Tropomyosin receptor kinase A: Difference between revisions

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{{Short description|A receptor tyrosine kinase involved in the development and function of the nervous system}}
== Tropomyosin Receptor Kinase A ==
{{Use dmy dates|date=October 2023}}


'''Tropomyosin receptor kinase A''' ('''TrkA'''), also known as '''NTRK1''', is a [[receptor tyrosine kinase]] that is encoded by the ''NTRK1'' gene in humans. It is a member of the [[neurotrophic tyrosine kinase receptor]] family and plays a crucial role in the development and function of the [[nervous system]].
[[File:Wikipedia_trka.png|thumb|right|Diagram of Tropomyosin Receptor Kinase A]]


==Structure==
'''Tropomyosin receptor kinase A''' (TrkA) is a [[protein]] that in humans is encoded by the ''NTRK1'' gene. TrkA is a member of the [[neurotrophin receptor]] family, which are [[tyrosine kinase]] receptors. These receptors are critical for the development and function of the [[nervous system]].
TrkA is a transmembrane protein that consists of an extracellular domain, a single transmembrane helix, and an intracellular tyrosine kinase domain. The extracellular domain is responsible for binding to its ligand, [[nerve growth factor]] (NGF), while the intracellular domain is involved in signal transduction.


==Function==
== Structure ==
TrkA is primarily activated by binding to NGF, which leads to receptor dimerization and autophosphorylation of specific tyrosine residues in the intracellular domain. This activation triggers several downstream signaling pathways, including the [[MAPK/ERK pathway]], the [[PI3K/AKT pathway]], and the [[PLC_ pathway]]. These pathways are involved in promoting neuronal survival, differentiation, and growth.
TrkA is a transmembrane receptor with an extracellular domain, a single transmembrane helix, and an intracellular tyrosine kinase domain. The extracellular domain is responsible for binding to its ligand, [[nerve growth factor]] (NGF), while the intracellular domain is involved in signal transduction.


==Role in Disease==
== Function ==
Mutations in the ''NTRK1'' gene can lead to a variety of disorders. For example, loss-of-function mutations are associated with [[congenital insensitivity to pain with anhidrosis]] (CIPA), a rare genetic disorder characterized by the inability to feel pain and the absence of sweat glands. On the other hand, gain-of-function mutations or gene fusions involving ''NTRK1'' can result in oncogenic activation, contributing to the development of certain cancers.
TrkA is primarily known for its role in the development and survival of [[neurons]]. It is activated by binding to NGF, which leads to receptor dimerization and autophosphorylation of tyrosine residues in the intracellular domain. This activation triggers several downstream signaling pathways, including the [[MAPK/ERK pathway]], the [[PI3K/AKT pathway]], and the [[PLC_ pathway]]. These pathways are involved in promoting neuronal survival, differentiation, and synaptic plasticity.


==Clinical Significance==
== Clinical Significance ==
TrkA is a target for cancer therapies, particularly in tumors that harbor ''NTRK1'' gene fusions. Inhibitors of TrkA, such as [[larotrectinib]] and [[entrectinib]], have been developed and approved for the treatment of cancers with these genetic alterations. These therapies have shown efficacy in reducing tumor size and improving patient outcomes.
Mutations in the ''NTRK1'' gene can lead to a rare genetic disorder known as [[congenital insensitivity to pain with anhidrosis]] (CIPA), which is characterized by the inability to feel pain and the absence of sweat glands. Additionally, aberrant TrkA signaling has been implicated in various [[cancers]], where it can act as an oncogene.


==Research==
== Related Pages ==
Ongoing research is focused on understanding the precise mechanisms of TrkA signaling and its role in various physiological and pathological processes. Studies are also exploring the potential of TrkA as a therapeutic target in neurodegenerative diseases and other conditions.
* [[Neurotrophin]]
 
==Related pages==
* [[Nerve growth factor]]
* [[Nerve growth factor]]
* [[Receptor tyrosine kinase]]
* [[Tyrosine kinase]]
* [[Neurotrophin]]
* [[Neurotrophin receptor]]


==References==
{{Receptor-stub}}
{{Reflist}}
{{Protein-stub}}


[[Category:Receptor tyrosine kinases]]
[[Category:Receptor tyrosine kinases]]
[[Category:Neurotrophin receptors]]
[[Category:Neurotrophin receptors]]
[[Category:Oncogenes]]
[[File:Wikipedia trka.png|thumb|right|Diagram of the TrkA receptor structure and signaling pathways.]]

Latest revision as of 16:25, 16 February 2025

Tropomyosin Receptor Kinase A[edit]

Diagram of Tropomyosin Receptor Kinase A

Tropomyosin receptor kinase A (TrkA) is a protein that in humans is encoded by the NTRK1 gene. TrkA is a member of the neurotrophin receptor family, which are tyrosine kinase receptors. These receptors are critical for the development and function of the nervous system.

Structure[edit]

TrkA is a transmembrane receptor with an extracellular domain, a single transmembrane helix, and an intracellular tyrosine kinase domain. The extracellular domain is responsible for binding to its ligand, nerve growth factor (NGF), while the intracellular domain is involved in signal transduction.

Function[edit]

TrkA is primarily known for its role in the development and survival of neurons. It is activated by binding to NGF, which leads to receptor dimerization and autophosphorylation of tyrosine residues in the intracellular domain. This activation triggers several downstream signaling pathways, including the MAPK/ERK pathway, the PI3K/AKT pathway, and the PLC_ pathway. These pathways are involved in promoting neuronal survival, differentiation, and synaptic plasticity.

Clinical Significance[edit]

Mutations in the NTRK1 gene can lead to a rare genetic disorder known as congenital insensitivity to pain with anhidrosis (CIPA), which is characterized by the inability to feel pain and the absence of sweat glands. Additionally, aberrant TrkA signaling has been implicated in various cancers, where it can act as an oncogene.

Related Pages[edit]


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