BNIP3L Protein, Human, Recombinant

Catalog No. TMPY-02376

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

BNIP3L Protein, Human, Recombinant

Catalog No. TMPY-02376

Pack Size	Price	Availability	Quantity
100 μg	$700	7-10 days

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Biological Activity	Activity testing is in progress. It is theoretically active, but we cannot guarantee it. If you require protein activity, we recommend choosing the eukaryotic expression version first.
Description	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
Species	Human
Expression System	E. coli
Tag	Tag Free
Accession Number	O60238-1
Synonyms	NIX,BNIP3a,BCL2/adenovirus E1B 19kDa interacting protein 3-like
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. Predicted N terminal: Met
Protein Purity	> 88 % as determined by SDS-PAGE
Molecular Weight	20.4 kDa (predicted); 36 kDa (reducing conditions)
Endotoxin	Please contact us for more information.
Formulation	Lyophilized from a solution filtered through a 0.22 μm filter, containing 50 mM Tris, 150 mM NaCl, 1 mM DTT, pH 8.0.Typically, a mixture containing 5% to 8% trehalose, mannitol, and 0.01% Tween 80 is incorporated as a protective agent before lyophilization.
Reconstitution	A Certificate of Analysis (CoA) containing reconstitution instructions is included with the products. Please refer to the CoA for detailed information.
Stability & Storage	It is recommended to store recombinant proteins at -20°C to -80°C for future use. Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at -80°C. For reconstituted protein solutions, the solution can be stored at -20°C to -80°C for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.
Shipping	In general, Lyophilized powders are shipping with blue ice.
Research 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

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