rbpms polyclonal antibodies  (ProSci Incorporated)


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    ProSci Incorporated rbpms polyclonal antibodies
    Rbpms Polyclonal Antibodies, supplied by ProSci Incorporated, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rbpms polyclonal antibodies/product/ProSci Incorporated
    Average 90 stars, based on 1 article reviews
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    anti rbpms  (ProSci Incorporated)


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    ProSci Incorporated anti rbpms
    GADD45a knockdown (KD) promotes RGC soma and axon survival and preserves visual function in SOHU glaucoma model (A) Representative confocal images of retina cross-sections showing GADD45a (red) mRNA expression in GCL <t>by</t> <t>immunostaining</t> at 1wpi. Scale bar, 20 μm. (B) Quantification of mean fluorescence intensity of GADD45α in GCL. n = 5. All the data are presented as means ± SEM. ∗∗∗p < 0.001, two-tailed unpaired t test. (C) IOP measurements at 3wpi. Naive, n = 13; WT SOHU, n = 13; GADD45a KD, n = 11. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, one-way ANOVA with Tukey’s multiple comparisons test. (D) Visual acuity measured by OKR at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 10. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, two-tailed unpaired t test. (E) Quantification of P1-N2 amplitude of PERG at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 6. Data are presented as means ± SEM, ∗p < 0.05, two-tailed unpaired t test. (F) Quantification of GCC thickness measured by OCT at 3wpi, represented as percentage of GCC thickness in the SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗∗p < 0.001, two-tailed unpaired t test. (G) Upper panel, representative confocal images of peripheral flat-mounted retinas showing surviving <t>RBPMS-positive</t> (red) RGCs at 3wpi. Scale bar, 20 μm. Lower panel, light microscope images of semi-thin transverse sections of ON with PPD staining at 3wpi. Scale bar, 10 μm. (H) Quantification of surviving RGC somata and axons at 3wpi, represented as percentage of glaucomatous eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗p < 0.01, two-tailed unpaired t test.
    Anti Rbpms, supplied by ProSci Incorporated, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 86 stars, based on 1 article reviews
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    Images

    1) Product Images from "RGC-specific ATF4 and/or CHOP deletion rescues glaucomatous neurodegeneration and visual function"

    Article Title: RGC-specific ATF4 and/or CHOP deletion rescues glaucomatous neurodegeneration and visual function

    Journal: Molecular Therapy. Nucleic Acids

    doi: 10.1016/j.omtn.2023.07.015

    GADD45a knockdown (KD) promotes RGC soma and axon survival and preserves visual function in SOHU glaucoma model (A) Representative confocal images of retina cross-sections showing GADD45a (red) mRNA expression in GCL by immunostaining at 1wpi. Scale bar, 20 μm. (B) Quantification of mean fluorescence intensity of GADD45α in GCL. n = 5. All the data are presented as means ± SEM. ∗∗∗p < 0.001, two-tailed unpaired t test. (C) IOP measurements at 3wpi. Naive, n = 13; WT SOHU, n = 13; GADD45a KD, n = 11. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, one-way ANOVA with Tukey’s multiple comparisons test. (D) Visual acuity measured by OKR at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 10. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, two-tailed unpaired t test. (E) Quantification of P1-N2 amplitude of PERG at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 6. Data are presented as means ± SEM, ∗p < 0.05, two-tailed unpaired t test. (F) Quantification of GCC thickness measured by OCT at 3wpi, represented as percentage of GCC thickness in the SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗∗p < 0.001, two-tailed unpaired t test. (G) Upper panel, representative confocal images of peripheral flat-mounted retinas showing surviving RBPMS-positive (red) RGCs at 3wpi. Scale bar, 20 μm. Lower panel, light microscope images of semi-thin transverse sections of ON with PPD staining at 3wpi. Scale bar, 10 μm. (H) Quantification of surviving RGC somata and axons at 3wpi, represented as percentage of glaucomatous eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗p < 0.01, two-tailed unpaired t test.
    Figure Legend Snippet: GADD45a knockdown (KD) promotes RGC soma and axon survival and preserves visual function in SOHU glaucoma model (A) Representative confocal images of retina cross-sections showing GADD45a (red) mRNA expression in GCL by immunostaining at 1wpi. Scale bar, 20 μm. (B) Quantification of mean fluorescence intensity of GADD45α in GCL. n = 5. All the data are presented as means ± SEM. ∗∗∗p < 0.001, two-tailed unpaired t test. (C) IOP measurements at 3wpi. Naive, n = 13; WT SOHU, n = 13; GADD45a KD, n = 11. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, one-way ANOVA with Tukey’s multiple comparisons test. (D) Visual acuity measured by OKR at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 10. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, two-tailed unpaired t test. (E) Quantification of P1-N2 amplitude of PERG at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 6. Data are presented as means ± SEM, ∗p < 0.05, two-tailed unpaired t test. (F) Quantification of GCC thickness measured by OCT at 3wpi, represented as percentage of GCC thickness in the SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗∗p < 0.001, two-tailed unpaired t test. (G) Upper panel, representative confocal images of peripheral flat-mounted retinas showing surviving RBPMS-positive (red) RGCs at 3wpi. Scale bar, 20 μm. Lower panel, light microscope images of semi-thin transverse sections of ON with PPD staining at 3wpi. Scale bar, 10 μm. (H) Quantification of surviving RGC somata and axons at 3wpi, represented as percentage of glaucomatous eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗p < 0.01, two-tailed unpaired t test.

