F162A Antibody (C-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, E |
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Primary Accession | Q96A26 |
Other Accession | NP_055182.3 |
Reactivity | Human, Mouse |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 17342 Da |
Antigen Region | 118-146 aa |
Gene ID | 26355 |
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Other Names | Protein FAM162A, E2-induced gene 5 protein, Growth and transformation-dependent protein, HGTD-P, FAM162A, C3orf28, E2IG5 |
Target/Specificity | This F162A antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 118-146 amino acids from the C-terminal region of human F162A. |
Dilution | WB~~1:1000 |
Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | F162A Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | FAM162A |
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Synonyms | C3orf28, E2IG5 |
Function | Proposed to be involved in regulation of apoptosis; the exact mechanism may differ between cell types/tissues (PubMed:15082785). May be involved in hypoxia-induced cell death of transformed cells implicating cytochrome C release and caspase activation (such as CASP9) and inducing mitochondrial permeability transition (PubMed:15082785). May be involved in hypoxia-induced cell death of neuronal cells probably by promoting release of AIFM1 from mitochondria to cytoplasm and its translocation to the nucleus; however, the involvement of caspases has been reported conflictingly (By similarity). |
Cellular Location | Mitochondrion membrane; Single-pass membrane protein |
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Provided below are standard protocols that you may find useful for product applications.
References
O'Seaghdha, C.M., et al. Hum. Mol. Genet. 19(21):4296-4303(2010)
Qu, Y., et al. Stroke 40(8):2843-2848(2009)
Cho, Y.E., et al. Hum. Pathol. 40(7):975-981(2009)
Kim, J.Y., et al. FEBS Lett. 580(13):3270-3275(2006)
Lee, M.J., et al. Mol. Cell. Biol. 24(9):3918-3927(2004)
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