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Mouse Anti-BNIP3L (C-Terminus) Recombinant Antibody (CBYY-0711) (CBMAB-0714-YY)

This product is mouse antibody that recognizes BNIP3L. The antibody CBYY-0711 can be used for immunoassay techniques such as: ELISA, FC, ICC, IF, WB
See all BNIP3L antibodies

Summary

Host Animal
Mouse
Specificity
Human, Mouse
Clone
CBYY-0711
Antibody Isotype
IgG1, κ
Application
ELISA, FC, ICC, IF, WB

Basic Information

Immunogen
Synthetic peptide derived from the internal region of human, mouse and rat Nix proteins
Specificity
Human, Mouse
Antibody Isotype
IgG1, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

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

Format
Liquid
Concentration
0.5 mg/mL
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.
Epitope
C-Terminus

Target

Full Name
BCL2 interacting protein 3 like
Introduction
This gene encodes a protein that belongs to the pro-apoptotic subfamily within the Bcl-2 family of proteins. The encoded protein binds to Bcl-2 and possesses the BH3 domain. The protein directly targets mitochondria and causes apoptotic changes, including loss of membrane potential and the release of cytochrome c. [provided by RefSeq, Feb 2015]
Entrez Gene ID
Human665
Mouse12177
UniProt ID
HumanO60238
MouseQ9Z2F7
Alternative Names
BCL2 Interacting Protein 3 Like; BCL2/Adenovirus E1B 19 KDa Protein-Interacting Protein 3A; BCL2/Adenovirus E1B 19kDa Interacting Protein 3 Like; NIP3-Like Protein X; BNIP3a; NIP3L; NIX;
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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For research use only. Not intended for any clinical use.

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