BNIP3 / DyLight 650 / Polyclonal

Product Details

Description	BNIP3 Polyclonal Antibody, DyLight 650 conjugate. BNIP3, formerly NIP3 (nineteen kDa interacting protein-3), is a pro-apoptotic, mitochondrial protein classified in the Bcl 2 family based on limited sequence homology to the Bcl 2 homology 3 (BH3) domain (amino acids 110-118) and C-terminal TM domain. BNIP3 expressed in yeast and mammalian cells interacts with survival promoting proteins Bcl 2, Bcl XL, CED9 and the adenovirus E1B 19K protein. Typically the BH3 domain of pro-apoptotic Bcl-2 homologues mediates Bcl 2/Bcl XL heterodimerization and confers pro-apoptotic activity. BNIP3 represents a subfamily of Bcl 2 related proteins, which functions without a typical BH3 domain to regulate apoptosis from both mitochondrial and nonmitochondrial sites by selective Bcl 2/Bcl XL interactions. The N-terminus (residues 1-49) and the C-terminus TM domain of BNIP3 are critical for Bcl 2 heterodimerization, and either region is sufficient for Bcl XL interaction. The TM domain of BNIP3 is critical for homodimerization, pro-apoptotic function, and mitochondrial targeting. BNIP3 contains PEST sequences suggesting that the protein may be susceptible to rapid degradation by proteases. PEST sequences commonly contain high local concentrations of amino acids P, E, S, T, and D flanked by charged amino acids and these are abundantly present in NIP3. Thus, the posttranslational control of BNIP3 expression through rapid protein degradation may constitute a mechanism for regulating the intracellular levels of a potentially lethal protein. Homologues of BNIP3 sharing both structural and functional similarity have been identified in mammals: Nix (also called BNIP3L/BNIP3alpha\/B5) and, in C. elegans, ceBNIP3. The TM domain of BNIP3 and Nix share 80% identity. Endogenous BNIP3 is loosely associated with mitochondrial membrane in normal tissue but fully integrates into the mitochondrial outer membrane with the N-terminus in the cytoplasm and the C-terminus in the membrane during induction of cell death. This is accompanied by rapid and profound mitochondrial dysfunction characterized by opening of the mitochondrial permeability transition (PT) pore, proton electrochemical gradient suppression, and increased reactive oxygen species production. BNIP3 has been reported to localize to the nuclear envelope when co-expressed with E1B 19K. Endogenous BNIP3 protein is abundant in murine andhuman skeletal muscle and is not detectable in lysates of all other nonskeletal muscle-bearing tissues and many cell lines, including myoblasts and differentiated myocytes. BNIP3 also plays a role in autophagy. Hypoxia-induced autophagy requires expression of this protein. Beclin, an autophagy protein, is kept in check by Bcl2 (normoxic). When Bcl2 lets go of Beclin it then binds BNIP3/L3 (hypoxic), causing autophagy.ICC 1:50-1:200, IF 1:50-1:200, WB 1:500-1:1000
Conjugate	DyLight 650
Clone	Polyclonal
Target Species	Human
Applications	IF, ICC, WB
Supplier	Thermo Fisher Scientific
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About BNIP3
This gene is encodes a mitochondrial protein that contains a BH3 domain and acts as a pro-apoptotic factor. The encoded protein interacts with anti-apoptotic proteins, including the E1B 19 kDa protein and Bcl2. This gene is silenced in tumors by DNA methylation. [provided by RefSeq, Dec 2014]

About DyLight 650
DyLight™ 650 is a red-emitting fluorophore that excited by the 640 nm laser and collected using a 670/30 nm bandpass filter. DyLight™ 650 has an excitation peak at 652 nm and an emission peak at 672 nm, and is spectrally similar to Alexa Fluor™ 647 and Cy5. DyLight™ 650 is most commonly used in flow cytometery and fluorescence microscopy applications.

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