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'''ING2''' or '''Inhibitor of Growth Family, Member 2''' is a [[protein]] that in humans is encoded by the ING2 [[gene]]. This protein is a member of the ING family of [[tumor suppressor]] proteins.
{{Infobox protein
 
| name = Inhibitor of growth protein 2
| symbol = ING2
| image = <!-- Image removed -->
| width =
| caption =
| HGNCid = 6059
| EntrezGene = 3622
| OMIM = 608053
| RefSeq = NM_001564
| UniProt = Q9H160
}}
'''Inhibitor of growth protein 2''' ('''ING2''') is a protein that in humans is encoded by the [[ING2 gene]].
== Function ==
== Function ==
ING2 is a member of the [[inhibitor of growth family]] of proteins, which are involved in [[chromatin remodeling]] and [[gene expression]]. ING2 plays a role in the regulation of [[cell cycle]], [[apoptosis]], and [[DNA repair]]. It is known to interact with the [[p53]] tumor suppressor protein and is involved in the [[p53 signaling pathway]].


The ING2 protein is a [[nuclear protein]] that physically interacts with the [[tumor suppressor]] protein [[p53]] and is a component of the [[mSin3a]] family of [[histone deacetylase]] complexes (HDAC). The ING2 protein is involved in numerous cellular processes including [[cell cycle]] control, [[apoptosis]], and [[DNA repair]].
== Clinical significance ==
 
Alterations in the expression of ING2 have been associated with various types of [[cancer]], including [[breast cancer]], [[colorectal cancer]], and [[melanoma]]. ING2 is considered a potential [[tumor suppressor gene]], and its loss of function may contribute to tumorigenesis.
== Structure ==
 
The ING2 protein contains a [[PHD finger]], a protein module that is implicated in [[chromatin]] recognition and [[nuclear import]]. The PHD finger of ING2 has been shown to bind to [[histone]] H3 trimethylated at lysine 4 (H3K4me3), a mark associated with [[gene activation]].
 
== Clinical Significance ==
 
Alterations in the ING2 gene have been associated with several types of [[cancer]], including [[breast cancer]], [[colorectal cancer]], and [[lung cancer]]. The ING2 protein may serve as a potential [[biomarker]] for these types of cancer.
 
[[File:ING2 protein structure.jpg|thumb|right|300px|Structure of the ING2 protein. Image from Wikimedia Commons.]]
 
== See Also ==
 
* [[ING1]]
* [[ING3]]
* [[ING4]]
* [[ING5]]
 
== References ==


<references />
== Interactions ==
ING2 has been shown to interact with several proteins, including:
* [[TP53]] (p53)
* [[Histone acetyltransferase]]s
* [[Histone deacetylase]]s


{{medicine-stub}}
These interactions suggest that ING2 is involved in the regulation of [[chromatin structure]] and [[gene transcription]].


[[Category:Proteins]]
== See also ==
* [[Inhibitor of growth family]]
* [[Tumor suppressor gene]]
* [[Chromatin remodeling]]
== External links ==
* [https://www.ncbi.nlm.nih.gov/gene/3622 ING2 gene - NCBI Gene]
* [https://www.uniprot.org/uniprot/Q9H160 ING2 protein - UniProt]
[[Category:Human proteins]]
[[Category:Tumor suppressor genes]]
[[Category:Tumor suppressor genes]]
[[Category:Genes]]
[[Category:Chromatin remodeling]]
[[Category:Oncology]]
[[Category:Medical genetics]]

Latest revision as of 01:50, 5 February 2025

Inhibitor of growth protein 2 (ING2) is a protein that in humans is encoded by the ING2 gene.

Function[edit]

ING2 is a member of the inhibitor of growth family of proteins, which are involved in chromatin remodeling and gene expression. ING2 plays a role in the regulation of cell cycle, apoptosis, and DNA repair. It is known to interact with the p53 tumor suppressor protein and is involved in the p53 signaling pathway.

Clinical significance[edit]

Alterations in the expression of ING2 have been associated with various types of cancer, including breast cancer, colorectal cancer, and melanoma. ING2 is considered a potential tumor suppressor gene, and its loss of function may contribute to tumorigenesis.

Interactions[edit]

ING2 has been shown to interact with several proteins, including:

These interactions suggest that ING2 is involved in the regulation of chromatin structure and gene transcription.

See also[edit]

External links[edit]