Jump to content

HEMGN

From Wikipedia, the free encyclopedia
(Redirected from HEMGN (gene))

HEMGN
Identifiers
AliasesHEMGN, CT155, EDAG, EDAG-1, NDR, hemogen
External IDsOMIM: 610715; MGI: 2136910; HomoloGene: 14223; GeneCards: HEMGN; OMA:HEMGN - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_018437
NM_197978

NM_053149

RefSeq (protein)

NP_060907
NP_932095

NP_444379

Location (UCSC)Chr 9: 97.93 – 97.94 MbChr 4: 46.39 – 46.41 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Hemogen is a protein that in humans is encoded by the HEMGN gene.[5] Hemgn Expression Regulation by Gfi1 Gfi1 (growth factor independence 1) is a transcriptional repressor involved in hematopoiesis, and it plays a crucial role in protecting hematopoietic cells from stress-induced apoptosis. The Hemgn gene is regulated by Gfi1 through a 16-bp promoter region, which is specifically located between +47 and +63 bp relative to the transcription start site (TSS). This regulation is dependent on Gfi1's interaction with the histone demethylase LSD1.

The key interaction mechanisms are as follows:

Gfi1 activates Hemgn expression through binding to its promoter region. Gfi1's activation is enhanced by its interaction with LSD1, which facilitates epigenetic modifications to increase the transcription of Hemgn.

Ikaros, another transcription factor, works synergistically with Gfi1 to further increase Hemgn expression. While Ikaros enhances Hemgn expression, it is not absolutely required for the Gfi1-mediated upregulation.

PU.1, another transcription factor, acts as a repressor of Hemgn. Gfi1 represses PU.1 expression, which precedes and correlates with the upregulation of Hemgn. In the absence of PU.1 (e.g., during knockdown or deficiency), Hemgn expression is augmented, showing that Gfi1 achieves Hemgn upregulation by suppressing PU.1.

The upregulation of Hemgn contributes significantly to the anti-apoptotic activity of Gfi1, allowing for cell survival under conditions of stress. This process occurs in a p53-independent manner, meaning that the anti-apoptotic effects of Gfi1 are not mediated through p53 pathways but rather through Hemgn regulation.[6]

References

[edit]
  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000136929Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000028332Ensembl, 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. ^ "Entrez Gene: HEMGN hemogen".
  6. ^ G C B, Hoyt LJ, Dovat S, Dong F (2024). "Upregulation of nuclear protein Hemgn by transcriptional repressor Gfi1 through repressing PU.1 contributes to the anti-apoptotic activity of Gfi1". Journal of Biological Chemistry. 300 (11). doi:10.1016/j.jbc.2024.107860. PMID 39374784.

Further reading

[edit]