    Techniques Used: Expressing, Immunostaining, Fluorescence, Two Tailed Test, Light Microscopy, Staining

    anti rbpms  (ProSci Incorporated)


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    ProSci Incorporated anti rbpms
    Intravitreal injection of SARM1 ASO significantly inhibits SARM1 in retina and protects RGC axons, but not RGC somata, in the mouse ONC model (A) Representative confocal images of retina cross sections showing widespread ASO distribution in <t>RBPMS</t> + RGCs within the ganglion cell layer (GCL) and other layers of retina 2 weeks after intravitreal ASO injection. ASO was immunostained with ASO antibody. Scale bar, 20 μm. (B) Quantitative real-time RT-PCR showing significant downregulation of SARM1 mRNA in retinas 4 weeks after intravitreal ASO injection in naive mice. Data are normalized to the control ASO group. Data are presented as means ± SEM; n = 3; ∗∗∗p < 0.001; two-tailed paired t test. (C) Top panel: representative confocal images of peripheral flat-mounted retinas showing surviving RBPMS + RGCs (red) at 14 days post-ONC (14 days post-crush [dpc]). Scale bar, 20 μm. Bottom panel: representative light microscope images of semi-thin transverse ON sections with PPD staining at 14 dpc. Scale bar, 5 μm. (D) Quantification of surviving RGC somata (left panel) and axons (right panel) at 14 dpc, represented as percentage of crush-injured eyes compared with the sham contralateral control eyes. Data are presented as means ± SEM, n = 5 of WT and SARM1 KO- and SARM1 ASO-treated mice; ns, no significant difference; ∗∗p < 0.01, ∗∗∗p < 0.001; one-way ANOVA with Tukey’s multiple comparisons test.
    Anti Rbpms, supplied by ProSci Incorporated, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti rbpms - by Bioz Stars, 2024-02
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    Images

    1) Product Images from "Differential effects of SARM1 inhibition in traumatic glaucoma and EAE optic neuropathies"

    Article Title: Differential effects of SARM1 inhibition in traumatic glaucoma and EAE optic neuropathies

    Journal: Molecular Therapy. Nucleic Acids

    doi: 10.1016/j.omtn.2023.02.029

    Intravitreal injection of SARM1 ASO significantly inhibits SARM1 in retina and protects RGC axons, but not RGC somata, in the mouse ONC model (A) Representative confocal images of retina cross sections showing widespread ASO distribution in RBPMS + RGCs within the ganglion cell layer (GCL) and other layers of retina 2 weeks after intravitreal ASO injection. ASO was immunostained with ASO antibody. Scale bar, 20 μm. (B) Quantitative real-time RT-PCR showing significant downregulation of SARM1 mRNA in retinas 4 weeks after intravitreal ASO injection in naive mice. Data are normalized to the control ASO group. Data are presented as means ± SEM; n = 3; ∗∗∗p < 0.001; two-tailed paired t test. (C) Top panel: representative confocal images of peripheral flat-mounted retinas showing surviving RBPMS + RGCs (red) at 14 days post-ONC (14 days post-crush [dpc]). Scale bar, 20 μm. Bottom panel: representative light microscope images of semi-thin transverse ON sections with PPD staining at 14 dpc. Scale bar, 5 μm. (D) Quantification of surviving RGC somata (left panel) and axons (right panel) at 14 dpc, represented as percentage of crush-injured eyes compared with the sham contralateral control eyes. Data are presented as means ± SEM, n = 5 of WT and SARM1 KO- and SARM1 ASO-treated mice; ns, no significant difference; ∗∗p < 0.01, ∗∗∗p < 0.001; one-way ANOVA with Tukey’s multiple comparisons test.
    Figure Legend Snippet: Intravitreal injection of SARM1 ASO significantly inhibits SARM1 in retina and protects RGC axons, but not RGC somata, in the mouse ONC model (A) Representative confocal images of retina cross sections showing widespread ASO distribution in RBPMS + RGCs within the ganglion cell layer (GCL) and other layers of retina 2 weeks after intravitreal ASO injection. ASO was immunostained with ASO antibody. Scale bar, 20 μm. (B) Quantitative real-time RT-PCR showing significant downregulation of SARM1 mRNA in retinas 4 weeks after intravitreal ASO injection in naive mice. Data are normalized to the control ASO group. Data are presented as means ± SEM; n = 3; ∗∗∗p < 0.001; two-tailed paired t test. (C) Top panel: representative confocal images of peripheral flat-mounted retinas showing surviving RBPMS + RGCs (red) at 14 days post-ONC (14 days post-crush [dpc]). Scale bar, 20 μm. Bottom panel: representative light microscope images of semi-thin transverse ON sections with PPD staining at 14 dpc. Scale bar, 5 μm. (D) Quantification of surviving RGC somata (left panel) and axons (right panel) at 14 dpc, represented as percentage of crush-injured eyes compared with the sham contralateral control eyes. Data are presented as means ± SEM, n = 5 of WT and SARM1 KO- and SARM1 ASO-treated mice; ns, no significant difference; ∗∗p < 0.01, ∗∗∗p < 0.001; one-way ANOVA with Tukey’s multiple comparisons test.

