HES and HERP families: Multiple effectors of the notch signaling pathway

By T. Iso, L. Kedes, Y. Hamamori. Journal of Cellular Physiology, 2003

1,296 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/b9805b68b9ae190186a7280ed8b308a3c2e76e3c

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Citations in the corpus

BMP receptor signaling: transcriptional targets, regulation of signals, and signaling cross-talk. (2005, background): “Upon complex formation between CSL and NICD, they induce transcription of target genes, including the Hey and Hes genes encoding basic HLH transcriptional regulators [109].”
Notch regulation of lymphocyte development and function (2004, background): “6 ) and the related Herp (Hes-related repressor protein) transcription factor famil”
The Notch target genes Hey1 and Hey2 are required for embryonic vascular development. (2004, background): “There is only a small number of target genes to mediate Notch function, and most of them belong to the Hes and Hey gene families (Iso et al. 2003).”
Notch signaling maintains bone marrow mesenchymal progenitors by suppressing osteoblast differentiation (2008, background): “Of the six potential targets of Notch, Hes1, Hes5, Hes7, Hey1, Hey2 and HeyL (ref”
Epithelial stem cells: turning over new leaves. (2007, neutral): “(1–7) and Hey (1–3) (Iso et al., 2003).”
Notch signaling in the mammalian central nervous system: insights from mouse mutants (2005, background): “In addition, it has become clear that although CBF1 (also called RBP-J or CSL) and the Hes gene”
When NRF2 Talks, Who's Listening? (2010, neutral): “Several lines of differential microarray analyses using RNAs isolated from MEFs prepared from Nrf2-=- and wildtype mice have shown that Notch1 and its direct downstream genes (Hes, Herp) (62) displayed decreased expression in Nrf2-=- MEF.”
Presenilin 1 mutants impair the self-renewal and differentiation of adult murine SVZ-neuronal progenitors via cell autonomous mechanisms involving Notch signaling (2010, background): “…and preferential differentiation into MAP2 or III-tubulin neurons; these defects have been attributed to reduced expression of Notch target genes, Hes1 and Hes5 (Shen et al., 1997; Wong et al., 1997; Kim and Shen, 2008) that would otherwise antagonize neuronal differentiation (Iso et al., 2003).”
The Glial Nature of Embryonic and Adult Neural Stem Cells (2009, background): “Notch also activates target genes such as hes1 and hes5 (Gaiano et al. 2000, Iso et al. 2003) to antagonize proneural genes and block cell differentiation.”