Homeobox protein CDX-1

Homeobox protein CDX-1 is a protein in humans that is encoded by the CDX1 gene.[5][6] CDX-1 is expressed in the developing endoderm and its expression persists in the intestine throughout adulthood.[7] CDX-1 protein expression varies along the intestine, with high expression in intestinal crypts and diminishing expression along intestinal villi.[8]

CDX1
Identifiers
AliasesCDX1, caudal type homeobox 1, Homeobox protein CDX-1
External IDsOMIM: 600746; MGI: 88360; HomoloGene: 1366; GeneCards: CDX1; OMA:CDX1 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001804

NM_009880

RefSeq (protein)

NP_001795

NP_034010

Location (UCSC)Chr 5: 150.17 – 150.18 MbChr 18: 61.15 – 61.17 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Function

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This gene is a member of the caudal-related homeobox transcription factor family. The encoded DNA-binding protein regulates intestine-specific gene expression and enterocyte differentiation. It has been shown to induce expression of the intestinal alkaline phosphatase gene, and inhibit beta-catenin/T-cell factor transcriptional activity.[6]

CDX1 has also been shown to play an important role in embryonic epicardial development. It has been demonstrated that CDX proteins suppress cardiac differentiation in both zebrafish and mouse embryonic stem cells, but the overall mechanism for how this happens is poorly understood.[9] However, CDX1 has been shown to be transiently expressed in the embryonic heart 11.5 days post coitum (dpc). This transient expression is thought to induce epicardial epithelial-to-mesenchymal transition and thus proper cardiovascular formation. It has been shown that low-dose CDX1 induction caused enhanced migration and differentiation of epicardium-derived cells into vascular smooth muscle, where as continued high dose induction of CDX1 or CDX1 deficiency diminished the ability of these cells to migrate and differentiate into smooth muscle by the actions of TGF-β1. Furthermore, CDX1 induction also altered transcript expression of genes related to cell adhesions for EMT and angiogenesis.[10] Therefore, along with its known roles in intestinal patterning and differentiation, CDX1 is also shown to be important in epicardial development.

References

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  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000113722Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000024619Ensembl, 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. ^ Bonner CA, Loftus SK, Wasmuth JJ (July 1995). "Isolation, characterization, and precise physical localization of human CDX1, a caudal-type homeobox gene". Genomics. 28 (2): 206–211. doi:10.1006/geno.1995.1132. PMID 8530027.
  6. ^ a b "Entrez Gene: CDX1 caudal type homeobox transcription factor 1".
  7. ^ Grainger S, Hryniuk A, Lohnes D (2013). "Cdx1 and Cdx2 exhibit transcriptional specificity in the intestine". PLOS ONE. 8 (1): e54757. Bibcode:2013PLoSO...854757G. doi:10.1371/journal.pone.0054757. PMC 3559873. PMID 23382958.
  8. ^ Barker N, van Es JH, Kuipers J, Kujala P, van den Born M, Cozijnsen M, et al. (October 2007). "Identification of stem cells in small intestine and colon by marker gene Lgr5". Nature. 449 (7165): 1003–1007. Bibcode:2007Natur.449.1003B. doi:10.1038/nature06196. PMID 17934449. S2CID 4349637.
  9. ^ Lengerke C, Wingert R, Beeretz M, Grauer M, Schmidt AG, Konantz M, et al. (June 2011). "Interactions between Cdx genes and retinoic acid modulate early cardiogenesis". Developmental Biology. 354 (1): 134–142. doi:10.1016/j.ydbio.2011.03.027. PMC 3502019. PMID 21466798.
  10. ^ Chu M, Wang L, Wang H, Shen T, Yang Y, Sun Y, et al. (2014). "A novel role of CDX1 in embryonic epicardial development". PLOS ONE. 9 (7): e103271. Bibcode:2014PLoSO...9j3271C. doi:10.1371/journal.pone.0103271. PMC 4113346. PMID 25068460.

Further reading

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