    Techniques Used: Injection, Quantitative RT-PCR, Two Tailed Test, Light Microscopy, Staining

    SARM1 ASO significantly protects RGC somata and axons in the SOHU glaucoma model (A) IOP measured at 3 wpi. SOHU eyes are injected with SO intracamerally; mock eyes are contralateral eyes injected with PBS intracamerally. Data are presented as means ± SEM; control ASO, n = 18; SARM1 ASO, n = 18; ns, no significance; ∗∗∗p < 0.001; one-way ANOVA with Tukey’s multiple comparisons test. (B) Left panel: representative in vivo OCT images of mouse retina at 3 wpi. GCC, indicated as red double-ended arrows. Right panel: quantification of GCC thickness, represented as percentage of GCC thickness in the SOHU glaucomatous eyes compared with the mock contralateral control eyes. Control ASO, n = 20; SARM1 ASO, n = 21. Data are presented as means ± SEM; ∗p < 0.05; two-tailed t test. (C) Top panel: representative confocal images of flat-mounted whole retinas and peripheral retinas showing surviving RBPMS + RGCs (red) at 3 wpi. Bottom panel: representative light microscope images of semi-thin transverse sections of ON with PPD staining at 3 wpi. Scale bar: whole retina, 500 μm; peripheral retina, 20 μm; semi-thin sections of ON, 5 μm. (D) Top panel: quantification of surviving RGC somata in inner, middle, and peripheral retinas at 3 wpi, represented as percentage of RGC number in the SOHU glaucomatous eyes compared with the mock contralateral control eyes. Bottom panel: quantification of surviving axons, represented as percentage of axon number in the SOHU glaucomatous eyes compared with the mock contralateral control eyes. Control ASO, n = 21; SARM1 ASO, n = 21. Data are presented as means ± SEM; ∗p < 0.05, ∗∗∗p < 0.001; two-tailed t test. (E) Left panel: representative wave forms of PERG at 3 wpi. Black, SOHU glaucomatous eye; red, contralateral mock control eye. Right panel: quantification of P1-N2 amplitude of PERG in the SOHU glaucomatous eyes compared with the mock contralateral control eyes at 3 wpi. Control ASO, n = 19; SARM1 ASO, n = 18. Data are presented as means ± SEM; ns, no significance; two-tailed t test.
    Figure Legend Snippet: SARM1 ASO significantly protects RGC somata and axons in the SOHU glaucoma model (A) IOP measured at 3 wpi. SOHU eyes are injected with SO intracamerally; mock eyes are contralateral eyes injected with PBS intracamerally. Data are presented as means ± SEM; control ASO, n = 18; SARM1 ASO, n = 18; ns, no significance; ∗∗∗p < 0.001; one-way ANOVA with Tukey’s multiple comparisons test. (B) Left panel: representative in vivo OCT images of mouse retina at 3 wpi. GCC, indicated as red double-ended arrows. Right panel: quantification of GCC thickness, represented as percentage of GCC thickness in the SOHU glaucomatous eyes compared with the mock contralateral control eyes. Control ASO, n = 20; SARM1 ASO, n = 21. Data are presented as means ± SEM; ∗p < 0.05; two-tailed t test. (C) Top panel: representative confocal images of flat-mounted whole retinas and peripheral retinas showing surviving RBPMS + RGCs (red) at 3 wpi. Bottom panel: representative light microscope images of semi-thin transverse sections of ON with PPD staining at 3 wpi. Scale bar: whole retina, 500 μm; peripheral retina, 20 μm; semi-thin sections of ON, 5 μm. (D) Top panel: quantification of surviving RGC somata in inner, middle, and peripheral retinas at 3 wpi, represented as percentage of RGC number in the SOHU glaucomatous eyes compared with the mock contralateral control eyes. Bottom panel: quantification of surviving axons, represented as percentage of axon number in the SOHU glaucomatous eyes compared with the mock contralateral control eyes. Control ASO, n = 21; SARM1 ASO, n = 21. Data are presented as means ± SEM; ∗p < 0.05, ∗∗∗p < 0.001; two-tailed t test. (E) Left panel: representative wave forms of PERG at 3 wpi. Black, SOHU glaucomatous eye; red, contralateral mock control eye. Right panel: quantification of P1-N2 amplitude of PERG in the SOHU glaucomatous eyes compared with the mock contralateral control eyes at 3 wpi. Control ASO, n = 19; SARM1 ASO, n = 18. Data are presented as means ± SEM; ns, no significance; two-tailed t test.

