Widely expressed in fetal brain.
The protein expressed by the NTRK2 gene functions as a receptor for BDNF/brain-derived neurotrophic factor and NTF4/neurotrophin-4, and can also bind to NTF3/neurotrophin-3, although this interaction is less efficient. Upon binding with its ligands, the receptor undergoes homodimerization, autophosphorylation, and activation, enabling it to recruit, phosphorylate, and/or activate several downstream effectors like SHC1, FRS2, SH2B1, SH2B2, and PLCG1. These effectors regulate distinct but overlapping signaling cascades. Through SHC1, FRS2, SH2B1, and SH2B2, NTRK2 activates the GRB2-Ras-MAPK cascade, which regulates neuronal differentiation including neurite outgrowth, as well as the Ras-PI3 kinase-AKT1 signaling cascade, which is primarily involved in growth and survival. The PLCG1 pathway, which influences synaptic plasticity, plays a role in learning and memory by affecting both short-term synaptic function and long-term potentiation. Additionally, PLCG1 activation leads to NF-Kappa-B activation, promoting the transcription of genes related to cell survival, thereby suppressing anoikis. NTRK2 may also be involved in neurotrophin-dependent calcium signaling in glial cells and in mediating communication between neurons and glial cells. This supplementary information is collated from multiple sources and compiled automatically.
Developmental and epileptic encephalopathy 58
DEE58
A form of epileptic encephalopathy, a heterogeneous group of severe early-onset epilepsies characterized by refractory seizures, neurodevelopmental impairment, and poor prognosis. Development is normal prior to seizure onset, after which cognitive and motor delays become apparent. DEE58 is an autosomal dominant condition characterized by onset of refractory seizures in the first days or months of life.
None
The disease may be caused by variants affecting the gene represented in this entry.
Obesity, hyperphagia, and developmental delay
OBHD
A disorder characterized by early-onset obesity, hyperphagia, and severe developmental delay in motor function, speech, and language.
None
The disease is caused by variants affecting the gene represented in this entry.
Phosphorylated. Undergoes ligand-mediated autophosphorylation that is required for interaction with SHC1 and PLCG1 and other downstream effectors. Isoform TrkB-T-Shc is not phosphorylated.
Ubiquitinated. Undergoes polyubiquitination upon activation; regulated by NGFR. Ubiquitination regulates the internalization of the receptor (By similarity).
Belongs to the protein kinase superfamily. Tyr protein kinase family. Insulin receptor subfamily.
Isoform TrkB is expressed in the central and peripheral nervous system. In the central nervous system (CNS), expression is observed in the cerebral cortex, hippocampus, thalamus, choroid plexus, granular layer of the cerebellum, brain stem, and spinal cord. In the peripheral nervous system, it is expressed in many cranial ganglia, the ophthalmic nerve, the vestibular system, multiple facial structures, the submaxillary glands, and dorsal root ganglia. Isoform TrkB-T1 is mainly expressed in the brain but also detected in other tissues including pancreas, kidney and heart. Isoform TrkB-T-Shc is predominantly expressed in the brain.
TRKB, NTRK2, BDNF/NT-3 growth factors receptor, GP145-TrkB, Neurotrophic tyrosine kinase receptor type 2, TrkB tyrosine kinase, Tropomyosin-related kinase B, Trk-B
Proteins
Oncology
91999Da
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