BCL2 proteins are important regulators of cell death and survival. They are recognized as cellular oncogenes that are often deregulated in cancers.
Inmunógeno
Synthetic peptide directed towards the C terminal region of human BCL2A1
Aplicación
Anti- BCL2A1 antibody produced in rabbit is suitable for western blotting at a concentration of 1 μg/ml.
Acciones bioquímicas o fisiológicas
The expression of BCL2A1 protein is regulated by NF-κB transcription factor. It has prosurvival and metastatic effects and facilitates survival of leukocytes subsets and inflammation. It is upregulated in melanomas and chronic inflammatory diseases.
Secuencia
Synthetic peptide located within the following region: FIMNNTGEWIRQNGGWENGFVKKFEPKSGWMTFLEVTGKICEMLSLLKQY
Forma física
Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.
Cláusula de descargo de responsabilidad
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Cell death and differentiation, 19(1), 67-74 (2011-11-15)
B-cell lymphoma 2 (BCL2) proteins are important cell death regulators, whose main function is to control the release of cytochrome c from mitochondria in the intrinsic apoptotic pathway. They comprise both pro- and anti-apoptotic proteins, which interact in various ways
Metastatic spread of melanoma to the central nervous system (CNS) is a common and devastating manifestation of disease progression, which, despite its clinical importance, remains poorly understood with respect to underlying molecular mechanisms. Using a recently developed preclinical model of
Proceedings of the National Academy of Sciences of the United States of America, 110(11), 4321-4326 (2013-03-01)
Although targeting oncogenic mutations in the BRAF serine/threonine kinase with small molecule inhibitors can lead to significant clinical responses in melanoma, it fails to eradicate tumors in nearly all patients. Successful therapy will be aided by identification of intrinsic mechanisms
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