Human Recombinant BNIP3L protein (V2LY-0526-LY2381)

Name: Human Recombinant BNIP3L protein
SKU: V2LY-0526-LY2381
Rating: 5 (1 reviews)

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Datasheet

SDS

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Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Expressed Host

E. coli

Protein Species

Human

Protein Construction

This product is Human Recombinant BNIP3L protein consist of Amino Acid: 2-187 and predicts a molecular mass of 20.4 kDa.

Molecule Mass

20.4 kDa

Sequence

Amino Acid: 2-187

Species

Human

Formulations & Storage [For reference only, actual COA shall prevail!]

Purity

>88% as determined by SDS-PAGE

Endotoxin

Please contact us for more information.

Format

Lyophilized

Reconstitution

Allow the vial and reconstitution buffer to equilibrate to room temperature. Briefly centrifuge or tap down the vial to ensure that all lyophilized powder is collected at the bottom of the vial. For the reconstitution of this product, we recommend adding PBS or sterile water to achieve a final antibody concentration of 1 mg/mL. Allow the vial to reconstitute for 10-15 minutes at room temperature with gentle agitation. Avoid vigorous shaking that can cause foaming and antibody denaturation. Aliquot into volumes based on your experiment and store liquid protein at -20°C or -80°C for long time.

Buffer

Lyophilized from sterile PBS

Preservative

None

Storage

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

More Infomation

Target

Full Name

BCL2 interacting protein 3 like

Function

Induces apoptosis. Interacts with viral and cellular anti-apoptosis proteins. Can overcome the suppressors BCL-2 and BCL-XL, although high levels of BCL-XL expression will inhibit apoptosis. Inhibits apoptosis induced by BNIP3. Involved in mitochondrial quality control via its interaction with SPATA18/MIEAP: in response to mitochondrial damage, participates in mitochondrial protein catabolic process (also named MALM) leading to the degradation of damaged proteins inside mitochondria. The physical interaction of SPATA18/MIEAP, BNIP3 and BNIP3L/NIX at the mitochondrial outer membrane regulates the opening of a pore in the mitochondrial double membrane in order to mediate the translocation of lysosomal proteins from the cytoplasm to the mitochondrial matrix. May function as a tumor suppressor.

Biological Process

Cellular response to hypoxia Source: MGI
Defense response to virus Source: UniProtKB
Mitochondrial outer membrane permeabilization Source: GO_Central
Mitochondrial protein catabolic process Source: UniProtKB
Negative regulation of apoptotic process Source: UniProtKB
Negative regulation of cell death Source: MGI
Negative regulation of mitochondrial membrane potential Source: Ensembl
Positive regulation of apoptotic process Source: UniProtKB
Positive regulation of macroautophagy Source: MGI
Regulation of apoptotic process Source: Reactome
Regulation of autophagy of mitochondrion Source: Ensembl
Regulation of programmed cell death Source: GO_Central
Regulation of protein targeting to mitochondrion Source: Ensembl
Viral process Source: UniProtKB-KW

Cellular Location

Mitochondrion outer membrane; Endoplasmic reticulum; Nucleus envelope; Membrane. Colocalizes with SPATA18 at the mitochondrion outer membrane.

Topology

Helical: 188-208 aa

PTM

Undergoes progressive proteolysis to an 11 kDa C-terminal fragment, which is blocked by the proteasome inhibitor lactacystin.

Li, R., Chen, G., Dang, Y., He, R., Liu, A., Ma, J., & Ling, Z. (2021). Expression and Clinical Significance of BCL2 Interacting Protein 3 Like in Multiple Myeloma. Technology in cancer research & treatment, 20, 15330338211024551.

Kim, Y. J., Choo, O. S., Lee, J. S., Jang, J. H., Woo, H. G., & Choung, Y. H. (2021). BCL2 Interacting Protein 3-like/NIX-mediated Mitophagy Plays an Important Role in the Process of Age-related Hearing Loss. Neuroscience, 455, 39-51.

Marinković, M., Šprung, M., & Novak, I. (2021). Dimerization of mitophagy receptor BNIP3L/NIX is essential for recruitment of autophagic machinery. Autophagy, 17(5), 1232-1243.

Wu, X., Zheng, Y., Liu, M., Li, Y., Ma, S., Tang, W., ... & Zhang, X. (2021). BNIP3L/NIX degradation leads to mitophagy deficiency in ischemic brains. Autophagy, 17(8), 1934-1946.

Yazdankhah, M., Ghosh, S., Shang, P., Stepicheva, N., Hose, S., Liu, H., ... & Sinha, D. (2021). BNIP3L-mediated mitophagy is required for mitochondrial remodeling during the differentiation of optic nerve oligodendrocytes. Autophagy, 1-20.

Ouyang, S., Chen, W., Zeng, G., Lei, C., Tian, G., Zhu, M., ... & Yang, M. (2020). MicroRNA-183-3p up-regulated by vagus nerve stimulation mitigates chronic systolic heart failure via the reduction of BNIP3L-mediated autophagy. Gene, 726, 144136.

da Silva Rosa, S. C., Martens, M. D., Field, J. T., Nguyen, L., Kereliuk, S. M., Hai, Y., ... & Gordon, J. W. (2020). BNIP3L/Nix-induced mitochondrial fission, mitophagy, and impaired myocyte glucose uptake are abrogated by PRKA/PKA phosphorylation. Autophagy, 1-16.

Lampert, M. A., Orogo, A. M., Najor, R. H., Hammerling, B. C., Leon, L. J., Wang, B. J., ... & Gustafsson, Å. B. (2019). BNIP3L/NIX and FUNDC1-mediated mitophagy is required for mitochondrial network remodeling during cardiac progenitor cell differentiation. Autophagy, 15(7), 1182-1198.

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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme Linked Immunospot (ELISpot)
Proteogenomic
Other Protocols

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Isotype control

For research use only. Not intended for any clinical use.

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