV-9, which does not pass the BBB, containing the general CAG driver. The last brain (right) is from an animal injected intraperitoneally (i.p.) with the AAV-PHP.eB Gfap -driven construct. Note that only the brains of animals that received the AAV-PHP.eb i.v. display significant fluorescent signal after 3 weeks (orange and yellow color). (B) Fluorescent imaging of whole brains 2 months after injection of the AAV-PHP.eB. Note that the fluorescence is still maintained after 2 months post injection and that even the i.p. injected AAV-PHP.eB Gfap is showing signal in the brain now. (C) Sorting of neurons and astrocytes by flow cytometry from brain tissue including the nucleus accumbens (NAc). The left panel shows the removal of debris from a single cell suspension, showing the distribution of debris in the forward as well as in the side scatter (FSC and SSC, respectively). The middle panel shows the removal of CD11b + cells (microglia) from the cell suspension (lower left corner from left panel). The CD11b - cells (bottom half from middle panel) were then sorted into two distinct cell populations corresponding to astrocytes (GLT1 + <t>/CD90.2</t> - ) and neurons (CD90.2 + /GLT1 - ) (right panel). (D) PCR analysis of astrocytes and neurons from the cell sorting. Microglia (CD11 + ) as well as astrocytes (GLT1 + /CD90.2 - ), but not neurons (CD90.2 + /GLT1 - ) from PHP.eB Gfap-iCre infected animals show the presence of iCre , indicating that only glia and not neurons could express iCre in order to delete Per2 in the Per2 fl/fl mice. (E) Immunohistochemistry of vG Per2 brain tissue from nucleus accumbens (NAc) isolated at ZT6. The signal for PER2 (green) mainly overlaps with neuronal NeuN signal (red) giving rise to the yellow color. Scale bar: 100 µm. (F) Immobility time in the forced swim test (FST) of vG Per2 (PHP.eB Gfap-iCre , green) and control (PHP.eB control, blue) animals are shown (n = 5, two-tailed t-test, *p
    Cd90 2 Antibody Anti Mouse, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Alomone Labs drug preparation 206 iberiotoxin
    Adeno-associated virus (AAV)-mediated deletion of Per2 in glial cells of adult mice leads to a depression resistant behavior. (A) Fluorescent imaging of whole brains 3 weeks after no injection (left), intravenous (i.v.) injection of the engineered AAV-PHP.eB, which can pass the blood-brain barrier (BBB), containing the general CAG driver (second from left) or the glial Gfap driver (middle). The second to last brain is from an animal with i.v. injected AAV-9, which does not pass the BBB, containing the general CAG driver. The last brain (right) is from an animal injected intraperitoneally (i.p.) with the AAV-PHP.eB Gfap -driven construct. Note that only the brains of animals that received the AAV-PHP.eb i.v. display significant fluorescent signal after 3 weeks (orange and yellow color). (B) Fluorescent imaging of whole brains 2 months after injection of the AAV-PHP.eB. Note that the fluorescence is still maintained after 2 months post injection and that even the i.p. injected AAV-PHP.eB Gfap is showing signal in the brain now. (C) Sorting of neurons and astrocytes by flow cytometry from brain tissue including the nucleus accumbens (NAc). The left panel shows the removal of debris from a single cell suspension, showing the distribution of debris in the forward as well as in the side scatter (FSC and SSC, respectively). The middle panel shows the removal of CD11b + cells (microglia) from the cell suspension (lower left corner from left panel). The CD11b - cells (bottom half from middle panel) were then sorted into two distinct cell populations corresponding to astrocytes (GLT1 + <t>/CD90.2</t> - ) and neurons (CD90.2 + /GLT1 - ) (right panel). (D) PCR analysis of astrocytes and neurons from the cell sorting. Microglia (CD11 + ) as well as astrocytes (GLT1 + /CD90.2 - ), but not neurons (CD90.2 + /GLT1 - ) from PHP.eB Gfap-iCre infected animals show the presence of iCre , indicating that only glia and not neurons could express iCre in order to delete Per2 in the Per2 fl/fl mice. (E) Immunohistochemistry of vG Per2 brain tissue from nucleus accumbens (NAc) isolated at ZT6. The signal for PER2 (green) mainly overlaps with neuronal NeuN signal (red) giving rise to the yellow color. Scale bar: 100 µm. (F) Immobility time in the forced swim test (FST) of vG Per2 (PHP.eB Gfap-iCre , green) and control (PHP.eB control, blue) animals are shown (n = 5, two-tailed t-test, *p
    Drug Preparation 206 Iberiotoxin, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 93 stars, based on 1 article reviews
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    Effects of a 24 h treatment with various signaling pathway inhibitors on IL-10 and IL-8 expression and effects of the 24 h treatment with the ERK1/2 inhibitor, SCH772984 and JNK inhibitor, SP600125 on IL-10 and IL-8 secretion in THP-1-derived M 2 macrophages. ( A , D ): Real-time PCR examination of IL-10 ( A ) and IL-8 ( D ) expression in SCH772964 (1 μM)-, SP600125 (10 μM)-, PD169316 (10 μM)-, LY294002 (10 μM)-, AZD5363 (2 μM)-, everolimus (10 nM)-, LY364947 (10 μM)-, ciclosporin A (CsA, 1 μM)-, T-5224 (10 μM)-, and Bay11-7082 (10 μM)-treated THP-1-derived M 2 macrophages for 24 h. Relative mRNA expression in the vehicle control is expressed as 1.0 (n = 4 for each). ( B , C , E , F ): Quantitative detection of IL-10 ( B , C ) and/or IL-8 ( E , F ) secretion by an ELISA assay in SCH772964 ( B , E )- and SP600125 ( C , F )-treated THP-1-derived M 2 macrophages. Relative cytokine secretion in the vehicle control is expressed as 1.0 (n = 4 for each). **: p

