phospho t37 t46 4e bp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho t37 t46 4e bp1
    Phospho T37 T46 4e Bp1, supplied by Cell Signaling Technology Inc, 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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    4e bp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc 4e bp1
    4e Bp1, supplied by Cell Signaling Technology Inc, 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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    4e bp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc 4e bp1
    S6K1 activation and inhibition <t>of</t> <t>4E-BP1</t> are necessary for caRheb-induced axon regeneration following ONC. (A) DN-S6K1 decreased p-S6 expression while caS6K1 increased p-S6 expression. Immunofluorescence of retinal sections using p-S6 (red) or Tuj1 (green) antibodies from mice transfected with AAV-DN-S6K1 or AAV-caS6K1. (B) Delivery of 4E-BP1-4A increased 4E-BP1 expression while sh4E-BP1 decreased 4E-BP1 expression. Immunofluorescence analysis for 4E-BP1 levels in RGCs transfected with AAV-4E-BP1-4A or AAV-sh4E-BP1. Cells were stained with antibodies for 4E-BP1 (red) or Tuj1 (green). (C) Mixed injection of AAV was administrated intravitreally to mice 2 weeks before ONC. CTB was intravitreally injected 12 days after ONC and eyes were harvested on days 14 after ONC. (D) DN-S6K1 and 4E-BP1-4A decreased the regenerating axons induced by caRheb. Images of optic nerve sections showing regenerating axons labeled by anterograde transport of CTB on days 14 after ONC from eyes injected with AAV-caRheb, AAV-caRheb + DN-S6K1, AAV-caRheb + caS6K1, AAV-caRheb + 4E-BP1-4A, or AAV-EGFP. Red asterisk indicates crush site. Scale bars: 40 µm (A, B), 100 µm (D). (E) Quantification of regenerating axons 14 days post-crush from eyes injected with AAV-caRheb, AAV-caRheb + DN-S6K1, AAV-caRheb + caS6K1, or AAV-caRheb + 4E-BP1-4A at different distances distal to the lesion site. (F) Quantification of regenerating axons on day 14 post-crush from eyes injected with AAV-EGFP, AAV-caRheb + 4E-BP1-4A, or AAV-caRheb + DN-S6K1 at different distances distal to the lesion site. Data are presented as mean ± SD ( n = 8–10). * P < 0.05, ** P < 0.01, *** P < 0.001, *** *P < 0.0001 (two-way analysis of variance with Bonferroni’s post hoc test). 4E-BP1-4A: Non-phosphorylatable 4E-BP1 mutant; AAV: adeno-associated virus; caRheb: constitutively active Ras homolog enriched in brain; caS6K1: constitutively active S6K1; CTB: cholera toxin B subunit; DN-S6K1: dominate negative S6K1; dpc: days post crush; EGFP: enhanced green fluorescent protein; GCL: ganglion cell layer; INL: inner nuclear layer; ONC: optic nerve crush; ONL: outer nuclear layer; p-S6: phospho-S6 ribosomal protein; RGC: retinal ganglion cell; S6K1: mammalian target of rapamycin complex 1 downstream effector; Tuj1: β3-tubulin.
    4e Bp1, supplied by Cell Signaling Technology Inc, 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 "Phosphorylated S6K1 and 4E-BP1 play different roles in constitutively active Rheb-mediated retinal ganglion cell survival and axon regeneration after optic nerve injury"

    Article Title: Phosphorylated S6K1 and 4E-BP1 play different roles in constitutively active Rheb-mediated retinal ganglion cell survival and axon regeneration after optic nerve injury

