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1                                              GRH value has decreased significantly in thick phenotype
2 nt sites revealed that the motifs YP, CP and GRH, are preferred in drivers, whereas SI, IQ and TVI ar
3 ences matching binding sites for JUN/FOS and GRH transcription factors, but vary widely in trans- and
4                            Mechanisms behind GRH uncoupling were diverse but could generally be attri
5                                           Ce-GRH-1 binds DNA in a sequence-specific manner identical
6                              In addition, Ce-GRH-1 binds to sequences upstream of the C.elegans gene
7                     The C.elegans member, Ce-GRH-1, groups with the Grainyhead subfamily, while the X
8                                 Grainy head (GRH) is a key transcription factor responsible for epide
9 attachment level (CAL) and recession height (GRH), recession width (GRW) and KGW measurements were re
10                 However, it is not known how GRH function is reactivated to repair differentiated epi
11                                     However, GRH with mutant ERK phosphorylation sites can still prom
12                  The growth rate hypothesis (GRH) posits that variation in organismal stoichiometry (
13        Serine 91 is the principal residue in GRH that is phosphorylated by ERK.
14 r its DNA binding function, the ERK sites in GRH are required to activate Dopa decarboxylase (Ddc) an
15 utations of the ERK phosphorylation sites in GRH do not impair its DNA binding function, the ERK site
16 ur phylogenetic analysis of the expanded LSF/GRH family (including other previously unrecognized prot
17           We propose that the combination of GRH and FOS is part of an ancient wound-response pathway
18 s required for wound-dependent expression of GRH target genes in epidermal cells.
19                           Here, we show that GRH is directly regulated by extracellular signal-regula
20                                          The GRH has found broad but not uniform support in studies a
21 e growth-RNA-P relationship predicted by the GRH may be uncoupled and outline paths for both theoreti
22 sting that ERK sites are dispensable for the GRH function in establishing epidermal barrier integrity
23 d be accounted for in empirical tests of the GRH and formalised mathematically to facilitate a predic
24  needed to broaden the working domain of the GRH.
25                                Together, the GRH was supported in ~50% of studies.