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Caspase 3 Antibody (9H19L2), ABfinity(TM) Rabbit Monoclonal

RRID:AB_2532293

Antibody ID

AB_2532293

Target Antigen

Caspase 3 human

Proper Citation

(Thermo Fisher Scientific Cat# 700182, RRID:AB_2532293)

Clonality

monoclonal antibody

Comments

Applications: WB (0.1-0.2 µg/mL), IHC (P) (1:10-1:50), ICC (1-2 µg/mL), IF (1-2 µg/mL)

Clone ID

Clone 9H19L2

Host Organism

rabbit

Vendor

Thermo Fisher Scientific Go To Vendor

Cat Num

700182

Publications that use this research resource

Epitranscriptomic m6A Regulation of Axon Regeneration in the Adult Mammalian Nervous System.

  • Weng YL
  • Neuron
  • 2018 Jan 17

Literature context:


Abstract:

N6-methyladenosine (m6A) affects multiple aspects of mRNA metabolism and regulates developmental transitions by promoting mRNA decay. Little is known about the role of m6A in the adult mammalian nervous system. Here we report that sciatic nerve lesion elevates levels of m6A-tagged transcripts encoding many regeneration-associated genes and protein translation machinery components in the adult mouse dorsal root ganglion (DRG). Single-base resolution m6A-CLIP mapping further reveals a dynamic m6A landscape in the adult DRG upon injury. Loss of either m6A methyltransferase complex component Mettl14 or m6A-binding protein Ythdf1 globally attenuates injury-induced protein translation in adult DRGs and reduces functional axon regeneration in the peripheral nervous system in vivo. Furthermore, Pten deletion-induced axon regeneration of retinal ganglion neurons in the adult central nervous system is attenuated upon Mettl14 knockdown. Our study reveals a critical epitranscriptomic mechanism in promoting injury-induced protein synthesis and axon regeneration in the adult mammalian nervous system.

Funding information:
  • NCI NIH HHS - U01 CA84243(United States)
  • NHGRI NIH HHS - RM1 HG008935()
  • NINDS NIH HHS - P01 NS097206()
  • NINDS NIH HHS - R35 NS097370()

An Intrinsic Epigenetic Barrier for Functional Axon Regeneration.

  • Weng YL
  • Neuron
  • 2017 Apr 19

Literature context:


Abstract:

Mature neurons in the adult peripheral nervous system can effectively switch from a dormant state with little axonal growth to robust axon regeneration upon injury. The mechanisms by which injury unlocks mature neurons' intrinsic axonal growth competence are not well understood. Here, we show that peripheral sciatic nerve lesion in adult mice leads to elevated levels of Tet3 and 5-hydroxylmethylcytosine in dorsal root ganglion (DRG) neurons. Functionally, Tet3 is required for robust axon regeneration of DRG neurons and behavioral recovery. Mechanistically, peripheral nerve injury induces DNA demethylation and upregulation of multiple regeneration-associated genes in a Tet3- and thymine DNA glycosylase-dependent fashion in DRG neurons. In addition, Pten deletion-induced axon regeneration of retinal ganglion neurons in the adult CNS is attenuated upon Tet1 knockdown. Together, our study suggests an epigenetic barrier that can be removed by active DNA demethylation to permit axon regeneration in the adult mammalian nervous system.

Funding information:
  • NIGMS NIH HHS - T32 GM007814()