    Techniques Used: Injection, In Vivo, Two Tailed Test, Light Microscopy, Staining

    RGC-specific SARM1 KD by AAV-mediated CRISPR shows similar neuroprotective effects as SARM1 ASO in both the ONC and SOHU glaucoma models (A) Schematic diagram of AAV vectors for Cas9 and SARM1 gRNAs expression. (B) Top panel: representative confocal images of peripheral flat-mounted retinas showing surviving RBPMS + RGCs (red) at 14 dpc following ONC. Scale bar, 20 μm. Bottom panel: representative light microscope images of semi-thin transverse ON sections with PPD staining at 14 dpc. Scale bar, 5 μm. (C) Quantification of surviving RGC somata (left panel) and axons (right panel) at 14 dpc, represented as percentage of crush-injured eyes compared with the sham contralateral control eyes. Control gRNA, n = 10; SARM1 gRNAs, n = 10. (D) IOP measured at 3 wpi. Control gRNA, n = 13; SARM1 gRNAs, n = 13. (E) Top panel: representative confocal images of flat-mounted whole retinas and peripheral retinas showing surviving RBPMS + RGCs (red) at 3 wpi in the SOHU glaucoma model. Bottom panel: representative light microscope images of semi-thin transverse sections of ON with PPD staining at 3 wpi. Scale bar: whole retina, 500 μm; peripheral retina, 20 μm; semi-thin sections of ON, 5 μm. (F) Top panel: quantification of surviving RGC somata in inner, middle, and peripheral retinas at 3 wpi, represented as percentage of RGC number in the SOHU glaucomatous eyes compared with the mock contralateral control eyes. Bottom panel: quantification of surviving axons, represented as percentage of axon number in the SOHU glaucomatous eyes compared with the mock contralateral control eyes. Control gRNA, n = 13; SARM1 gRNAs, n = 13. (G) Left panel: representative in vivo OCT images of mouse retina at 3 wpi. GCC, indicated as red double-ended arrows. Right panel: quantification of GCC thickness, represented as percentage of GCC thickness in the SOHU glaucomatous eyes compared with the mock contralateral control eyes. Control gRNA, n = 11; SARM1 gRNA, n = 10. (H) Left panel: representative wave forms of PERG at 3 wpi. Black, SOHU glaucomatous eye; red, mock contralateral control eye. Right panel: quantification of P1-N2 amplitude of PERG in the SOHU glaucomatous eye compared with the mock contralateral control eye at 3 wpi. Control gRNA, n = 12; SARM1 gRNA, n = 12. All data are presented as means ± SEM; ns, no significant difference; ∗∗p < 0.01, ∗∗∗p < 0.001; two-tailed t test, except in (D), with one-way ANOVA with Tukey’s multiple comparisons test.
    Figure Legend Snippet: RGC-specific SARM1 KD by AAV-mediated CRISPR shows similar neuroprotective effects as SARM1 ASO in both the ONC and SOHU glaucoma models (A) Schematic diagram of AAV vectors for Cas9 and SARM1 gRNAs expression. (B) Top panel: representative confocal images of peripheral flat-mounted retinas showing surviving RBPMS + RGCs (red) at 14 dpc following ONC. Scale bar, 20 μm. Bottom panel: representative light microscope images of semi-thin transverse ON sections with PPD staining at 14 dpc. Scale bar, 5 μm. (C) Quantification of surviving RGC somata (left panel) and axons (right panel) at 14 dpc, represented as percentage of crush-injured eyes compared with the sham contralateral control eyes. Control gRNA, n = 10; SARM1 gRNAs, n = 10. (D) IOP measured at 3 wpi. Control gRNA, n = 13; SARM1 gRNAs, n = 13. (E) Top panel: representative confocal images of flat-mounted whole retinas and peripheral retinas showing surviving RBPMS + RGCs (red) at 3 wpi in the SOHU glaucoma model. Bottom panel: representative light microscope images of semi-thin transverse sections of ON with PPD staining at 3 wpi. Scale bar: whole retina, 500 μm; peripheral retina, 20 μm; semi-thin sections of ON, 5 μm. (F) Top panel: quantification of surviving RGC somata in inner, middle, and peripheral retinas at 3 wpi, represented as percentage of RGC number in the SOHU glaucomatous eyes compared with the mock contralateral control eyes. Bottom panel: quantification of surviving axons, represented as percentage of axon number in the SOHU glaucomatous eyes compared with the mock contralateral control eyes. Control gRNA, n = 13; SARM1 gRNAs, n = 13. (G) Left panel: representative in vivo OCT images of mouse retina at 3 wpi. GCC, indicated as red double-ended arrows. Right panel: quantification of GCC thickness, represented as percentage of GCC thickness in the SOHU glaucomatous eyes compared with the mock contralateral control eyes. Control gRNA, n = 11; SARM1 gRNA, n = 10. (H) Left panel: representative wave forms of PERG at 3 wpi. Black, SOHU glaucomatous eye; red, mock contralateral control eye. Right panel: quantification of P1-N2 amplitude of PERG in the SOHU glaucomatous eye compared with the mock contralateral control eye at 3 wpi. Control gRNA, n = 12; SARM1 gRNA, n = 12. All data are presented as means ± SEM; ns, no significant difference; ∗∗p < 0.01, ∗∗∗p < 0.001; two-tailed t test, except in (D), with one-way ANOVA with Tukey’s multiple comparisons test.

