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DRAM polyclonal antibody



ADI-905-738-100	100 µg	395.00 USD
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Product Specification

Alternative Name:	Damage-regulated autophagy modulator

Host:	Rabbit

Immunogen:	Synthetic peptide corresponding to the sequence near the N-terminus of human DRAM.

UniProt ID:	Q8N682

Species reactivity:	Human, Mouse, Rat

Applications:	IHC, WB

Recommended Dilutions/Conditions:	Immunohistochemistry (2.5µg/ml) Western Blot (0.5-1.0µg/ml) Suggested dilutions/conditions may not be available for all applications. Optimal conditions must be determined individually for each application.

Application Notes:	Detects a band of ~31kDa by Western blot.

Purity Detail:	Peptide affinity purified.

Formulation:	Liquid. In PBS containing 0.02% sodium azide.

Shipping:	Blue Ice Not Frozen

Long Term Storage:	+4°C

Scientific Background:	Damage-regulated autophagy modulator (DRAM) is a p53 target gene encoding a lysosomal protein that induces autophagy, a process that degrades cytosolic proteins and organelles. It has been suggested that activation of DRAM by p53 is simultaneous to the activation by p53 of one or more proapoptotic genes such as PUMA and Bax, and that the signaling pathways regulated by these genes together promote a full cell death response.

Regulatory Status:	RUO - Research Use Only

Western blot analysis of DRAM in K562 cell lysate with DRAM antibody at (A) 0.5, (B) 1 and (C) 2µg/ml.

DRAM polyclonal antibody Immunohistochemistry

Immunohistochemistry analysis of DRAM in human liver tissue with DRAM antibody at 2.5µg/ml.

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Product Literature References

DRAM1 regulates autophagy flux through lysosomes: X.D. Zhang, et al.; PLoS One 8, e63245 (2013), Application(s): WB using A549 cells, Abstract; Full Text

Propofol prevents cerebral ischemia-triggered autophagy activation and cell death in the rat hippocampus through the NF-κB/p53 signaling pathway: D.R. Cui, et al.; Neuroscience 246, 117 (2013), Application(s): WB using rat tissue homogenates, Abstract;

p53 induction contributes to excitotoxic neuronal death in rat striatum through apoptotic and autophagic mechanisms: Y. Wang, et al.; Eur. J. Neurosci. 30, 2258 (2009), Abstract;