May play a role in host B-cell survival by preventing host apoptosis. The survival of infected B-cells is a key step to induce host cell differentiation into memory cells, thereby assuring long term infection of the organism. May also play an active part in oncogenesis in Burkitt's lymphomy and nasopharyngeal carcinoma (By similarity).
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Protein type: Apoptosis; Autophagy; Membrane protein, integral; Oncoprotein
Cellular Component: cytoplasm; cytosol; endoplasmic reticulum; endoplasmic reticulum membrane; intracellular; membrane; mitochondrial membrane; mitochondrial outer membrane; mitochondrion; myelin sheath; nuclear membrane; nucleus; perinuclear region of cytoplasm; pore complex
Molecular Function: BH domain binding; BH3 domain binding; channel activity; channel inhibitor activity; identical protein binding; protease binding; protein binding; protein heterodimerization activity; protein homodimerization activity; protein phosphatase 2A binding; protein phosphatase binding; sequence-specific DNA binding; transcription factor binding; ubiquitin protein ligase binding
Biological Process: actin filament organization; aging; apoptosis; apoptotic mitochondrial changes; axon regeneration; axonogenesis; B cell differentiation; B cell homeostasis; B cell lineage commitment; B cell proliferation; B cell receptor signaling pathway; behavioral fear response; brain development; CD8-positive, alpha-beta T cell lineage commitment; cell aging; cell growth; cell morphogenesis; cell proliferation; cell-cell adhesion; cellular calcium ion homeostasis; cellular response to glucose starvation; cerebral cortex development; cochlear nucleus development; defense response to virus; developmental growth; digestive tract morphogenesis; DNA damage response, signal transduction resulting in induction of apoptosis; ear development; endoplasmic reticulum calcium ion homeostasis; focal adhesion formation; gland morphogenesis; glomerulus development; growth; hair follicle morphogenesis; hemopoiesis; homeostasis of number of cells within a tissue; immune system development; induction of apoptosis by oxidative stress; induction of apoptosis via death domain receptors; kidney development; leukocyte homeostasis; lymphocyte homeostasis; lymphoid progenitor cell differentiation; male gonad development; melanin metabolic process; melanocyte differentiation; mesenchymal cell development; metanephros development; negative regulation of apoptosis; negative regulation of autophagy; negative regulation of cell growth; negative regulation of cell migration; negative regulation of cell proliferation; negative regulation of cellular pH reduction; negative regulation of mitotic cell cycle; negative regulation of myeloid cell apoptosis; negative regulation of neuron apoptosis; negative regulation of ossification; negative regulation of osteoblast proliferation; negative regulation of retinal cell programmed cell death; neuron apoptosis; oligodendrocyte differentiation; oocyte development; organ growth; organ morphogenesis; ossification; ovarian follicle development; peptidyl-serine phosphorylation; peptidyl-threonine phosphorylation; pigment granule organization and biogenesis; pigmentation; pigmentation during development; positive regulation of B cell proliferation; positive regulation of catalytic activity; positive regulation of cell growth; positive regulation of cell proliferation; positive regulation of melanocyte differentiation; positive regulation of multicellular organism growth; positive regulation of neuron maturation; positive regulation of peptidyl-serine phosphorylation; positive regulation of pigmentation; positive regulation of skeletal muscle fiber development; positive regulation of smooth muscle cell migration; post-embryonic development; protein amino acid dephosphorylation; protein polyubiquitination; regulation of apoptosis; regulation of autophagy; regulation of calcium ion transport; regulation of catalytic activity; regulation of cell cycle; regulation of cell-matrix adhesion; regulation of gene expression; regulation of mitochondrial membrane permeability; regulation of mitochondrial membrane potential; regulation of nitrogen utilization; regulation of pigmentation during development; regulation of programmed cell death; regulation of protein heterodimerization activity; regulation of protein homodimerization activity; regulation of protein localization; regulation of protein stability; regulation of transmembrane transporter activity; regulation of viral genome replication; release of cytochrome c from mitochondria; renal system process; response to aluminum ion; response to caffeine; response to cAMP; response to copper ion; response to corticosterone stimulus; response to cytokine stimulus; response to DNA damage stimulus; response to drug; response to electrical stimulus; response to estrogen stimulus; response to ethanol; response to folic acid; response to gamma radiation; response to glucocorticoid stimulus; response to heat; response to hydrogen peroxide; response to hypoxia; response to inorganic substance; response to insulin stimulus; response to iron ion; response to L-ascorbic acid; response to nicotine; response to nutrient; response to organic cyclic substance; response to organic substance; response to oxidative stress; response to peptide hormone stimulus; response to steroid hormone stimulus; response to toxin; response to UV-B; response to vitamin E; spleen development; T cell differentiation; T cell differentiation in the thymus; T cell homeostasis; T cell lineage commitment; thymus development; ureteric bud branching; ureteric bud development
Prevents premature death of the host cell during virus production, which would otherwise reduce the amount of progeny virus. Acts as a host B-cell leukemia/lymphoma 2 (Bcl-2) homolog, and interacts with pro-apoptotic proteins to prevent mitochondria permeabilization, release of cytochrome c and subsequent apoptosis of the host cell ().
Plays a major role in programmed cell death (PCD, apoptosis). Egl-1 binds to and directly inhibits the activity of ced-9, releasing the cell death activator ced-4 from a ced-9/ced-4 containing protein complex and allowing ced-4 to activate the cell-killing caspase ced-3.
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