    Journal: Neural Regeneration Research

    doi: 10.4103/1673-5374.371372

    S6K1 activation and inhibition of 4E-BP1 are necessary for caRheb-induced axon regeneration following ONC. (A) DN-S6K1 decreased p-S6 expression while caS6K1 increased p-S6 expression. Immunofluorescence of retinal sections using p-S6 (red) or Tuj1 (green) antibodies from mice transfected with AAV-DN-S6K1 or AAV-caS6K1. (B) Delivery of 4E-BP1-4A increased 4E-BP1 expression while sh4E-BP1 decreased 4E-BP1 expression. Immunofluorescence analysis for 4E-BP1 levels in RGCs transfected with AAV-4E-BP1-4A or AAV-sh4E-BP1. Cells were stained with antibodies for 4E-BP1 (red) or Tuj1 (green). (C) Mixed injection of AAV was administrated intravitreally to mice 2 weeks before ONC. CTB was intravitreally injected 12 days after ONC and eyes were harvested on days 14 after ONC. (D) DN-S6K1 and 4E-BP1-4A decreased the regenerating axons induced by caRheb. Images of optic nerve sections showing regenerating axons labeled by anterograde transport of CTB on days 14 after ONC from eyes injected with AAV-caRheb, AAV-caRheb + DN-S6K1, AAV-caRheb + caS6K1, AAV-caRheb + 4E-BP1-4A, or AAV-EGFP. Red asterisk indicates crush site. Scale bars: 40 µm (A, B), 100 µm (D). (E) Quantification of regenerating axons 14 days post-crush from eyes injected with AAV-caRheb, AAV-caRheb + DN-S6K1, AAV-caRheb + caS6K1, or AAV-caRheb + 4E-BP1-4A at different distances distal to the lesion site. (F) Quantification of regenerating axons on day 14 post-crush from eyes injected with AAV-EGFP, AAV-caRheb + 4E-BP1-4A, or AAV-caRheb + DN-S6K1 at different distances distal to the lesion site. Data are presented as mean ± SD ( n = 8–10). * P < 0.05, ** P < 0.01, *** P < 0.001, *** *P < 0.0001 (two-way analysis of variance with Bonferroni’s post hoc test). 4E-BP1-4A: Non-phosphorylatable 4E-BP1 mutant; AAV: adeno-associated virus; caRheb: constitutively active Ras homolog enriched in brain; caS6K1: constitutively active S6K1; CTB: cholera toxin B subunit; DN-S6K1: dominate negative S6K1; dpc: days post crush; EGFP: enhanced green fluorescent protein; GCL: ganglion cell layer; INL: inner nuclear layer; ONC: optic nerve crush; ONL: outer nuclear layer; p-S6: phospho-S6 ribosomal protein; RGC: retinal ganglion cell; S6K1: mammalian target of rapamycin complex 1 downstream effector; Tuj1: β3-tubulin.
    Figure Legend Snippet: S6K1 activation and inhibition of 4E-BP1 are necessary for caRheb-induced axon regeneration following ONC. (A) DN-S6K1 decreased p-S6 expression while caS6K1 increased p-S6 expression. Immunofluorescence of retinal sections using p-S6 (red) or Tuj1 (green) antibodies from mice transfected with AAV-DN-S6K1 or AAV-caS6K1. (B) Delivery of 4E-BP1-4A increased 4E-BP1 expression while sh4E-BP1 decreased 4E-BP1 expression. Immunofluorescence analysis for 4E-BP1 levels in RGCs transfected with AAV-4E-BP1-4A or AAV-sh4E-BP1. Cells were stained with antibodies for 4E-BP1 (red) or Tuj1 (green). (C) Mixed injection of AAV was administrated intravitreally to mice 2 weeks before ONC. CTB was intravitreally injected 12 days after ONC and eyes were harvested on days 14 after ONC. (D) DN-S6K1 and 4E-BP1-4A decreased the regenerating axons induced by caRheb. Images of optic nerve sections showing regenerating axons labeled by anterograde transport of CTB on days 14 after ONC from eyes injected with AAV-caRheb, AAV-caRheb + DN-S6K1, AAV-caRheb + caS6K1, AAV-caRheb + 4E-BP1-4A, or AAV-EGFP. Red asterisk indicates crush site. Scale bars: 40 µm (A, B), 100 µm (D). (E) Quantification of regenerating axons 14 days post-crush from eyes injected with AAV-caRheb, AAV-caRheb + DN-S6K1, AAV-caRheb + caS6K1, or AAV-caRheb + 4E-BP1-4A at different distances distal to the lesion site. (F) Quantification of regenerating axons on day 14 post-crush from eyes injected with AAV-EGFP, AAV-caRheb + 4E-BP1-4A, or AAV-caRheb + DN-S6K1 at different distances distal to the lesion site. Data are presented as mean ± SD ( n = 8–10). * P < 0.05, ** P < 0.01, *** P < 0.001, *** *P < 0.0001 (two-way analysis of variance with Bonferroni’s post hoc test). 4E-BP1-4A: Non-phosphorylatable 4E-BP1 mutant; AAV: adeno-associated virus; caRheb: constitutively active Ras homolog enriched in brain; caS6K1: constitutively active S6K1; CTB: cholera toxin B subunit; DN-S6K1: dominate negative S6K1; dpc: days post crush; EGFP: enhanced green fluorescent protein; GCL: ganglion cell layer; INL: inner nuclear layer; ONC: optic nerve crush; ONL: outer nuclear layer; p-S6: phospho-S6 ribosomal protein; RGC: retinal ganglion cell; S6K1: mammalian target of rapamycin complex 1 downstream effector; Tuj1: β3-tubulin.