    Journal: International Journal of Molecular Sciences

    Article Title: Downregulation of IL-8 and IL-10 by the Activation of Ca2+-Activated K+ Channel KCa3.1 in THP-1-Derived M2 Macrophages

    doi: 10.3390/ijms23158603

    Figure Lengend Snippet: Effects of a 24 h treatment with various signaling pathway inhibitors on IL-10 and IL-8 expression and effects of the 24 h treatment with the ERK1/2 inhibitor, SCH772984 and JNK inhibitor, SP600125 on IL-10 and IL-8 secretion in THP-1-derived M 2 macrophages. ( A , D ): Real-time PCR examination of IL-10 ( A ) and IL-8 ( D ) expression in SCH772964 (1 μM)-, SP600125 (10 μM)-, PD169316 (10 μM)-, LY294002 (10 μM)-, AZD5363 (2 μM)-, everolimus (10 nM)-, LY364947 (10 μM)-, ciclosporin A (CsA, 1 μM)-, T-5224 (10 μM)-, and Bay11-7082 (10 μM)-treated THP-1-derived M 2 macrophages for 24 h. Relative mRNA expression in the vehicle control is expressed as 1.0 (n = 4 for each). ( B , C , E , F ): Quantitative detection of IL-10 ( B , C ) and/or IL-8 ( E , F ) secretion by an ELISA assay in SCH772964 ( B , E )- and SP600125 ( C , F )-treated THP-1-derived M 2 macrophages. Relative cytokine secretion in the vehicle control is expressed as 1.0 (n = 4 for each). **: p

    Article Snippet: Primary antibodies against KCa 3.1 (rabbit polyclonal), ERK1/2 (rabbit polyclonal), phospho-ERK1(T202/Y204)/ERK2(T185/Y187) (rabbit monoclonal), JNK (rabbit polyclonal), phospho-JNK(Y185) (rabbit polyclonal), c-Jun (rabbit polyclonal), CREB (rabbit polyclonal), phospho-CREB(S133) (rabbit polyclonal), and β-actin (ACTB) (mouse monoclonal) were from Alomone Labs (Jerusalem, Israel), BioLegend (San Diego, CA, USA), R & D Systems (Minneapolis, MN, USA), GeneTex (Alton Pkwy Irvine, CA, USA), ProteinTech (Rosemont, IL, USA), Medical & Biological Laboratories (Nagoya, Japan), and ABclonal (Tokyo, Japan).

    Techniques: Expressing, Derivative Assay, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

    Protein expression levels of phosphorylated ERK1/2 (P-ERK1/2) and P-JNK in THP-1-derived M 2 macrophages following the SKA-121 treatment and high [K + ] e exposure. A – D : Western blot showing P-ERK1/2, total ERK1/2 (ERK1/2) ( A,B ), P-JNK, and total JNK (JNK) ( C , D ) in 1 μM SKA-121-treated ( A , C ) and high [K + ] e -exposed ( B , D ) THP-1-derived M 2 macrophages. Specific band signals were observed at 42 (P-ERK2), 42 (ERK2), 43/50 (P-JNK), and 43/50 (JNK) kDa. E – H : Summarized results of the relative protein expression of P-ERK2/ERK2 ( E , F ) and P-JNK/JNK ( G , H ) in 1 μM SKA-121-treated ( E , G ) and high [K + ] e -exposed ( F , H ) THP-1-derived M 2 macrophages. After compensation with the optical density of the ACTB signal (43 kDa), the expression level in the vehicle control or 5 mM K + is expressed as 1.0 (n = 4 for each). **: p

