Name :
Recombinant Human BNIP3L Protein

Biological Activity :

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

Biological Activity :
Testing in progress

Expression Host :
Human

Source :
E. coli

Tag :

Protein Accession No. :
NP_004322.1

NCBI Gene ID :

Synonyms :

Synonyms :
BCL2/adenovirus E1B 19kDa interacting protein 3-like

Amino Acid Sequence :

Molecular Weight :
The recombinant human BNIP3L consists of 186 amino acids and has a calculated molecular mass of 20.4 kDa. It migrates as an approximately 36 kDa band in SDS-PAGE under reducing conditions.

Purity :
> 88 % as determined by SDS-PAGE

State of Matter :

Product Concentration :

Storage and Stability :
Samples are stable for up to twelve months from date of receipt at -20℃ to -80℃. Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.

Endotoxin Level :
Please contact us for more information.

Protein Construction :
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.

Buffer Solution :
Lyophilized from sterile 50mM Tris, 150mM NaCl, 1mM DTT, pH 8.0Please contact us for any concerns or special requirements. Normally 5 % – 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization. Please refer to the specific buffer information in the hardcopy of datasheet.

Shipping :
In general, recombinant proteins are provided as lyophilized powder which are shipped at ambient temperature.Bulk packages of recombinant proteins are provided as frozen liquid. They are shipped out with blue ice unless customers require otherwise.

Redissolution :
A hardcopy of datasheet with reconstitution instructions is sent along with the products. Please refer to it for detailed information.

Synonyms :
BNIP3a Protein, Human; NIX Protein, Human BNIP3L 背景信息 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

References & Citations :
Imazu T, et al. (1999) Bcl-2 / E1B 19 kDa-interacting protein 3-like protein (Bnip3L) interacts with bcl-2 / Bcl-xL and induces apoptosis by altering mitochondrial membrane permeability. Oncogene. 18(32): 4523-9.Sun JL, et al. (2004) Expression and structure of BNIP3L in lung cancer. Ai Zheng. 23(1): 8-14.

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