MYB (gene): Difference between revisions

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'''MYB (gene)'''


The '''MYB''' gene is a [[gene]] that encodes a [[protein]] known as MYB proto-oncogene, transcription factor. This protein is a member of the MYB family of [[transcription factor]]s and plays a crucial role in the regulation of [[gene expression]], [[cell proliferation]], [[differentiation]], and [[apoptosis]].
{{Infobox gene
| name = MYB
| symbol = MYB
| HGNCid = 7553
| OMIM = 189990
| EntrezGene = 4602
| RefSeq = NM_001130173
| UniProt = P10242
| chromosome = 6
| arm = q
| band = 23
}}
 
'''MYB''' is a [[gene]] that encodes a [[transcription factor]] involved in the regulation of [[gene expression]], [[cell cycle]], and [[apoptosis]]. The MYB protein is a key player in the control of [[hematopoiesis]], the process by which [[blood cells]] are formed.


== Function ==
== Function ==
 
The MYB gene is crucial for the proper development and function of [[hematopoietic stem cells]]. It acts as a transcriptional activator that binds to specific DNA sequences, thereby regulating the expression of target genes involved in cell proliferation and differentiation. MYB is particularly important in the development of [[erythrocytes]], [[megakaryocytes]], and [[lymphocytes]].
The MYB gene is responsible for producing the MYB protein, which is a transcription factor. Transcription factors are proteins that help turn specific genes "on" or "off" by binding to nearby [[DNA]]. The MYB protein binds to DNA and regulates the activity of other genes, thereby controlling many cellular processes.
 
== Structure ==
 
The MYB protein consists of several domains, including the MYB DNA-binding domain, the transactivation domain, and the negative regulatory domain. The MYB DNA-binding domain is responsible for binding to specific sequences of DNA, while the transactivation domain is involved in activating the transcription of target genes. The negative regulatory domain helps control the activity of the MYB protein.


== Clinical Significance ==
== Clinical Significance ==
Mutations or dysregulation of the MYB gene have been implicated in various [[cancers]], particularly [[leukemias]] and [[breast cancer]]. Overexpression of MYB is often associated with [[acute myeloid leukemia]] (AML) and [[T-cell acute lymphoblastic leukemia]] (T-ALL). MYB is also a potential target for therapeutic intervention in these malignancies.


Mutations in the MYB gene have been associated with several types of [[cancer]], including [[leukemia]], [[colorectal cancer]], and [[adenoid cystic carcinoma]]. These mutations can lead to the production of an abnormal MYB protein that can disrupt normal cell processes and lead to the development of cancer.
== Interactions ==
MYB interacts with several other proteins to exert its function. It forms complexes with [[coactivators]] such as [[CBP]] and [[p300]], which are necessary for its transcriptional activity. MYB also interacts with [[corepressors]] like [[N-CoR]] and [[SMRT]], which modulate its activity in different cellular contexts.


== Research ==
== Research ==
 
Ongoing research is focused on understanding the precise mechanisms by which MYB regulates gene expression and contributes to oncogenesis. Studies are also exploring the potential of MYB as a biomarker for cancer diagnosis and prognosis, as well as a target for novel therapeutic strategies.
Research is ongoing to better understand the role of the MYB gene in normal cell function and in disease. This research may lead to new treatments for diseases associated with mutations in the MYB gene.
 
[[File:MYB gene location.png|thumb|right|300px|Location of the MYB gene on chromosome 6.]]


== See Also ==
== See Also ==
* [[Oncogene]]
* [[Transcription factor]]
* [[Transcription factor]]
* [[Hematopoiesis]]
* [[Leukemia]]
* [[Gene expression]]
* [[Gene expression]]
* [[Cell proliferation]]
* [[Differentiation]]
* [[Apoptosis]]


== References ==
== References ==
{{Reflist}}


<references />
== External Links ==
* [https://www.ncbi.nlm.nih.gov/gene/4602 MYB gene - NCBI]
* [https://www.uniprot.org/uniprot/P10242 MYB protein - UniProt]


[[Category:Genes]]
[[Category:Genes on human chromosome 6]]
[[Category:Transcription factors]]
[[Category:Oncogenes]]
[[Category:Oncogenes]]
[[Category:Transcription factors]]
{{medicine-stub}}

Latest revision as of 17:01, 29 December 2024


MYB
Symbol MYB
HGNC ID 7553
Alternative symbols
Entrez Gene 4602
OMIM 189990
RefSeq NM_001130173
UniProt P10242
Chromosome 6q23
Locus supplementary data


MYB is a gene that encodes a transcription factor involved in the regulation of gene expression, cell cycle, and apoptosis. The MYB protein is a key player in the control of hematopoiesis, the process by which blood cells are formed.

Function[edit]

The MYB gene is crucial for the proper development and function of hematopoietic stem cells. It acts as a transcriptional activator that binds to specific DNA sequences, thereby regulating the expression of target genes involved in cell proliferation and differentiation. MYB is particularly important in the development of erythrocytes, megakaryocytes, and lymphocytes.

Clinical Significance[edit]

Mutations or dysregulation of the MYB gene have been implicated in various cancers, particularly leukemias and breast cancer. Overexpression of MYB is often associated with acute myeloid leukemia (AML) and T-cell acute lymphoblastic leukemia (T-ALL). MYB is also a potential target for therapeutic intervention in these malignancies.

Interactions[edit]

MYB interacts with several other proteins to exert its function. It forms complexes with coactivators such as CBP and p300, which are necessary for its transcriptional activity. MYB also interacts with corepressors like N-CoR and SMRT, which modulate its activity in different cellular contexts.

Research[edit]

Ongoing research is focused on understanding the precise mechanisms by which MYB regulates gene expression and contributes to oncogenesis. Studies are also exploring the potential of MYB as a biomarker for cancer diagnosis and prognosis, as well as a target for novel therapeutic strategies.

See Also[edit]

References[edit]

<references group="" responsive="1"></references>


External Links[edit]