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BNIP3L/NIX Protein

Recombinant BNIP3L/NIX protein expressed in Escherichia coli (E. coli).
Catalog No. ABIN7317369

Quick Overview for BNIP3L/NIX Protein (ABIN7317369)

Target

See all BNIP3L/NIX (BNIP3L) Proteins
BNIP3L/NIX (BNIP3L) (BCL2/adenovirus E1B 19kDa Interacting Protein 3-Like (BNIP3L))

Protein Type

Recombinant

Origin

  • 4
  • 2
Human

Source

  • 2
  • 2
  • 1
  • 1
Escherichia coli (E. coli)

Purity

> 88 % as determined by reducing SDS-PAGE.
  • Purpose

    Recombinant Human BNIP3L Protein

    Sequence

    Ser 2-Lys 187

    Characteristics

    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.
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  • Restrictions

    For Research Use only
  • Format

    Lyophilized

    Reconstitution

    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

    Storage

    4 °C,-20 °C,-80 °C

    Storage Comment

    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.
  • Target

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

    Alternative Name

    BNIP3L

    Background

    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

    Molecular Weight

    20.4 kDa

    Pathways

    Autophagy
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