    Journal: International Journal of Molecular Sciences

    Article Title: Downregulation of IL-8 and IL-10 by the Activation of Ca2+-Activated K+ Channel KCa3.1 in THP-1-Derived M2 Macrophages

    doi: 10.3390/ijms23158603

    Figure Lengend Snippet: Protein expression levels of phosphorylated ERK1/2 (P-ERK1/2) and P-JNK in THP-1-derived M 2 macrophages following the SKA-121 treatment and high [K + ] e exposure. A – D : Western blot showing P-ERK1/2, total ERK1/2 (ERK1/2) ( A,B ), P-JNK, and total JNK (JNK) ( C , D ) in 1 μM SKA-121-treated ( A , C ) and high [K + ] e -exposed ( B , D ) THP-1-derived M 2 macrophages. Specific band signals were observed at 42 (P-ERK2), 42 (ERK2), 43/50 (P-JNK), and 43/50 (JNK) kDa. E – H : Summarized results of the relative protein expression of P-ERK2/ERK2 ( E , F ) and P-JNK/JNK ( G , H ) in 1 μM SKA-121-treated ( E , G ) and high [K + ] e -exposed ( F , H ) THP-1-derived M 2 macrophages. After compensation with the optical density of the ACTB signal (43 kDa), the expression level in the vehicle control or 5 mM K + is expressed as 1.0 (n = 4 for each). **: p

    Article Snippet: Primary antibodies against KCa 3.1 (rabbit polyclonal), ERK1/2 (rabbit polyclonal), phospho-ERK1(T202/Y204)/ERK2(T185/Y187) (rabbit monoclonal), JNK (rabbit polyclonal), phospho-JNK(Y185) (rabbit polyclonal), c-Jun (rabbit polyclonal), CREB (rabbit polyclonal), phospho-CREB(S133) (rabbit polyclonal), and β-actin (ACTB) (mouse monoclonal) were from Alomone Labs (Jerusalem, Israel), BioLegend (San Diego, CA, USA), R & D Systems (Minneapolis, MN, USA), GeneTex (Alton Pkwy Irvine, CA, USA), ProteinTech (Rosemont, IL, USA), Medical & Biological Laboratories (Nagoya, Japan), and ABclonal (Tokyo, Japan).

    Techniques: Expressing, Derivative Assay, Western Blot

    ( A ) Expression of P-ERK 1/2 in neonatal rat cardiomyocytes. Total proteins were extracted from neonatal rat ventricular cardiomyocytes. Cells were treated with 1 µM Norepinephrine (NE) for 4–24 h or pre-treated with either U0126 (P-ERK1/2 inhibitor) or metoprolol tartrate (β1-blocker) for 1 h followed by treatment with NE for 24 h. Proteins were separated on an 8% SDS-polyacrylamide gel, transferred to a nitrocellulose membrane, and probed with anti-P-ERK, anti-total-ERK antibodies overnight and then incubated with HRP-conjugated goat anti-rabbit secondary antibody. Lanes were loaded with 30 μg of proteins. NE: cardiomyocytes treated with 1 µM norepinephrine, 24 h + U0126: Cardiomyocytes pre-treated with U0126 for 1 h followed by treatment with NE for 24 h. 24 h + β1-blocker: Cardiomyocytes pre-treated with metoprolol tartrate (β1-blocker) for 1 h followed by treatment with NE for 24 h. ( B ) Graph showing the total protein expression of P-ERK normalized to total-ERK. * p

    Journal: Cells

    Article Title: Sympathetic Stimulation Upregulates the Ca2+ Channel Subunit, CaVα2δ1, via the β1 and ERK 1/2 Pathway in Neonatal Ventricular Cardiomyocytes

    doi: 10.3390/cells11020188

    Figure Lengend Snippet: ( A ) Expression of P-ERK 1/2 in neonatal rat cardiomyocytes. Total proteins were extracted from neonatal rat ventricular cardiomyocytes. Cells were treated with 1 µM Norepinephrine (NE) for 4–24 h or pre-treated with either U0126 (P-ERK1/2 inhibitor) or metoprolol tartrate (β1-blocker) for 1 h followed by treatment with NE for 24 h. Proteins were separated on an 8% SDS-polyacrylamide gel, transferred to a nitrocellulose membrane, and probed with anti-P-ERK, anti-total-ERK antibodies overnight and then incubated with HRP-conjugated goat anti-rabbit secondary antibody. Lanes were loaded with 30 μg of proteins. NE: cardiomyocytes treated with 1 µM norepinephrine, 24 h + U0126: Cardiomyocytes pre-treated with U0126 for 1 h followed by treatment with NE for 24 h. 24 h + β1-blocker: Cardiomyocytes pre-treated with metoprolol tartrate (β1-blocker) for 1 h followed by treatment with NE for 24 h. ( B ) Graph showing the total protein expression of P-ERK normalized to total-ERK. * p

