Description
Product Characteristics:
The adenovirus E1B protein is a viral homolog of the Bcl-2 family of proteins that are involved in regulating cell death. A family of interacting proteins, which are designated Nip or Bnip and include BNIP-1, BNIP-2, BNIP-3 and Nix, associate with both the E1B protein and Bcl-2 proteins to mediate apoptotic signaling. BNIP-1 contains a hydrophobic transmembrane domain, which enables its localization to the nuclear envelope, endoplasmic recticulum and mitochondria. BNIP-2, (previously designated Nip2 and Nip21 in human and mouse respectively), shares homology with the non-catalytic domain of Cdc42 GTPase-activating protein (Cdc42GAP). Through binding to Cdc42GAP, BNIP-2 enhances the GTPase activity of Cdc42GAP, facilitating the hydrolysis of GTP bound to Cdc42 and thereby, mediating the signaling pathways involving receptor kinases, small GTPases and apoptotic proteins. Nix, which is also designated Nip3L or Bnip3L, is highly related to BNIP-3, and both proteins localize to the mitochondria where they associate with Bcl-2 proteins. BNIP-3 preferentially binds to Bcl-xL and induces apoptosis by suppressing the anti-apoptosis activity of Bcl-xL.
Subcellular location: Cytoplasm, Cell membrane
Synonyms: BNIP3 phospho S95, p-BNIP3 phospho S95, BCL2 Adenovirus E1B 19 kDa Interacting Protein 3, BCL2/adenovirus E1B 19 kDa protein interacting protein 3, BCL2/adenovirus E1B 19 kDa protein-interacting protein 3, BNIP 3, BNIP3, BNIP3_HUMAN, NIP 3, NIP3.
Target Information: This gene is a member of the BCL2/adenovirus E1B 19 kd-interacting protein (BNIP) family. It interacts with the E1B 19 kDa protein, which protects cells from virally-induced cell death. The encoded protein also interacts with E1B 19 kDa-like sequences of BCL2, another apoptotic protector. This protein contains a BH3 domain and a transmembrane domain, which have been associated with pro-apoptotic function. The dimeric mitochondrial protein encoded by this gene is known to induce apoptosis, even in the presence of BCL2. [provided by RefSeq, Mar 2011]