HOXA5

Source: Wikipedia, the free encyclopedia.
HOXA5
Gene ontology
Molecular function
Cellular component
Biological process
Sources:Amigo / QuickGO
Ensembl
UniProt
RefSeq (mRNA)

NM_019102

NM_010453

RefSeq (protein)

NP_061975

NP_034583

Location (UCSC)Chr 7: 27.14 – 27.14 MbChr 6: 52.18 – 52.18 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Homeobox protein Hox-A5 is a protein that in humans is encoded by the HOXA5 gene.[5][6][7]

Function

In vertebrates, the genes encoding the class of

tumorigenesis.[7]

HoxA5 is controlled, at least in part, by

Comparison of the HoxA5

promoter methylation profile across cell types from the least differentiated (human embryonic stem cells) to the most endothelial-like (human umbilical vein endothelial cells, or HUVECs) shows that the HoxA5 promoter is normally heavily methylated in non-differentiated cells and becomes demethylated as cells differentiate down the endothelial lineage.[14] HoxA5 contains a C-Amp Response Elements (CRE) in its promoter.[8] POL2 and CTCF binding are enriched at the CpG-dense HoxA5 promoter in HUVECs, demonstrating transcriptional activity.[14]

Clinical significance

HoxA5 is suppressed in

DNMT inhibitor decitabine (5Aza) is used to treat this disease. While HoxA5 is known to be hypermethylated in AML, it has not yet been shown whether decitabine directly targets these genes for demethylation.[15][16] HOXA5 has also been nominated as an oncogene in glioblastoma. [17]

See also

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000106004 - Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000038253 - Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. PMID 1973146
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  7. ^ a b "Entrez Gene: HOXA5 homeobox A5".
  8. ^
    PMID 25953647
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External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.


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