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.
Beta-actin (ACTB/ACTB) is one of six different actin isoforms in humans. Actins are highly conserved proteins that are involved in cell motility,structure and integrity. Beta actin is a major constituent of the contractile apparatus and one of the two nonmuscle cytoskeletal actins. Beta-actin gene is stably and constitutively expressed at high levels in most tissues and cells,and commonly used as a loading control for western blot and as a control for qPCR.
The protein encoded by this gene is part of a complex of proteins that constitute adherens junctions (AJs). AJs are necessary for the creation and maintenance of epithelial cell layers by regulating cell growth and adhesion between cells. The encoded protein also anchors the actin cytoskeleton and may be responsible for transmitting the contact inhibition signal that causes cells to stop dividing once the epithelial sheet is complete. Finally, this protein binds to the product of the APC gene, which is mutated in adenomatous polyposis of the colon. Mutations in this gene are a cause of colorectal cancer (CRC), pilomatrixoma (PTR), medulloblastoma (MDB), and ovarian cancer. Alternative splicing results in multiple transcript variants.
CTNNB1,also known as β-Catenin,is an evolutionarily conserved,multifunctional intracellular protein. CTNNB1 was originally identified in cell adherens junctions (Ajs) where it functions to bridge the cytoplasmic domain of cadherins to a-catenin and the actin cytoskeleton. Besides its essential role in the Ajs,CTNNB1 is also a key downstream component of the canonical Wnt pathway that plays diverse and critical roles in embryonic development and adult tissue homeostasis. Deregulation of CTNNB1 activity is associated with multiple diseases including cancers. .
Beta III Tubulin (TUBB3) is one of six β-tubulin isoforms and is expressed highly during fetal and postnatal development (axon guidance and maturation). Its expression levels decrease in the adult central nervous system (CNS) but remain high in the peripheral nervous system (PNS). Microtubules enriched in β3-tubulin are more dynamic than those composed of other β-tubulin isoforms. Research studies have shown that mutations in the β3-tubulin gene TUBB3 cause ocular motility defects and other nervous system disorders. Furthermore, β3-tubulin is present in neoplastic but not in normal differentiated glial cells. Thus, β3-tubulin is a great neuronal marker.
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