|Other Names||Vesicle transport protein SEC20, BCL2/adenovirus E1B 19 kDa protein-interacting protein 1, Transformation-related gene 8 protein, TRG-8, BNIP1, NIP1, SEC20L|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP1315a was selected from the region of human NIP1 BH3 Domain. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||SNARE that may be involved in targeting and fusion of Golgi-derived retrograde transport vesicles with the ER. Required for maintenance of ER network. Implicated in the suppression of cell death. May be involved in mitochondrial autophagy.|
|Cellular Location||Mitochondrion. Endoplasmic reticulum membrane; Single-pass type IV membrane protein|
|Tissue Location||Isoform 1 is highly expressed in heart, brain, liver skeletal muscle and pancreas. Isoform 3 is moderately expressed in placenta, lung and kidney. Isoform 4 is highly expressed in testis and small intestine|
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Provided below are standard protocols that you may find useful for product applications.
This gene is a member of the BCL2/adenovirus E1B 19 kd-interacting protein (BNIP) family. It interacts with the E1B 19 kDa protein which is responsible for the protection of virally-induced cell death, as well as E1B 19 kDa-like sequences of BCL2, also an apoptotic protector. Alternative splicing of this gene results in four products of unknown function. Transcript variant BNIP1 contains the entire coding region of the gene. This variant contains a fully conserved BH3 domain, which has been associated with pro-apoptotic function.
Zhang, H., et al., FEBS Lett. 448(1):23-27 (1999).Boyd, J.M., et al., Cell 79(2):341-351 (1994).
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