ETS1: Difference between revisions

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'''ETS1''' is a [[gene]] that encodes the ETS proto-oncogene 1, a [[transcription factor]]. This gene is part of the ETS family of transcription factors, which are characterized by the presence of a conserved ETS DNA-binding domain that recognizes the core consensus DNA sequence GGAA/T in target genes.
{{Infobox gene
| name = ETS1
| image = <!-- Image removed -->
| caption = <!-- Image caption -->
| symbol = ETS1
| alt_symbols = c-ets-1
| HGNCid = 3487
| OMIM = 164720
| EntrezGene = 2113
| HUGO = 3487
| RefSeq = NM_005238
| UniProt = P14921
| chromosomal_location = 11q24.3
}}
 
'''ETS1''' is a [[gene]] that encodes a member of the [[ETS family]] of [[transcription factors]]. This family of transcription factors is characterized by the presence of a conserved [[ETS domain]], which is responsible for binding to specific [[DNA sequences]].


== Function ==
== Function ==
The ETS1 gene product is a transcription factor that activates or represses the transcription of a variety of genes, including those involved in [[cell growth]], [[cell differentiation]], [[apoptosis]], and the [[immune response]]. It is involved in the regulation of [[hematopoiesis]] and [[angiogenesis]], and it plays a role in various diseases, including [[cancer]] and [[autoimmune diseases]].
The ETS1 protein plays a crucial role in the regulation of [[gene expression]] during various biological processes, including [[cell proliferation]], [[differentiation]], [[apoptosis]], and [[angiogenesis]]. It is involved in the [[development]] of [[lymphoid]] and [[vascular systems]] and is essential for [[embryonic development]].
 
== Structure ==
The ETS1 protein consists of several domains, including the ETS domain, which is responsible for DNA binding, and the Pointed (PNT) domain, which is involved in protein-protein interactions. The ETS domain is highly conserved among ETS family members, while the PNT domain is unique to ETS1 and a few other ETS proteins.


== Clinical significance ==
== Clinical Significance ==
Alterations in the ETS1 gene have been associated with various types of cancer, including [[breast cancer]], [[lung cancer]], and [[leukemia]]. Overexpression of ETS1 has been observed in many tumors, and it has been suggested that ETS1 may contribute to tumor progression by promoting cell proliferation, angiogenesis, and metastasis.
Mutations or dysregulation of the ETS1 gene have been associated with various [[cancers]], including [[leukemia]], [[lymphoma]], and [[breast cancer]]. Overexpression of ETS1 has been observed in [[tumor cells]], where it may contribute to [[tumor progression]] and [[metastasis]].


In addition to its role in cancer, ETS1 has been implicated in autoimmune diseases such as [[systemic lupus erythematosus]] (SLE) and [[rheumatoid arthritis]] (RA). Studies have shown that ETS1 is involved in the regulation of immune cell function, and alterations in ETS1 expression or function may contribute to the development of these diseases.
== Interactions ==
ETS1 interacts with several other proteins and transcription factors to modulate gene expression. It can form complexes with [[cofactors]] such as [[CBP/p300]] and [[AP-1]], enhancing its transcriptional activity. These interactions are crucial for its role in [[cell signaling pathways]].


[[File:ETS1 protein structure.jpg|thumb|right|300px|Structure of the ETS1 protein. The ETS domain (red) is responsible for DNA binding, while the PNT domain (blue) is involved in protein-protein interactions.]]
== Research ==
Ongoing research is focused on understanding the precise mechanisms by which ETS1 regulates gene expression and contributes to disease. Targeting ETS1 and its pathways is being explored as a potential therapeutic strategy in cancer treatment.


== See also ==
== See Also ==
* [[ETS family]]
* [[Transcription factor]]
* [[Transcription factor]]
* [[Oncogene]]
* [[Gene expression]]
* [[Cancer biology]]


== References ==
== References ==
<references />
<references/>
 
== External Links ==
* [https://www.ncbi.nlm.nih.gov/gene/2113 ETS1 Gene - NCBI]
* [https://www.uniprot.org/uniprot/P14921 ETS1 Protein - UniProt]


[[Category:Genes]]
{{Transcription factors}}
{{Genes on human chromosome 11}}
[[Category:Transcription factors]]
[[Category:Transcription factors]]
[[Category:Genes on human chromosome 11]]
[[Category:Oncogenes]]
[[Category:Oncogenes]]
[[Category:Autoimmune diseases]]
[[Category:Cancer]]
{{Genes on human chromosome 11}}
{{Transcription factors}}
{{Oncogenes}}
{{Autoimmune diseases}}
{{Cancer}}
{{medicine-stub}}

Latest revision as of 20:41, 30 December 2024

ETS1
Symbol ETS1
HGNC ID 3487
Alternative symbols
Entrez Gene 2113
OMIM 164720
RefSeq NM_005238
UniProt P14921
Chromosome
Locus supplementary data


ETS1 is a gene that encodes a member of the ETS family of transcription factors. This family of transcription factors is characterized by the presence of a conserved ETS domain, which is responsible for binding to specific DNA sequences.

Function[edit]

The ETS1 protein plays a crucial role in the regulation of gene expression during various biological processes, including cell proliferation, differentiation, apoptosis, and angiogenesis. It is involved in the development of lymphoid and vascular systems and is essential for embryonic development.

Clinical Significance[edit]

Mutations or dysregulation of the ETS1 gene have been associated with various cancers, including leukemia, lymphoma, and breast cancer. Overexpression of ETS1 has been observed in tumor cells, where it may contribute to tumor progression and metastasis.

Interactions[edit]

ETS1 interacts with several other proteins and transcription factors to modulate gene expression. It can form complexes with cofactors such as CBP/p300 and AP-1, enhancing its transcriptional activity. These interactions are crucial for its role in cell signaling pathways.

Research[edit]

Ongoing research is focused on understanding the precise mechanisms by which ETS1 regulates gene expression and contributes to disease. Targeting ETS1 and its pathways is being explored as a potential therapeutic strategy in cancer treatment.

See Also[edit]

References[edit]

<references/>

External Links[edit]