    Techniques Used: Activation Assay, Inhibition, Expressing, Immunofluorescence, Transfection, Staining, Injection, Labeling, Mutagenesis

    S6K1 activation, but not the knockdown of 4E-BP1, is sufficient to promote axon regeneration. (A) AAV-caS6K1 and AAV-sh4E-BP1 were administrated intravitreally to mice 2 weeks before ONC. CTB was intravitreally injected 12 days after ONC and optic nerves were harvested on day 14 after ONC. (B) Expression of caS6K1 induced axon regeneration. Images of optic nerve sections show regenerating axons labeled by anterograde transport of CTB on day 14 after optic nerve crush from AAV-EGFP- and AAV-caS6K1-injected eyes. (C) Quantification of regenerating axons 14 days post-crush from AAV-EGFP- and AAV-caS6K1-injected eyes at different distances distal from the crushing site (mean ± SD, n = 6–9). (D) Knockdown of 4E-BP1 did not induce axon regeneration. Images of optic nerve sections show regenerating axons labeled by anterograde transport of CTB on day 14 after ONC from AAV-shscramble and AAV-sh4E-BP1-injected eyes. Red asterisk indicates crush site. Scale bars: 100 µm (B, D). (E) Quantification of regenerating axons 14 days post-crush from AAV-shscramble- and AAV-sh4E-BP1-injected eyes at different distances from the crushing site (means ± SD, n = 6). ** P < 0.01, **** P < 0.0001 (two-way analysis of variance with Bonferroni’s post hoc test). 4E-BP1: Mammalian target of rapamycin complex 1 downstream effector; AAV: adeno-associated virus; caS6K1: constitutively active S6K1; CTB: cholera toxin B subunit; dpc: days post crush; EGFP: enhanced green fluorescent protein; ONC: optic nerve crush; RGC: retinal ganglion cell; S6K1: mammalian target of rapamycin complex 1 downstream effector.
    Figure Legend Snippet: S6K1 activation, but not the knockdown of 4E-BP1, is sufficient to promote axon regeneration. (A) AAV-caS6K1 and AAV-sh4E-BP1 were administrated intravitreally to mice 2 weeks before ONC. CTB was intravitreally injected 12 days after ONC and optic nerves were harvested on day 14 after ONC. (B) Expression of caS6K1 induced axon regeneration. Images of optic nerve sections show regenerating axons labeled by anterograde transport of CTB on day 14 after optic nerve crush from AAV-EGFP- and AAV-caS6K1-injected eyes. (C) Quantification of regenerating axons 14 days post-crush from AAV-EGFP- and AAV-caS6K1-injected eyes at different distances distal from the crushing site (mean ± SD, n = 6–9). (D) Knockdown of 4E-BP1 did not induce axon regeneration. Images of optic nerve sections show regenerating axons labeled by anterograde transport of CTB on day 14 after ONC from AAV-shscramble and AAV-sh4E-BP1-injected eyes. Red asterisk indicates crush site. Scale bars: 100 µm (B, D). (E) Quantification of regenerating axons 14 days post-crush from AAV-shscramble- and AAV-sh4E-BP1-injected eyes at different distances from the crushing site (means ± SD, n = 6). ** P < 0.01, **** P < 0.0001 (two-way analysis of variance with Bonferroni’s post hoc test). 4E-BP1: Mammalian target of rapamycin complex 1 downstream effector; AAV: adeno-associated virus; caS6K1: constitutively active S6K1; CTB: cholera toxin B subunit; dpc: days post crush; EGFP: enhanced green fluorescent protein; ONC: optic nerve crush; RGC: retinal ganglion cell; S6K1: mammalian target of rapamycin complex 1 downstream effector.

