Disease relevance of HES6

• These findings demonstrate that it is possible to utilize longitudinal samples from an in vivo model of colon carcinoma to identify genes up-regulated in metastases and that HES-6 may be an important marker of a range of primary cancers as well as metastatic colon carcinoma [1].

High impact information on HES6

• On N box-containing promoters, HES6 cooperated with HES1 to achieve maximal repression [2].
• HES6 interacted with the corepressor transducin-like Enhancer of split 1 in yeast and mammalian cells through its WRPW COOH-terminal motif [2].
• We have analyzed the biochemical and functional roles of HES6 in myoblasts [2].
• Our results show that HES6 is an important regulator of myogenesis and suggest that MyoR is a target for HES6-dependent transcriptional repression [2].
• The expression of HES6 was induced when myoblasts fused to become differentiated myotubes [2].

Biological context of HES6

• Expression of mouse HES-6, a new member of the Hairy/Enhancer of split family of bHLH transcription factors [3].
• Detection of differentially expressed HES-6 gene in metastatic colon carcinoma by combination of suppression subtractive hybridization and cDNA library array [1].

Anatomical context of HES6

• An HES6-VP16 activation domain fusion protein activated the N box-containing reporter, confirming that HES6 bound the N box in muscle cells [2].
• HES-6 is also expressed in the trunk, in the dorsal root ganglia and in the myotomes [3].
• In the limb buds HES-6 is expressed in skeletal muscle and presumptive tendons [3].
• Consistent with these findings, Hes6 inhibits Hes1-mediated transcriptional repression in cortical neural progenitor cells and promotes the differentiation of cortical neurons, a process that is normally inhibited by Hes1 [4].
• Subsequently, the expression of Hes6 is restricted to morphologically differentiated hair cells [5].

Physical interactions of HES6

• We further show that Hes6 directly interacts with CREB-binding protein (CBP), one of the key components of PML-NB, via its basic domain [6].

References