    Techniques Used: CRISPR, Expressing, Light Microscopy, Staining, In Vivo, Two Tailed Test

    Local retina delivery of SARM1 ASO does not protect RGCs or ONs in the EAE/optic neuritis model (A) Representative in vivo OCT images of mouse retina at 5 wpi. BL, baseline; wpi, weeks post-immunization. GCC, indicated as red double-ended arrows. OD: right eye, control ASO; OS: left eye, SARM1 ASO. (B) Quantification of GCC thickness. Naive, n = 6; sham, n = 6; EAE, n = 12. Control ASO and SARM1 ASO were intravitreally injected into the two eyes of each animal for comparison. Data are presented as means ± SEM; ns, no significance; ∗∗∗p < 0.001; two-way ANOVA with Tukey’s multiple comparisons test. (C) Top panel: representative confocal images of peripheral flat-mounted retinas showing surviving RBPMS + RGCs (red) at 5 wpi. Bottom panel: representative light microscope images of semi-thin transverse sections of ON with PPD staining at 5 wpi. Scale bar: flat-mounted retina, 20 μm; semi-thin sections of ON, 5 μm. (D) Left panel: quantification of surviving RGC somata in peripheral retinas at 5 wpi. Right panel: quantification of surviving axons. Naive, n = 4; sham, n = 4; EAE, n = 11. Data are presented as means ± SEM; ns, no significance; ∗∗∗p < 0.001; two-way ANOVA with Tukey’s multiple comparisons test. (E) Left panel: representative TEM images of ON transverse section at 5 wpi in EAE mice. Scale bar, 1 μm. Right panel: quantification of surviving axons imaged by TEM. n = 3. Data are presented as means ± SEM; ns, no significance; paired two-tailed t test. (F) Left panel: representative wave forms of PERG at baseline (BL) and 5 wpi. Black, SARM1 ASO-injected eyes; red, control ASO-injected eyes. Right panel: quantification of P1-N2 amplitude of PERG at 5 wpi. Naive, n = 6; sham, n = 6; EAE, n = 12. Data are presented as means ± SEM; ns, no significance; ∗∗∗p < 0.001; two-way ANOVA with Tukey’s multiple comparisons test.
    Figure Legend Snippet: Local retina delivery of SARM1 ASO does not protect RGCs or ONs in the EAE/optic neuritis model (A) Representative in vivo OCT images of mouse retina at 5 wpi. BL, baseline; wpi, weeks post-immunization. GCC, indicated as red double-ended arrows. OD: right eye, control ASO; OS: left eye, SARM1 ASO. (B) Quantification of GCC thickness. Naive, n = 6; sham, n = 6; EAE, n = 12. Control ASO and SARM1 ASO were intravitreally injected into the two eyes of each animal for comparison. Data are presented as means ± SEM; ns, no significance; ∗∗∗p < 0.001; two-way ANOVA with Tukey’s multiple comparisons test. (C) Top panel: representative confocal images of peripheral flat-mounted retinas showing surviving RBPMS + RGCs (red) at 5 wpi. Bottom panel: representative light microscope images of semi-thin transverse sections of ON with PPD staining at 5 wpi. Scale bar: flat-mounted retina, 20 μm; semi-thin sections of ON, 5 μm. (D) Left panel: quantification of surviving RGC somata in peripheral retinas at 5 wpi. Right panel: quantification of surviving axons. Naive, n = 4; sham, n = 4; EAE, n = 11. Data are presented as means ± SEM; ns, no significance; ∗∗∗p < 0.001; two-way ANOVA with Tukey’s multiple comparisons test. (E) Left panel: representative TEM images of ON transverse section at 5 wpi in EAE mice. Scale bar, 1 μm. Right panel: quantification of surviving axons imaged by TEM. n = 3. Data are presented as means ± SEM; ns, no significance; paired two-tailed t test. (F) Left panel: representative wave forms of PERG at baseline (BL) and 5 wpi. Black, SARM1 ASO-injected eyes; red, control ASO-injected eyes. Right panel: quantification of P1-N2 amplitude of PERG at 5 wpi. Naive, n = 6; sham, n = 6; EAE, n = 12. Data are presented as means ± SEM; ns, no significance; ∗∗∗p < 0.001; two-way ANOVA with Tukey’s multiple comparisons test.

    Techniques Used: In Vivo, Injection, Light Microscopy, Staining, Two Tailed Test

    rbpms polypeptide  (ProSci Incorporated)


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    ProSci Incorporated rbpms polypeptide
    Rbpms Polypeptide, supplied by ProSci Incorporated, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rbpms polyclonal antibodies  (ProSci Incorporated)


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    ProSci Incorporated rbpms polyclonal antibodies
    Rbpms Polyclonal Antibodies, supplied by ProSci Incorporated, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rna binding protein multiple splice rbpms polypeptide  (ProSci Incorporated)


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    ProSci Incorporated rna binding protein multiple splice rbpms polypeptide
    Rna Binding Protein Multiple Splice Rbpms Polypeptide, supplied by ProSci Incorporated, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rna binding protein multiple splice rbpms polypeptide  (ProSci Incorporated)


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    ProSci Incorporated rbpms
    Loss of RGCs and glial reactivity two weeks after pONT. Double immunohistochemistry of <t>RBPMS</t> <t>and</t> <t>GFAP</t> was performed on retinal wholemounts. Compared to the contralateral control ( A – C ), noticeable dropout of RGCs was detected and reactive astrocytes were present in the nasal quadrant after pONT ( D – F ). A more dramatic loss of RGCs and increased astrocytic reactivity were noted in the temporal quadrant after pONT ( G – I ). N = nasal; T = temporal; RBPMS = RNA binding protein with multiple splicing; GFAP = glial fibrillary acidic protein; 2 wk = 2 weeks; pONT = partial optic nerve transection; CTL = control.
    Rbpms, supplied by ProSci Incorporated, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Differential Retinal Protein Expression in Primary and Secondary Retinal Ganglion Cell Degeneration Identified by Integrated SWATH and Target-Based Proteomics"

