BNIP3 Rabbit pAb (一抗) | Bioss

bs-4239R

宠物抗体、农牧业/家禽抗体

BNIP3 Rabbit pAb

促凋亡调节蛋白BNIP3抗体

HABON; NIP3; BNIP3_HUMAN; BNIP3; BNIP3_MOUSE;

Rabbit

KLH conjugated synthetic peptide derived from human BNIP3: 101-194/194

IgG

Liquid

affinity purified by Protein A

Polyclonal

22 kDa

1mg/ml

0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.

Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles.

This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

BNIP3蛋白在缺氧条件下可诱导细胞发生细胞凋亡。BNIP3促细胞凋亡线粒体途径根据有无caspase的参与而具有不同的作用机制，也是研究的热点。BNIP3还可诱导细胞自噬。BNIP3全称为Bcl2/腺病毒E1B19kD相互作用蛋白3。(Bcl2/adenovirusE1B19kDainteractingprotein3，BNIP3)，是新近发现的BH3only亚家族成员之一，也是低氧敏感的凋亡基因。在化学性低氧诱导细胞凋亡的过程中，ATP是BNIP3导致细胞凋亡的关键性因素之一。单独ATP下降不诱导细胞凋亡，但ATP下降到一定程度能促进BNIP3向线粒体转位，从而诱导了BNIP3相关的凋亡。这可能是低氧诱导BNIP3表达导致细胞凋亡的重要机制之一。

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.