ErbB-2 receptor: Difference between revisions
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In [[biochemistry]], '''erbB-2''' ('''Human Epidermal growth factor Receptor 2''', '''HER2''', '''HER-2''', '''HER2/neu''') is a [[cell surface receptor]] that is a "[[protein-tyrosine kinase receptor]] that is found to be overexpressed in a significant number of adenocarcinomas. It has extensive homology to and can heterodimerize with the EGF receptor ([[epidermal growth factor receptor]]), the [[erbB-3 receptor]] and the erbB-4 receptor. | In [[biochemistry]], '''erbB-2''' ('''Human Epidermal growth factor Receptor 2''', '''HER2''', '''HER-2''', '''HER2/neu''') is a [[cell surface receptor]] that is a "[[protein-tyrosine kinase receptor]] that is found to be overexpressed in a significant number of adenocarcinomas including gastric, esophageal, salivary, colon, bladder and lung cancers (8-9). It has extensive homology to and can heterodimerize with the EGF receptor ([[epidermal growth factor receptor]]), the [[erbB-3 receptor]] and the erbB-4 receptor. "<ref>{{MeSH}}</ref> | ||
The ErbB-2 gene is located on chromosome 17q21 and encodes a protein of 1255 amino acids which weighs, when glycosylated, 185 kDa. The human ErbB-2 was cloned by homology screening with v-ErbB (3) and has the highest homology to the [[epidermal growth factor receptor | EGFR]] among ErbB family members. It is mostly related to EGFR in its [[kinase]] domain (82%) and mostly distinct in the C-terminus, which contains most of the autophosphorylation sites. ErbB-2 is the only orphan receptor of the ErbB family, since no ligand binding it has been found up to date. Activation of ErbB-2 is, therefore, highly dependent on the expression of other family members, to which it is recruited as a preferred heterodimeric partner (4). On the other hand, overexpression and/or mutation of ErbB-2 are thought to lead to spontaneous dimerisation and the stabilization of the receptor dimmers in a ligandindependent manner (5-7). | |||
== | [[Trastuzumab]] is a [[monoclonal antibody]] against the ErbB-2 receptor that lengthens remission time in metastatic [[breast cancer]].<ref name="pmid17611206">{{cite journal| author=Hudis CA| title=Trastuzumab--mechanism of action and use in clinical practice. | journal=N Engl J Med | year= 2007 | volume= 357 | issue= 1 | pages= 39-51 | pmid=17611206 | ||
<references/> | | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=17611206 | doi=10.1056/NEJMra043186 }} </ref> | ||
==Attribution== | |||
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==Footnotes== | |||
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Latest revision as of 10:31, 2 September 2024
In biochemistry, erbB-2 (Human Epidermal growth factor Receptor 2, HER2, HER-2, HER2/neu) is a cell surface receptor that is a "protein-tyrosine kinase receptor that is found to be overexpressed in a significant number of adenocarcinomas including gastric, esophageal, salivary, colon, bladder and lung cancers (8-9). It has extensive homology to and can heterodimerize with the EGF receptor (epidermal growth factor receptor), the erbB-3 receptor and the erbB-4 receptor. "[1] The ErbB-2 gene is located on chromosome 17q21 and encodes a protein of 1255 amino acids which weighs, when glycosylated, 185 kDa. The human ErbB-2 was cloned by homology screening with v-ErbB (3) and has the highest homology to the EGFR among ErbB family members. It is mostly related to EGFR in its kinase domain (82%) and mostly distinct in the C-terminus, which contains most of the autophosphorylation sites. ErbB-2 is the only orphan receptor of the ErbB family, since no ligand binding it has been found up to date. Activation of ErbB-2 is, therefore, highly dependent on the expression of other family members, to which it is recruited as a preferred heterodimeric partner (4). On the other hand, overexpression and/or mutation of ErbB-2 are thought to lead to spontaneous dimerisation and the stabilization of the receptor dimmers in a ligandindependent manner (5-7).
Trastuzumab is a monoclonal antibody against the ErbB-2 receptor that lengthens remission time in metastatic breast cancer.[2]
Attribution
- Some content on this page may previously have appeared on Wikipedia.
Footnotes
- ↑ Anonymous (2024), ErbB-2 receptor (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ Hudis CA (2007). "Trastuzumab--mechanism of action and use in clinical practice.". N Engl J Med 357 (1): 39-51. DOI:10.1056/NEJMra043186. PMID 17611206. Research Blogging.