Break point cluster region protein (Bcr) is encoded by the Bcr gene. The Bcr gene, mapping on chromosome22, was orginally identified by its presence in the chimeric Bcr-Abl oncogene. Although the BCR-ABL fusion protein has been extensively studied, the function of the normal BCR gene product is not clear. The protein has serine / threonine kinase activity and is a GTPase-activating protein for RAC1 and CDC42. A chromosomal aberration involving BCR has been found in patients with chronic myeloid leukemia.
The protein encoded by this gene is a member of the nerve growth factor family. It is induced by cortical neurons, and is necessary for survival of striatal neurons in the brain. Expression of this gene is reduced in both Alzheimer's and Huntington disease patients. This gene may play a role in the regulation of stress response and in the biology of mood disorders. Multiple transcript variants encoding distinct isoforms have been described for this gene. During development, promotes the survival and differentiation of selected neuronal populations of the peripheral and central nervous systems. Participates in axonal growth, pathfinding and in the modulation of dendritic growth and morphology. Major regulator of synaptic transmission and plasticity at adult synapses in many regions of the CNS.
BECN1(beclin 1) Homo sapiens This gene encodes a protein that regulates autophagy, a catabolic process of degradation induced by starvation. The encoded protein is a component of the phosphatidylinositol-3-kinase (PI3K) complex which mediates vesicle-trafficking processes. This protein is thought to play a role in multiple cellular processes, including tumorigenesis, neurodegeneration and apoptosis. Alternative splicing results in multiple transcript variants.
Beclin-1 (BECN1), also known as ATG6 or VPS30, has a central role in autophagy, a process of programmed cell survival, which is increased during periods of cell stress and extinguished during the cell cycle. Beclin-1, may play a role in antiviral host defense. It protects against infection by a neurovirulent strain of Sindbis virus. Beclin-1 participates in the regulation of autophagy and has an important role in development, tumorigenesis, and neurodegeneration. A progressively reduced Beclin-1 expression is reported to correlate with the primary tumor growth of squamous cell carcinoma and adenocarcinoma of the lung. Caspase-mediated cleavage of Beclin 1 promotes crosstalk between apoptosis and autophagy.
Beta-adrenergic receptors mediate the catecholamine-induced activation of adenylate cyclase through the action of G proteins. The beta-2-adrenergic receptor binds epinephrine with an approximately 30-fold greater affinity than it does norepinephrine.
β2-microglobulin (B2M) is a principal component of the Major Histocompatibility Complex (MHC) class I molecule, a ternary membrane protein complex that displays fragments derived from proteolyzed cytosolic proteins on the surface of cells for recognition by the surveillance immune system. As an integral component of the MHC class I complex, β2-microglobulin plays a critically important role in immune system function. It has important relevance to cancer biology research; for example, research studies have shown that nearly one-third of diffuse large B cell lymphomas contain mutations that inactivate β2-microglobulin gene function, thereby allowing tumor cells to escape immune detection. In addition, β2-microglobulin has been identified as an amyloid preprotein with collagen-binding affinity; its accumulation in osteoarthritic lesions of long-term dialysis patients is reportedly a contributing factor to the condition known as amyloid osteoarthropathy.
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