    Article Title: Differential Retinal Protein Expression in Primary and Secondary Retinal Ganglion Cell Degeneration Identified by Integrated SWATH and Target-Based Proteomics

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms22168592

    Loss of RGCs and glial reactivity two weeks after pONT. Double immunohistochemistry of RBPMS and GFAP was performed on retinal wholemounts. Compared to the contralateral control ( A – C ), noticeable dropout of RGCs was detected and reactive astrocytes were present in the nasal quadrant after pONT ( D – F ). A more dramatic loss of RGCs and increased astrocytic reactivity were noted in the temporal quadrant after pONT ( G – I ). N = nasal; T = temporal; RBPMS = RNA binding protein with multiple splicing; GFAP = glial fibrillary acidic protein; 2 wk = 2 weeks; pONT = partial optic nerve transection; CTL = control.
    Figure Legend Snippet: Loss of RGCs and glial reactivity two weeks after pONT. Double immunohistochemistry of RBPMS and GFAP was performed on retinal wholemounts. Compared to the contralateral control ( A – C ), noticeable dropout of RGCs was detected and reactive astrocytes were present in the nasal quadrant after pONT ( D – F ). A more dramatic loss of RGCs and increased astrocytic reactivity were noted in the temporal quadrant after pONT ( G – I ). N = nasal; T = temporal; RBPMS = RNA binding protein with multiple splicing; GFAP = glial fibrillary acidic protein; 2 wk = 2 weeks; pONT = partial optic nerve transection; CTL = control.