    Article Snippet: Antibodies used were rabbit anti-CaV α2δ1 (1:1000, Alomone ACC-015), rabbit CaV α1C (1:1000, Alomone ACC-003), rabbit CaV β2 (1:5000, Alomone ACC-105), rabbit CaVβ3 (1:500, Alomone ACC-008), rabbit Phospho-ERK 1/2 (Cell Signaling Technology, Danvers, MA, USA, 9101S), Total ERK 1/2 (Cell Signaling Technology, 137F5) and rabbit GAPDH (Jackson, West Grove, PA, USA, 111-035-144).

    Techniques: Expressing, Incubation

    ( A ) Expression of p -ERK 1/2 in neonatal rat cardiomyocytes. Total proteins were extracted from neonatal rat ventricular cardiomyocytes. Proteins were separated on an 8% SDS-polyacrylamide gel, transferred to a nitrocellulose membrane, and probed with anti-P-ERK1/2 and anti-total-ERK antibodies overnight, and then incubated with HRP-conjugated goat anti-rabbit secondary antibody. Lanes were loaded with 30 μg of proteins. NE: cardiomyocytes treated with 1 µM norepinephrine. ( B ) Graph showing the total protein expression of P-ERK 1/2 normalized to total-ERK 1/2. * p

    Journal: Cells

    Article Title: Sympathetic Stimulation Upregulates the Ca2+ Channel Subunit, CaVα2δ1, via the β1 and ERK 1/2 Pathway in Neonatal Ventricular Cardiomyocytes

    doi: 10.3390/cells11020188

    Figure Lengend Snippet: ( A ) Expression of p -ERK 1/2 in neonatal rat cardiomyocytes. Total proteins were extracted from neonatal rat ventricular cardiomyocytes. Proteins were separated on an 8% SDS-polyacrylamide gel, transferred to a nitrocellulose membrane, and probed with anti-P-ERK1/2 and anti-total-ERK antibodies overnight, and then incubated with HRP-conjugated goat anti-rabbit secondary antibody. Lanes were loaded with 30 μg of proteins. NE: cardiomyocytes treated with 1 µM norepinephrine. ( B ) Graph showing the total protein expression of P-ERK 1/2 normalized to total-ERK 1/2. * p

    Article Snippet: Antibodies used were rabbit anti-CaV α2δ1 (1:1000, Alomone ACC-015), rabbit CaV α1C (1:1000, Alomone ACC-003), rabbit CaV β2 (1:5000, Alomone ACC-105), rabbit CaVβ3 (1:500, Alomone ACC-008), rabbit Phospho-ERK 1/2 (Cell Signaling Technology, Danvers, MA, USA, 9101S), Total ERK 1/2 (Cell Signaling Technology, 137F5) and rabbit GAPDH (Jackson, West Grove, PA, USA, 111-035-144).