    Techniques Used: Activation Assay, Injection, Expressing, Labeling

    The survival of RGCs after ONC requires the activity of S6K1 and 4E-BP1. (A) AAV-EGFP, AAV-caS6K1, and AAV-DN-S6K1 were administrated intravitreally to mice 2 weeks before ONC. Eyes were harvested on day 14 after ONC. (B) Overexpression of caS6K1 but not DN-S6K1 increased RGC survival. Fluorescent photomicrographs of retinal whole-mounts showing surviving Tuj1 + RGCs 14 dpc from eyes injected with AAV-EGFP, AAV-caS6K1, and AAV-DN-S6K1. (C) Quantification of sizes of surviving RGCs from AAV-EGFP, AAV-caS6K1, and AAV-DN-S6K1 groups (mean ± SD, n = 4). (D) Quantification of surviving Tuj1 + RGCs from eyes injected with AAV-EGFP, AAV-caS6K1, and AAV-DN-S6K1 (mean ± SD, n = 6–8). € AAV-EGFP, AAV-sh4E-BP1, and AAV-4E-BP1-4A were administrated intravitreally to mice 2 weeks before ONC. Eyes were harvested on day 14 after ONC. (F) Overexpression of 4E-BP1-4A increased RGC survival while knockdown of 4E-BP1 decreased RGC survival. Immunofluorescence of retinal whole-mounts showing surviving RGCs 14 dpc from AAV-EGFP, AAV-sh4E-BP1, and AAV-4E-BP1-4A groups. Scale bars: 60 µm (B, F). (G) Quantification of surviving RGCs from eyes injected with AAV-EGFP, sh4E-BP1, and 4E-BP1-4A (mean ± SD, n = 6–8). * P < 0.05, ** P < 0.01, *** P < 0.001, *** *P < 0.0001 (one-way analysis of variance with Bonferroni’s post hoc test). AAV: Adeno-associated virus; caS6K1: constitutively active S6K1; DN-S6K1: dominate negative S6K1; EGFP: enhanced green fluorescent protein; ONC: optic nerve crush; RGC: retinal ganglion cell; S6K1: mammalian target of rapamycin complex 1 downstream effector; Tuj1: β3-tubulin.
    Figure Legend Snippet: The survival of RGCs after ONC requires the activity of S6K1 and 4E-BP1. (A) AAV-EGFP, AAV-caS6K1, and AAV-DN-S6K1 were administrated intravitreally to mice 2 weeks before ONC. Eyes were harvested on day 14 after ONC. (B) Overexpression of caS6K1 but not DN-S6K1 increased RGC survival. Fluorescent photomicrographs of retinal whole-mounts showing surviving Tuj1 + RGCs 14 dpc from eyes injected with AAV-EGFP, AAV-caS6K1, and AAV-DN-S6K1. (C) Quantification of sizes of surviving RGCs from AAV-EGFP, AAV-caS6K1, and AAV-DN-S6K1 groups (mean ± SD, n = 4). (D) Quantification of surviving Tuj1 + RGCs from eyes injected with AAV-EGFP, AAV-caS6K1, and AAV-DN-S6K1 (mean ± SD, n = 6–8). € AAV-EGFP, AAV-sh4E-BP1, and AAV-4E-BP1-4A were administrated intravitreally to mice 2 weeks before ONC. Eyes were harvested on day 14 after ONC. (F) Overexpression of 4E-BP1-4A increased RGC survival while knockdown of 4E-BP1 decreased RGC survival. Immunofluorescence of retinal whole-mounts showing surviving RGCs 14 dpc from AAV-EGFP, AAV-sh4E-BP1, and AAV-4E-BP1-4A groups. Scale bars: 60 µm (B, F). (G) Quantification of surviving RGCs from eyes injected with AAV-EGFP, sh4E-BP1, and 4E-BP1-4A (mean ± SD, n = 6–8). * P < 0.05, ** P < 0.01, *** P < 0.001, *** *P < 0.0001 (one-way analysis of variance with Bonferroni’s post hoc test). AAV: Adeno-associated virus; caS6K1: constitutively active S6K1; DN-S6K1: dominate negative S6K1; EGFP: enhanced green fluorescent protein; ONC: optic nerve crush; RGC: retinal ganglion cell; S6K1: mammalian target of rapamycin complex 1 downstream effector; Tuj1: β3-tubulin.

