ITM2C Antibody (N-term) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Primary Accession | Q9NQX7 |
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Clone Names | 100712033 |
Gene ID | 81618 |
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Other Names | Integral membrane protein 2C, Cerebral protein 14, Transmembrane protein BRI3, CT-BRI3, ITM2C, BRI3 |
Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
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. |
Name | ITM2C |
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Synonyms | BRI3 |
Function | Negative regulator of amyloid-beta peptide production. May inhibit the processing of APP by blocking its access to alpha- and beta-secretase. Binding to the beta-secretase-cleaved APP C-terminal fragment is negligible, suggesting that ITM2C is a poor gamma-secretase cleavage inhibitor. May play a role in TNF-induced cell death and neuronal differentiation (By similarity). |
Cellular Location | Lysosome membrane; Single-pass type II membrane protein. Cell membrane; Single-pass type II membrane protein |
Tissue Location | High levels in the brain, specifically in the cerebral cortex, medulla, amygdala, hippocampus, thalamus, caudate nucleus, cerebellum, olfactory lobe and spinal cord. Very low levels in other organs. |
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Provided below are standard protocols that you may find useful for product applications.
Background
Negative regulator of beta amyloid peptide production. May inhibit the processing of APP by blocking its access to alpha-and beta-secretase. Binding to the beta-secretase-cleaved APP C-terminal fragment is negligible, suggesting that ITM2C is a poor gamma-secretase cleavage inhibitor. May play a role in TNF-induced cell death and neuronal differentiation (By similarity).
References
Yoshida, T., et al. Int. J. Mol. Med. 25(4):649-656(2010)Oguri, M., et al. Am. J. Hypertens. 23(1):70-77(2010)Matsuda, S., et al. J. Biol. Chem. 284(23):15815-15825(2009)Matsuda, S., et al. Mol Neurodegener 4, 41 (2009) :Gong, Y., et al. BMB Rep 41(4):287-293(2008)
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