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BNIP3L Protein, Human, Recombinant

カタログ番号 TMPY-02376
別名: BCL2/adenovirus E1B 19kDa interacting protein 3-like, NIX, BNIP3a

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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BNIP3L Protein, Human, Recombinant
パッケージサイズ 在庫状況 単価(税別)
100 μg 約5 days ¥ 161,000
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生物学的特性に関する説明
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参考文献
説明 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 Host E. coli
Tag Tag Free
Accession Number O60238-1
別名 BCL2/adenovirus E1B 19kDa interacting protein 3-like, NIX, BNIP3a
Construction 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.
Protein Purity > 88 % as determined by SDS-PAGE
分子量 20.4 kDa (predicted)
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℃. For reconstituted proteinsolutions, 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

参考文献

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Keywords

BNIP3L Protein, Human, Recombinant BCL2/adenovirus E1B 19kDa interacting protein 3-like NIX BNIP3a recombinant recombinant-proteins proteins protein