|Application ||WB, E|
|Other Accession||Q4R540, NP_001012532.1, NP_001012534.1|
|Calculated MW||30224 Da|
|Antigen Region||27-55 aa|
|Other Names||Integral membrane protein 2C, Cerebral protein 14, Transmembrane protein BRI3, CT-BRI3, ITM2C, BRI3|
|Target/Specificity||This ITM2C antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 27-55 amino acids from the N-terminal region of human ITM2C.|
|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||ITM2C Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||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).|
|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.
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).
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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