    Techniques Used: Immunohistochemistry, RNA Binding Assay

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    ProSci Incorporated rbpms polyclonal antibodies
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    GADD45a knockdown (KD) promotes RGC soma and axon survival and preserves visual function in SOHU glaucoma model (A) Representative confocal images of retina cross-sections showing GADD45a (red) mRNA expression in GCL <t>by</t> <t>immunostaining</t> at 1wpi. Scale bar, 20 μm. (B) Quantification of mean fluorescence intensity of GADD45α in GCL. n = 5. All the data are presented as means ± SEM. ∗∗∗p < 0.001, two-tailed unpaired t test. (C) IOP measurements at 3wpi. Naive, n = 13; WT SOHU, n = 13; GADD45a KD, n = 11. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, one-way ANOVA with Tukey’s multiple comparisons test. (D) Visual acuity measured by OKR at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 10. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, two-tailed unpaired t test. (E) Quantification of P1-N2 amplitude of PERG at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 6. Data are presented as means ± SEM, ∗p < 0.05, two-tailed unpaired t test. (F) Quantification of GCC thickness measured by OCT at 3wpi, represented as percentage of GCC thickness in the SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗∗p < 0.001, two-tailed unpaired t test. (G) Upper panel, representative confocal images of peripheral flat-mounted retinas showing surviving <t>RBPMS-positive</t> (red) RGCs at 3wpi. Scale bar, 20 μm. Lower panel, light microscope images of semi-thin transverse sections of ON with PPD staining at 3wpi. Scale bar, 10 μm. (H) Quantification of surviving RGC somata and axons at 3wpi, represented as percentage of glaucomatous eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗p < 0.01, two-tailed unpaired t test.
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    GADD45a knockdown (KD) promotes RGC soma and axon survival and preserves visual function in SOHU glaucoma model (A) Representative confocal images of retina cross-sections showing GADD45a (red) mRNA expression in GCL <t>by</t> <t>immunostaining</t> at 1wpi. Scale bar, 20 μm. (B) Quantification of mean fluorescence intensity of GADD45α in GCL. n = 5. All the data are presented as means ± SEM. ∗∗∗p < 0.001, two-tailed unpaired t test. (C) IOP measurements at 3wpi. Naive, n = 13; WT SOHU, n = 13; GADD45a KD, n = 11. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, one-way ANOVA with Tukey’s multiple comparisons test. (D) Visual acuity measured by OKR at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 10. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, two-tailed unpaired t test. (E) Quantification of P1-N2 amplitude of PERG at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 6. Data are presented as means ± SEM, ∗p < 0.05, two-tailed unpaired t test. (F) Quantification of GCC thickness measured by OCT at 3wpi, represented as percentage of GCC thickness in the SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗∗p < 0.001, two-tailed unpaired t test. (G) Upper panel, representative confocal images of peripheral flat-mounted retinas showing surviving <t>RBPMS-positive</t> (red) RGCs at 3wpi. Scale bar, 20 μm. Lower panel, light microscope images of semi-thin transverse sections of ON with PPD staining at 3wpi. Scale bar, 10 μm. (H) Quantification of surviving RGC somata and axons at 3wpi, represented as percentage of glaucomatous eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗p < 0.01, two-tailed unpaired t test.
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    GADD45a knockdown (KD) promotes RGC soma and axon survival and preserves visual function in SOHU glaucoma model (A) Representative confocal images of retina cross-sections showing GADD45a (red) mRNA expression in GCL <t>by</t> <t>immunostaining</t> at 1wpi. Scale bar, 20 μm. (B) Quantification of mean fluorescence intensity of GADD45α in GCL. n = 5. All the data are presented as means ± SEM. ∗∗∗p < 0.001, two-tailed unpaired t test. (C) IOP measurements at 3wpi. Naive, n = 13; WT SOHU, n = 13; GADD45a KD, n = 11. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, one-way ANOVA with Tukey’s multiple comparisons test. (D) Visual acuity measured by OKR at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 10. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, two-tailed unpaired t test. (E) Quantification of P1-N2 amplitude of PERG at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 6. Data are presented as means ± SEM, ∗p < 0.05, two-tailed unpaired t test. (F) Quantification of GCC thickness measured by OCT at 3wpi, represented as percentage of GCC thickness in the SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗∗p < 0.001, two-tailed unpaired t test. (G) Upper panel, representative confocal images of peripheral flat-mounted retinas showing surviving <t>RBPMS-positive</t> (red) RGCs at 3wpi. Scale bar, 20 μm. Lower panel, light microscope images of semi-thin transverse sections of ON with PPD staining at 3wpi. Scale bar, 10 μm. (H) Quantification of surviving RGC somata and axons at 3wpi, represented as percentage of glaucomatous eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗p < 0.01, two-tailed unpaired t test.
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    GADD45a knockdown (KD) promotes RGC soma and axon survival and preserves visual function in SOHU glaucoma model (A) Representative confocal images of retina cross-sections showing GADD45a (red) mRNA expression in GCL <t>by</t> <t>immunostaining</t> at 1wpi. Scale bar, 20 μm. (B) Quantification of mean fluorescence intensity of GADD45α in GCL. n = 5. All the data are presented as means ± SEM. ∗∗∗p < 0.001, two-tailed unpaired t test. (C) IOP measurements at 3wpi. Naive, n = 13; WT SOHU, n = 13; GADD45a KD, n = 11. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, one-way ANOVA with Tukey’s multiple comparisons test. (D) Visual acuity measured by OKR at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 10. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, two-tailed unpaired t test. (E) Quantification of P1-N2 amplitude of PERG at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 6. Data are presented as means ± SEM, ∗p < 0.05, two-tailed unpaired t test. (F) Quantification of GCC thickness measured by OCT at 3wpi, represented as percentage of GCC thickness in the SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗∗p < 0.001, two-tailed unpaired t test. (G) Upper panel, representative confocal images of peripheral flat-mounted retinas showing surviving <t>RBPMS-positive</t> (red) RGCs at 3wpi. Scale bar, 20 μm. Lower panel, light microscope images of semi-thin transverse sections of ON with PPD staining at 3wpi. Scale bar, 10 μm. (H) Quantification of surviving RGC somata and axons at 3wpi, represented as percentage of glaucomatous eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗p < 0.01, two-tailed unpaired t test.
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    GADD45a knockdown (KD) promotes RGC soma and axon survival and preserves visual function in SOHU glaucoma model (A) Representative confocal images of retina cross-sections showing GADD45a (red) mRNA expression in GCL <t>by</t> <t>immunostaining</t> at 1wpi. Scale bar, 20 μm. (B) Quantification of mean fluorescence intensity of GADD45α in GCL. n = 5. All the data are presented as means ± SEM. ∗∗∗p < 0.001, two-tailed unpaired t test. (C) IOP measurements at 3wpi. Naive, n = 13; WT SOHU, n = 13; GADD45a KD, n = 11. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, one-way ANOVA with Tukey’s multiple comparisons test. (D) Visual acuity measured by OKR at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 10. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, two-tailed unpaired t test. (E) Quantification of P1-N2 amplitude of PERG at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 6. Data are presented as means ± SEM, ∗p < 0.05, two-tailed unpaired t test. (F) Quantification of GCC thickness measured by OCT at 3wpi, represented as percentage of GCC thickness in the SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗∗p < 0.001, two-tailed unpaired t test. (G) Upper panel, representative confocal images of peripheral flat-mounted retinas showing surviving <t>RBPMS-positive</t> (red) RGCs at 3wpi. Scale bar, 20 μm. Lower panel, light microscope images of semi-thin transverse sections of ON with PPD staining at 3wpi. Scale bar, 10 μm. (H) Quantification of surviving RGC somata and axons at 3wpi, represented as percentage of glaucomatous eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗p < 0.01, two-tailed unpaired t test.
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    Loss of RGCs and glial reactivity two weeks after pONT. Double immunohistochemistry of <t>RBPMS</t> <t>and</t> <t>GFAP</t> was performed on retinal wholemounts. Compared to the contralateral control ( A – C ), noticeable dropout of RGCs was detected and reactive astrocytes were present in the nasal quadrant after pONT ( D – F ). A more dramatic loss of RGCs and increased astrocytic reactivity were noted in the temporal quadrant after pONT ( G – I ). N = nasal; T = temporal; RBPMS = RNA binding protein with multiple splicing; GFAP = glial fibrillary acidic protein; 2 wk = 2 weeks; pONT = partial optic nerve transection; CTL = control.
    Rbpms, supplied by ProSci Incorporated, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    GADD45a knockdown (KD) promotes RGC soma and axon survival and preserves visual function in SOHU glaucoma model (A) Representative confocal images of retina cross-sections showing GADD45a (red) mRNA expression in GCL by immunostaining at 1wpi. Scale bar, 20 μm. (B) Quantification of mean fluorescence intensity of GADD45α in GCL. n = 5. All the data are presented as means ± SEM. ∗∗∗p < 0.001, two-tailed unpaired t test. (C) IOP measurements at 3wpi. Naive, n = 13; WT SOHU, n = 13; GADD45a KD, n = 11. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, one-way ANOVA with Tukey’s multiple comparisons test. (D) Visual acuity measured by OKR at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 10. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, two-tailed unpaired t test. (E) Quantification of P1-N2 amplitude of PERG at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 6. Data are presented as means ± SEM, ∗p < 0.05, two-tailed unpaired t test. (F) Quantification of GCC thickness measured by OCT at 3wpi, represented as percentage of GCC thickness in the SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗∗p < 0.001, two-tailed unpaired t test. (G) Upper panel, representative confocal images of peripheral flat-mounted retinas showing surviving RBPMS-positive (red) RGCs at 3wpi. Scale bar, 20 μm. Lower panel, light microscope images of semi-thin transverse sections of ON with PPD staining at 3wpi. Scale bar, 10 μm. (H) Quantification of surviving RGC somata and axons at 3wpi, represented as percentage of glaucomatous eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗p < 0.01, two-tailed unpaired t test.