    Techniques: Expressing, Incubation

    Adeno-associated virus (AAV)-mediated deletion of Per2 in glial cells of adult mice leads to a depression resistant behavior. (A) Fluorescent imaging of whole brains 3 weeks after no injection (left), intravenous (i.v.) injection of the engineered AAV-PHP.eB, which can pass the blood-brain barrier (BBB), containing the general CAG driver (second from left) or the glial Gfap driver (middle). The second to last brain is from an animal with i.v. injected AAV-9, which does not pass the BBB, containing the general CAG driver. The last brain (right) is from an animal injected intraperitoneally (i.p.) with the AAV-PHP.eB Gfap -driven construct. Note that only the brains of animals that received the AAV-PHP.eb i.v. display significant fluorescent signal after 3 weeks (orange and yellow color). (B) Fluorescent imaging of whole brains 2 months after injection of the AAV-PHP.eB. Note that the fluorescence is still maintained after 2 months post injection and that even the i.p. injected AAV-PHP.eB Gfap is showing signal in the brain now. (C) Sorting of neurons and astrocytes by flow cytometry from brain tissue including the nucleus accumbens (NAc). The left panel shows the removal of debris from a single cell suspension, showing the distribution of debris in the forward as well as in the side scatter (FSC and SSC, respectively). The middle panel shows the removal of CD11b + cells (microglia) from the cell suspension (lower left corner from left panel). The CD11b - cells (bottom half from middle panel) were then sorted into two distinct cell populations corresponding to astrocytes (GLT1 + /CD90.2 - ) and neurons (CD90.2 + /GLT1 - ) (right panel). (D) PCR analysis of astrocytes and neurons from the cell sorting. Microglia (CD11 + ) as well as astrocytes (GLT1 + /CD90.2 - ), but not neurons (CD90.2 + /GLT1 - ) from PHP.eB Gfap-iCre infected animals show the presence of iCre , indicating that only glia and not neurons could express iCre in order to delete Per2 in the Per2 fl/fl mice. (E) Immunohistochemistry of vG Per2 brain tissue from nucleus accumbens (NAc) isolated at ZT6. The signal for PER2 (green) mainly overlaps with neuronal NeuN signal (red) giving rise to the yellow color. Scale bar: 100 µm. (F) Immobility time in the forced swim test (FST) of vG Per2 (PHP.eB Gfap-iCre , green) and control (PHP.eB control, blue) animals are shown (n = 5, two-tailed t-test, *p

    Journal: bioRxiv

    Article Title: Deletion of the Clock Gene Period2 (Per2) in Glial Cells Alters Mood-Related Behavior in Mice

    doi: 10.1101/2020.12.09.417162

    Figure Lengend Snippet: Adeno-associated virus (AAV)-mediated deletion of Per2 in glial cells of adult mice leads to a depression resistant behavior. (A) Fluorescent imaging of whole brains 3 weeks after no injection (left), intravenous (i.v.) injection of the engineered AAV-PHP.eB, which can pass the blood-brain barrier (BBB), containing the general CAG driver (second from left) or the glial Gfap driver (middle). The second to last brain is from an animal with i.v. injected AAV-9, which does not pass the BBB, containing the general CAG driver. The last brain (right) is from an animal injected intraperitoneally (i.p.) with the AAV-PHP.eB Gfap -driven construct. Note that only the brains of animals that received the AAV-PHP.eb i.v. display significant fluorescent signal after 3 weeks (orange and yellow color). (B) Fluorescent imaging of whole brains 2 months after injection of the AAV-PHP.eB. Note that the fluorescence is still maintained after 2 months post injection and that even the i.p. injected AAV-PHP.eB Gfap is showing signal in the brain now. (C) Sorting of neurons and astrocytes by flow cytometry from brain tissue including the nucleus accumbens (NAc). The left panel shows the removal of debris from a single cell suspension, showing the distribution of debris in the forward as well as in the side scatter (FSC and SSC, respectively). The middle panel shows the removal of CD11b + cells (microglia) from the cell suspension (lower left corner from left panel). The CD11b - cells (bottom half from middle panel) were then sorted into two distinct cell populations corresponding to astrocytes (GLT1 + /CD90.2 - ) and neurons (CD90.2 + /GLT1 - ) (right panel). (D) PCR analysis of astrocytes and neurons from the cell sorting. Microglia (CD11 + ) as well as astrocytes (GLT1 + /CD90.2 - ), but not neurons (CD90.2 + /GLT1 - ) from PHP.eB Gfap-iCre infected animals show the presence of iCre , indicating that only glia and not neurons could express iCre in order to delete Per2 in the Per2 fl/fl mice. (E) Immunohistochemistry of vG Per2 brain tissue from nucleus accumbens (NAc) isolated at ZT6. The signal for PER2 (green) mainly overlaps with neuronal NeuN signal (red) giving rise to the yellow color. Scale bar: 100 µm. (F) Immobility time in the forced swim test (FST) of vG Per2 (PHP.eB Gfap-iCre , green) and control (PHP.eB control, blue) animals are shown (n = 5, two-tailed t-test, *p

    Article Snippet: Antibodies targeted CD11b (fluorophore PECy7, ref. 552850, BD Pharmingen), CD90.2 (fluorophore PE, ref., 130-102-489, Miltenyi Biotech) and GLT1 (fluorophore ATTO 633, ref., AGC-022-FR, Alomone lab), and were used in a 1:100 dilution.

    Techniques: Mouse Assay, Imaging, Injection, Construct, Fluorescence, Flow Cytometry, Polymerase Chain Reaction, FACS, Infection, Immunohistochemistry, Isolation, Two Tailed Test