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ATF-2 (C-19) antibody

RRID:AB_630885

Antibody ID

AB_630885

Target Antigen

ATF-2 (C-19) mouse, human, rat, mouse, rat, human

Proper Citation

(Santa Cruz Biotechnology Cat# sc-187, RRID:AB_630885)

Clonality

polyclonal antibody

Comments

Discontinued: 2016; validation status unknown check with seller; recommendations: Immunocytochemistry; Immunoprecipitation; Immunofluorescence; ELISA; Immunohistochemistry; Western Blot; WB, IP, IF, IHC(P), ELISA

Host Organism

rabbit

Vendor

Santa Cruz Biotechnology

Cat Num

sc-187

Publications that use this research resource

Crosstalk control and limits of physiological c-Jun N-terminal kinase activity for cell viability and neurite stability in differentiated PC12 cells.

  • Waetzig V
  • Mol. Cell. Neurosci.
  • 2018 Apr 24

Literature context:


Abstract:

The c-Jun N-terminal kinases (JNKs) are important mediators of cell viability and structural integrity in postmitotic neurons, which is required for maintaining synaptic connections and neural plasticity. In the present study, we chose differentiated PC12 cells as a well-characterised neuronal model system to selectively examine the regulation of basal JNK activity by extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt. We detected a complex interaction between the kinases to prevent cell death and neurite loss. Especially the appropriate level of JNK activation determined cellular survival. Basal activity of ERK1/2 attenuated the potentiation of JNK phosphorylation and thereby the induction of apoptosis. Importantly, when JNK activity was too low, cell viability and the number of neurite-bearing cells also decreased, even though the activation of ERK1/2 was enhanced. In this case, the JNK-mediated survival signals via activating transcription factor-3 (ATF3) were inhibited. Furthermore, the phosphorylation of ERK1/2 induced by the JNK inhibitor SP600125 inhibited the basal activity of Akt, which normally supported cell viability. Thus, controlling JNK activity is crucial to promote survival and neurite stability of differentiated neuronal cells.

Enhanced Functional Genomic Screening Identifies Novel Mediators of Dual Leucine Zipper Kinase-Dependent Injury Signaling in Neurons.

  • Welsbie DS
  • Neuron
  • 2017 Jun 21

Literature context:


Abstract:

Dual leucine zipper kinase (DLK) has been implicated in cell death signaling secondary to axonal damage in retinal ganglion cells (RGCs) and other neurons. To better understand the pathway through which DLK acts, we developed enhanced functional genomic screens in primary RGCs, including use of arrayed, whole-genome, small interfering RNA libraries. Explaining why DLK inhibition is only partially protective, we identify leucine zipper kinase (LZK) as cooperating with DLK to activate downstream signaling and cell death in RGCs, including in a mouse model of optic nerve injury, and show that the same pathway is active in human stem cell-derived RGCs. Moreover, we identify four transcription factors, JUN, activating transcription factor 2 (ATF2), myocyte-specific enhancer factor 2A (MEF2A), and SRY-Box 11 (SOX11), as being the major downstream mediators through which DLK/LZK activation leads to RGC cell death. Increased understanding of the DLK pathway has implications for understanding and treating neurodegenerative diseases.