    Techniques Used: Activity Assay, Over Expression, Injection, Immunofluorescence

    Complementary modulation of Rheb and 4E-BP1 strikingly boosts RGC survival. (A) AAV-EGFP, AAV-caRheb, AAV-caRheb + DN-S6K1, and AAV-caRheb + 4E-BP1-4A were administrated intravitreally to mice 2 weeks before ONC. Eyes were harvested on day 14 after ONC. (B) CaRheb + 4E-BP1-4A significantly increased the survival of RGCs while caRheb + DN-S6K1 significantly decreased RGC survival compared with caRheb alone. Fluorescent photomicrographs of retinal whole-mounts showed surviving Tuj1 + RGCs 14 dpc from eyes injected with AAV-EGFP, AAV-caRheb, AAV-caRheb + DN-S6K1, and AAV-caRheb + 4E-BP1-4A. Scale bars: 60 µm. (C) Quantification of surviving Tuj1 + RGCs from eyes injected with AAV-EGFP, AAV-caRheb, AAV-caRheb + DN-S6K1, and AAV-caRheb + 4E-BP1-4A. Data are presented as mean ± SD ( n = 6–8). **** P < 0.0001 (one-way analysis of variance with Bonferroni’s post hoc test). AAV: Adeno-associated virus; caS6K1: constitutively active S6K1; DN-S6K1: dominate negative S6K1; dpc: days post crush; EGFP: enhanced green fluorescent protein; ONC: optic nerve crush; RGC: retinal ganglion cell; S6K1: mammalian target of rapamycin complex 1 downstream effector; Tuj1: β3-tubulin.
    Figure Legend Snippet: Complementary modulation of Rheb and 4E-BP1 strikingly boosts RGC survival. (A) AAV-EGFP, AAV-caRheb, AAV-caRheb + DN-S6K1, and AAV-caRheb + 4E-BP1-4A were administrated intravitreally to mice 2 weeks before ONC. Eyes were harvested on day 14 after ONC. (B) CaRheb + 4E-BP1-4A significantly increased the survival of RGCs while caRheb + DN-S6K1 significantly decreased RGC survival compared with caRheb alone. Fluorescent photomicrographs of retinal whole-mounts showed surviving Tuj1 + RGCs 14 dpc from eyes injected with AAV-EGFP, AAV-caRheb, AAV-caRheb + DN-S6K1, and AAV-caRheb + 4E-BP1-4A. Scale bars: 60 µm. (C) Quantification of surviving Tuj1 + RGCs from eyes injected with AAV-EGFP, AAV-caRheb, AAV-caRheb + DN-S6K1, and AAV-caRheb + 4E-BP1-4A. Data are presented as mean ± SD ( n = 6–8). **** P < 0.0001 (one-way analysis of variance with Bonferroni’s post hoc test). AAV: Adeno-associated virus; caS6K1: constitutively active S6K1; DN-S6K1: dominate negative S6K1; dpc: days post crush; EGFP: enhanced green fluorescent protein; ONC: optic nerve crush; RGC: retinal ganglion cell; S6K1: mammalian target of rapamycin complex 1 downstream effector; Tuj1: β3-tubulin.

