BNIP3L/NIX Protein

Produktnummer ABIN7317369

Recombinant BNIP3L/NIX-Protein exprimiert in Escherichia coli (E. coli).

Kurzübersicht für BNIP3L/NIX Protein (ABIN7317369)

Target: BNIP3L/NIX (BNIP3L) (BCL2/adenovirus E1B 19kDa Interacting Protein 3-Like (BNIP3L))

Protein-Typ: Recombinant

Spezies: Human

Quelle: Escherichia coli (E. coli)

Reinheit: > 88 % as determined by reducing SDS-PAGE.

Produktdetails

Verwendungszweck: Recombinant Human BNIP3L Protein

Sequenz: Ser 2-Lys 187

Produktmerkmale: A DNA sequence encoding the human BNIP3L (NP_004322.1) (Ser 2-Lys 187) was expressed and purified, with additional two amino acids (Gly & Pro) at the N-terminus.

Anwendungsinformationen

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Format: Lyophilized

Rekonstitution: Please refer to the printed manual for detailed information.

Buffer: Lyophilized from sterile 50 mM Tris, 150 mM NaCl, 1 mM DTT, pH 8.0

Lagerung: 4 °C,-20 °C,-80 °C

Informationen zur Lagerung: Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80°C. Reconstituted protein solution can be stored at 4-8°C for 2-7 days. Aliquots of reconstituted samples are stable at < -20°C for 3 months.

Antigendetails

Target: BNIP3L/NIX (BNIP3L) (BCL2/adenovirus E1B 19kDa Interacting Protein 3-Like (BNIP3L))

Andere Bezeichnung: BNIP3L

Hintergrund:

Background: The deletion of BNIP3L results in retention of mitochondria during lens fiber cell remodeling, and that deletion of BNIP3L also results in the retention of endoplasmic reticulum and Golgi apparatus. BNIP3L localizes to the endoplasmic reticulum and Golgi apparatus of wild-type newborn mouse lenses and is contained within mitochondria, endoplasmic reticulum and Golgi apparatus isolated from adult mouse liver. As the cells become packed with keratin bundles, Bnip3L expression triggers mitophagy to rid the cells of the last remaining 'living' characteristic, thus completing the march from 'living' to 'dead' within the hair follicle. during retinal development tissue hypoxia triggers HIF1A/HIF-1 stabilization, resulting in increased expression of the mitophagy receptor BNIP3L/NIX. BNIP3L-dependent mitophagy results in a metabolic shift toward glycolysis essential for RGC neurogenesis. BNIP3L could be a potential therapeutic target for ischemic stroke

Synonym: BNIP3a,NIX

Molekulargewicht: 20.4 kDa

Pathways: Autophagie