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HES5
Introduction
Transcription factor HES-5 is a protein that in humans is encoded by the HES5 gene.[1][2]
HES5 regulates brain development process.[3] HES5 expression significantly higher in squamous cervical carcinoma than in CIN as well as higher in CIN than normal cervical epithelia.[4] Human HES5 gene binds to Notch receptor and expression of HES5 decreases during cartilage differentiation.[5]
References
References
- β Takebayashi K, Akazawa C, Nakanishi S, Kageyama R (Feb 1995). “Structure and promoter analysis of the gene encoding the mouse helix-loop-helix factor HES-5. Identification of the neural precursor cell-specific promoter element”. J Biol Chem. 270 (3): 1342β9. doi:10.1074/jbc.270.3.1342. PMIDΒ 7836401.
- β “Entrez Gene: HES5 hairy and enhancer of split 5 (Drosophila)”.
- β Hatakeyama J, Bessho Y, Katoh K, Ookawara S, Fujioka M, Guillemot F, Kageyama R (November 2004). “Hes genes regulate size, shape and histogenesis of the nervous system by control of the timing of neural stem cell differentiation”. Development. 131 (22): 5539β50. doi:10.1242/dev.01436. PMIDΒ 15496443.
- β Liu J, Ye F, Chen H, LΓΌ W, Zhou C, Xie X (2007). “Expression of differentiation associated protein Hes1 and Hes5 in cervical squamous carcinoma and its precursors”. Int. J. Gynecol. Cancer. 17 (6): 1293β9. doi:10.1111/j.1525-1438.2007.00930.x. PMIDΒ 17388915.
- β Karlsson C, Jonsson M, Asp J, Brantsing C, Kageyama R, Lindahl A (March 2007). “Notch and HES5 are regulated during human cartilage differentiation”. Cell Tissue Res. 327 (3): 539β51. doi:10.1007/s00441-006-0307-0. PMIDΒ 17093926.
Further reading
Further reading
- Strausberg RL, Feingold EA, Grouse LH, et al. (2003). “Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences”. Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899β903. doi:10.1073/pnas.242603899. PMCΒ 139241. PMIDΒ 12477932.
- Gazit R, Krizhanovsky V, Ben-Arie N (2004). “Math1 controls cerebellar granule cell differentiation by regulating multiple components of the Notch signaling pathway”. Development. 131 (4): 903β13. doi:10.1242/dev.00982. PMIDΒ 14757642.
- Nakatani T, Mizuhara E, Minaki Y, et al. (2004). “Helt, a novel basic-helix-loop-helix transcriptional repressor expressed in the developing central nervous system”. J. Biol. Chem. 279 (16): 16356β67. doi:10.1074/jbc.M311740200. PMIDΒ 14764602.
- Kamakura S, Oishi K, Yoshimatsu T, et al. (2004). “Hes binding to STAT3 mediates crosstalk between Notch and JAK-STAT signalling”. Nat. Cell Biol. 6 (6): 547β54. doi:10.1038/ncb1138. PMIDΒ 15156153.
- Katoh M, Katoh M (2005). “Identification and characterization of human HES2, HES3, and HES5 genes in silico”. Int. J. Oncol. 25 (2): 529β34. doi:10.3892/ijo.25.2.529. PMIDΒ 15254753.
- Ohtsuka T, Imayoshi I, Shimojo H, et al. (2006). “Visualization of embryonic neural stem cells using Hes promoters in transgenic mice”. Mol. Cell. Neurosci. 31 (1): 109β22. doi:10.1016/j.mcn.2005.09.006. PMIDΒ 16214363.
- Ong CT, Cheng HT, Chang LW, et al. (2006). “Target selectivity of vertebrate notch proteins. Collaboration between discrete domains and CSL-binding site architecture determines activation probability”. J. Biol. Chem. 281 (8): 5106β19. doi:10.1074/jbc.M506108200. PMIDΒ 16365048.
- Gregory SG, Barlow KF, McLay KE, et al. (2006). “The DNA sequence and biological annotation of human chromosome 1”. Nature. 441 (7091): 315β21. doi:10.1038/nature04727. PMIDΒ 16710414.
- Karlsson C, Brantsing C, Svensson T, et al. (2007). “Differentiation of human mesenchymal stem cells and articular chondrocytes: analysis of chondrogenic potential and expression pattern of differentiation-related transcription factors”. J. Orthop. Res. 25 (2): 152β63. doi:10.1002/jor.20287. PMIDΒ 17072841.
- Karlsson C, Jonsson M, Asp J, et al. (2007). “Notch and HES5 are regulated during human cartilage differentiation”. Cell Tissue Res. 327 (3): 539β51. doi:10.1007/s00441-006-0307-0. PMIDΒ 17093926.
External links
External links
- HES5+protein,+human at the US National Library of Medicine Medical Subject Headings (MeSH)
This article incorporates text from the United States National Library of Medicine, which is in the public domain.
