EI24 (D3F6Z) Rabbit Antibody

INQUIRY

CAT. NO.: AMA-0511

Target Information
UniProt ID	O14681

Product Details
Size	100 µL
Reactivity	Human, Mouse, Rat
Host	Rabbit
Source/Isotype	Rabbit IgG
Storage	Store at -20°C. Do not aliquot the antibody.
Purification	Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ala31 of human EI24 protein.

Usage
Application	WB, IP
Product Usage Information Dilution	Western Blotting (1:1000); Immunoprecipitation (1:200)
MW (Target)	30 kDa

Background
Etoposide-induced 2.4 mRNA (EI24)/p53-induced gene 8 (PIG8) was identified as a DNA damage response gene induced by etoposide in a p53 dependent manner with roles in growth suppression and apoptosis As a pro-apoptotic gene, some evidence suggests that EI24 functions as a tumor suppressor gene in cases such as breast and cervical cancer The mechanism of EI24 is still unclear, but studies have shown that it can localize to the endoplasmic reticulum and associate with Bcl-2 and could regulate apoptosis through regulation of Bcl-2 function Liver-specific deletions of EI24 in mice show impaired autophagic flux, suggesting that it may also play a role in regulating basal autophagy EI24 was shown to be involved in the autophagic degradation of many RING E3 ligases In addition, decreased expression of EI24 in epithelial tumor cells induced epithelial-to-mesenchymal transition (EMT). Together these studies suggest multiple mechanisms for EI24 to regulate tumor progression that includes regulation of apoptosis, autophagy, and EMT.

Background

Etoposide-induced 2.4 mRNA (EI24)/p53-induced gene 8 (PIG8) was identified as a DNA damage response gene induced by etoposide in a p53 dependent manner with roles in growth suppression and apoptosis As a pro-apoptotic gene, some evidence suggests that EI24 functions as a tumor suppressor gene in cases such as breast and cervical cancer The mechanism of EI24 is still unclear, but studies have shown that it can localize to the endoplasmic reticulum and associate with Bcl-2 and could regulate apoptosis through regulation of Bcl-2 function Liver-specific deletions of EI24 in mice show impaired autophagic flux, suggesting that it may also play a role in regulating basal autophagy EI24 was shown to be involved in the autophagic degradation of many RING E3 ligases In addition, decreased expression of EI24 in epithelial tumor cells induced epithelial-to-mesenchymal transition (EMT). Together these studies suggest multiple mechanisms for EI24 to regulate tumor progression that includes regulation of apoptosis, autophagy, and EMT.

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