    Journal: Molecular Therapy. Nucleic Acids

    Article Title: RGC-specific ATF4 and/or CHOP deletion rescues glaucomatous neurodegeneration and visual function

    doi: 10.1016/j.omtn.2023.07.015

    Figure Lengend Snippet: GADD45a knockdown (KD) promotes RGC soma and axon survival and preserves visual function in SOHU glaucoma model (A) Representative confocal images of retina cross-sections showing GADD45a (red) mRNA expression in GCL by immunostaining at 1wpi. Scale bar, 20 μm. (B) Quantification of mean fluorescence intensity of GADD45α in GCL. n = 5. All the data are presented as means ± SEM. ∗∗∗p < 0.001, two-tailed unpaired t test. (C) IOP measurements at 3wpi. Naive, n = 13; WT SOHU, n = 13; GADD45a KD, n = 11. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, one-way ANOVA with Tukey’s multiple comparisons test. (D) Visual acuity measured by OKR at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 10. Data are presented as means ± SEM, ∗∗∗∗p < 0.0001, two-tailed unpaired t test. (E) Quantification of P1-N2 amplitude of PERG at 3wpi, represented as percentage of SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 6. Data are presented as means ± SEM, ∗p < 0.05, two-tailed unpaired t test. (F) Quantification of GCC thickness measured by OCT at 3wpi, represented as percentage of GCC thickness in the SOHU eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗∗p < 0.001, two-tailed unpaired t test. (G) Upper panel, representative confocal images of peripheral flat-mounted retinas showing surviving RBPMS-positive (red) RGCs at 3wpi. Scale bar, 20 μm. Lower panel, light microscope images of semi-thin transverse sections of ON with PPD staining at 3wpi. Scale bar, 10 μm. (H) Quantification of surviving RGC somata and axons at 3wpi, represented as percentage of glaucomatous eyes compared to the sham contralateral control eyes. WT, n = 13; GADD45a KD, n = 9. Data are presented as means ± SEM, ∗∗p < 0.01, two-tailed unpaired t test.

    Article Snippet: The primary antibodies used for immunostaining were as follows: anti-RBPMS at 1:4,000 (Custom made at ProSci) and anti-GADD45a at 1:200 (Santa Cruz, sc-6850).

    Techniques: Expressing, Immunostaining, Fluorescence, Two Tailed Test, Light Microscopy, Staining

    Loss of RGCs and glial reactivity two weeks after pONT. Double immunohistochemistry of RBPMS and GFAP was performed on retinal wholemounts. Compared to the contralateral control ( A – C ), noticeable dropout of RGCs was detected and reactive astrocytes were present in the nasal quadrant after pONT ( D – F ). A more dramatic loss of RGCs and increased astrocytic reactivity were noted in the temporal quadrant after pONT ( G – I ). N = nasal; T = temporal; RBPMS = RNA binding protein with multiple splicing; GFAP = glial fibrillary acidic protein; 2 wk = 2 weeks; pONT = partial optic nerve transection; CTL = control.

    Journal: International Journal of Molecular Sciences

    Article Title: Differential Retinal Protein Expression in Primary and Secondary Retinal Ganglion Cell Degeneration Identified by Integrated SWATH and Target-Based Proteomics

    doi: 10.3390/ijms22168592

    Figure Lengend Snippet: Loss of RGCs and glial reactivity two weeks after pONT. Double immunohistochemistry of RBPMS and GFAP was performed on retinal wholemounts. Compared to the contralateral control ( A – C ), noticeable dropout of RGCs was detected and reactive astrocytes were present in the nasal quadrant after pONT ( D – F ). A more dramatic loss of RGCs and increased astrocytic reactivity were noted in the temporal quadrant after pONT ( G – I ). N = nasal; T = temporal; RBPMS = RNA binding protein with multiple splicing; GFAP = glial fibrillary acidic protein; 2 wk = 2 weeks; pONT = partial optic nerve transection; CTL = control.

    Article Snippet: Briefly, the samples were incubated with 10% fetal bovine serum for 1 h to block non-specific staining and then in a solution of RBPMS (1:500; rabbit; ProSci, Polway, CA, USA) and GFAP (1:1000; chicken; Abcam, Waltham, MA, USA) antibodies in PBS containing 1% Triton, 0.5% bovine serum albumin (BSA), and 0.9% sodium chloride (PBS-T-BSA) overnight at 4 °C.

    Techniques: Immunohistochemistry, RNA Binding Assay