The precursor form of Brain-Derived Neurotrophic Factor (pro-BDNF) interacts preferentially with the pan-neurotrophin receptor p75 (p75NTR) and vps10p domain-containing receptor sortilin and induces neuronal apoptosis, whereas mature BDNF selectively binds with high affinity to the TrkB kinase receptor and promotes the survival, growth and differentiation of neurons. As proneurotrophins and mature neurotrophins elicit opposite biological effects, Pro-BDNF cleavage in the neuronal system is regulated in a specific and cell-context dependent manner. Pro-BDNF plays important role in negative regulation of neurotrophic actions in the brain.
Important signaling molecule that activates signaling cascades downstream of NTRK2.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. The versatility of BDNF is emphasized by its contribution to a range of adaptive neuronal responses including long-term potentiation (LTP), long-term depression (LTD), certain forms of short-term synaptic plasticity, as well as homeostatic regulation of intrinsic neuronal excitability.
The precursor form of Brain-Derived Neurotrophic Factor (pro-BDNF) interacts preferentially with the pan-neurotrophin receptor p75 (p75NTR) and vps10p domain-containing receptor sortilin and induces neuronal apoptosis; whereas mature BDNF selectively binds with high affinity to the TrkB kinase receptor and promotes the survival; growth and differentiation of neurons. As proneurotrophins and mature neurotrophins elicit opposite biological effects; Pro-BDNF cleavage in the neuronal system is regulated in a specific and cell-context dependent manner. Pro-BDNF plays important role in negative regulation of neurotrophic actions in the brain.
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.
β-2-Microglobulin (B2M) is a secreted protein with 1 Ig-like C1-type (immunoglobulin-like) domain which belongs to the beta-2-microglobulin family. B2M component of major histocompatibility complex (MHC) class I molecules; involved in the presentation of peptide antigens to the immune system. Polymers of beta 2-microglobulin can be found in tissues from patients on long-term hemodialysis. B2M is a protein found on the surface of many cells and plentiful on the surface of white blood cells. Serum B2M concentration is increased in renal diseases; various malignant diseases and some inflammatory and autoimmune disorders. B2M may adopt the fibrillar configuration of amyloid in certain pathologic states. The capacity to assemble into amyloid fibrils is concentration dependent. B2M has been shown as a marker for monitoring inflammatory disease activity and it appears likely to have a destructive role in amyloidosis-related arthritis. B2M might be involved in the OA (osteoarthritis) pathogenesis. Defects in B2M are the cause of hypercatabolic hypoproteinemia. Affected individuals show marked reduction in serum concentrations of immunoglobulin and albumin; probably due to rapid degradation. B2M could be a potential therapeutic target in ovarian cancer.
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