    Techniques Used: Injection

    Schematic diagram of the role of the Rheb/mTORC1/S6K1 and 4E-BP1 pathway in RGC survival and axon regeneration. (A) S16H mutation in Rheb results in a constitutively GTP-bound Rheb as an activated form. Constitutively active Rheb stimulates mTORC1, which subsequently phosphorylates both S6K1 and 4E-BP1 and results in the promotion of protein synthesis. S6K1 is activated by phosphorylation, whereas 4E-BP1 is inhibited by phosphorylation. Both S6K1 activation and 4E-BP1 inhibition contribute to axon regeneration. Activated S6K1 also contributes to RGC survival and enlarged neural size. In contrast, 4E-BP1 inhibits axon regeneration but increases surviving RGCs. We speculate that unknown downstream effectors of mTORC1 also contribute to axon regeneration. (B) Constitutively active Rheb activates mTORC1, which in turn phosphorylates the two downstream effectors S6K1 and 4E-BP1. Phosphorylation of S6K1 supports RGC survival, whereas phosphorylation of 4E-BP1 plays a contrary role. However, S6K1 activation seems to be dominating in this context, and the impact of 4E-BP1 phosphorylation is masked and compensated by the positive effect of active S6K1. (C) Overexpression of non-phosphorylatable 4E-BP1 (4E-BP1-4A) protects RGCs independent of mTORC1 activity. Thus, inactivation of endogenous 4E-BP1 upon caRheb becomes irrelevant, and 4E-BP1-4A compensates for the low level of endogenous 4E-BP1 activity and further promotes RGC survival under these conditions. 4E-BP1: mTORC1 downstream effector; caRheb: constitutively active Rheb; GTP: guanosine triphosphate; mTORC1: mammalian target of rapamycin complex 1; RGC: retinal ganglion cell; Rheb: Ras homolog enriched in brain; S6K1: mTORC1 downstream effector; WT: wild type.
    Figure Legend Snippet: Schematic diagram of the role of the Rheb/mTORC1/S6K1 and 4E-BP1 pathway in RGC survival and axon regeneration. (A) S16H mutation in Rheb results in a constitutively GTP-bound Rheb as an activated form. Constitutively active Rheb stimulates mTORC1, which subsequently phosphorylates both S6K1 and 4E-BP1 and results in the promotion of protein synthesis. S6K1 is activated by phosphorylation, whereas 4E-BP1 is inhibited by phosphorylation. Both S6K1 activation and 4E-BP1 inhibition contribute to axon regeneration. Activated S6K1 also contributes to RGC survival and enlarged neural size. In contrast, 4E-BP1 inhibits axon regeneration but increases surviving RGCs. We speculate that unknown downstream effectors of mTORC1 also contribute to axon regeneration. (B) Constitutively active Rheb activates mTORC1, which in turn phosphorylates the two downstream effectors S6K1 and 4E-BP1. Phosphorylation of S6K1 supports RGC survival, whereas phosphorylation of 4E-BP1 plays a contrary role. However, S6K1 activation seems to be dominating in this context, and the impact of 4E-BP1 phosphorylation is masked and compensated by the positive effect of active S6K1. (C) Overexpression of non-phosphorylatable 4E-BP1 (4E-BP1-4A) protects RGCs independent of mTORC1 activity. Thus, inactivation of endogenous 4E-BP1 upon caRheb becomes irrelevant, and 4E-BP1-4A compensates for the low level of endogenous 4E-BP1 activity and further promotes RGC survival under these conditions. 4E-BP1: mTORC1 downstream effector; caRheb: constitutively active Rheb; GTP: guanosine triphosphate; mTORC1: mammalian target of rapamycin complex 1; RGC: retinal ganglion cell; Rheb: Ras homolog enriched in brain; S6K1: mTORC1 downstream effector; WT: wild type.

    Techniques Used: Mutagenesis, Activation Assay, Inhibition, Over Expression, Activity Assay

    anti phospho 4e bp1 thr37 46  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti phospho 4e bp1 thr37 46
    Anti Phospho 4e Bp1 Thr37 46, supplied by Cell Signaling Technology Inc, 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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    Cell Signaling Technology Inc anti 4e bp1
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    phospho 4e bp1 ser65  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc 4e bp1
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    p 4e bp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p 4e bp1
    P 4e Bp1, supplied by Cell Signaling Technology Inc, 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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    4e bp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc 4e bp1
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    anti phospho 4e bp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti phospho 4e bp1

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    1) Product Images from "Loss of Ptpmt1 limits mitochondrial utilization of carbohydrates and leads to muscle atrophy and heart failure in tissue-specific knockout mice"

    Article Title: Loss of Ptpmt1 limits mitochondrial utilization of carbohydrates and leads to muscle atrophy and heart failure in tissue-specific knockout mice

    Journal: eLife

    doi: 10.7554/eLife.86944


    Figure Legend Snippet:

    Techniques Used:

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    Journal: eLife

    Article Title: Loss of Ptpmt1 limits mitochondrial utilization of carbohydrates and leads to muscle atrophy and heart failure in tissue-specific knockout mice

    doi: 10.7554/eLife.86944

    Figure Lengend Snippet:

    Article Snippet: Antibody , anti-phospho-4E-bp1 (Thr 37/46 ) (236B4) (Rabbit monoclonal) , Cell Signaling Technology , Cat# 2855 , WB (1:1000).

    Techniques: