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20篇 您的检索式：作者名="Nicholson RC"

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	题名	作者	年代	出处	被引量
1	Sequence of the mouse fibronectin -encoding gene promoter region显示文摘	Polly P Nicholson RC	1993	Gene1993，137，2：	1
2	Complex regulatory interactions control CRH gene expression显示文摘	Nicholson RC King BR Smith R	2004	Bioscience2004，1，9：	1
3	Corticotrophin releasing hormone and the timing of birth显示文摘	Smith R Nicholson RC	2007	Front Biosci2007，12，：	1
4	Prevalence of postpartum thyroid dysfunction: a quantitative review显示文摘	NICHOLSON W K ROBINSON K A SMALLRIDGE RC	2006	J Thyroid2006，16，6：	1
5	Microdeletions detected using chromosome microarray in children with suspected genetic movement disorders: a single-centre study显示文摘	Dale RC Grattan-Smith P Nicholson M	2012	Dev Med Child Neurol2012，54，7：	1
6	Microdeletions detected using chromosome microarray in children with suspected genetic movement disorders : a single-centre study 显示文摘	Dale RC Grattan-Smith P Nicholson M	2012	Dev Med Child Neurol2012，54，：	1
7	Microdeletions detected using chromosome microarray in children with suspected genetic movement disorders: a single-centre study显示文摘	Dale RC Grattan-Smith P Nicholson M	2012	Dev Med Child Neurol2012，54，：	1
8	The forestry refinery显示文摘	MYERY RC NICHOLSON MD Katzen R	1981	Chemtech1981，11，：	1
9	Antimicrobial - associated acute hepatitis 显示文摘	Nicholson Sc Webb CD Moellering RC Jr	2002	Pharmacotherapy2002，22，6：	1
10	Activation of the apoptotic protease CPP32 by cytotoxic T-cell-derived granzyme B显示文摘	Darmon AJ Nicholson DW Bleackley RC		0，，：	1
11	Activation of the apoptotic pretease CPP32 by cytotoxic T - cell - derived granzyme B 显示文摘	Darmon A J Nicholson DW Blcakly RC	1995	Nature1995，377，6548：	1
12	Prevalence of postpartum thyroid dysfunction: a quantitative review显示文摘	Nicholson WK Robinson KA Smallridge RC	2006	Thyroid2006，16，：	1
13	Prevalence of post- parturn thyroid dysfunction : a quantitative review 显示文摘	Nicholson WK Robinson KA Smallridge RC	2006	Thyroid2006，16，6：	1
14	Prevalence ofpostpartum thyroid dysfunction: a quantitative review 显示文摘	Nicholson WK Robinson KA Smallridge RC	2006	Thyroid2006，16，6：	1
15	Activation of the apoptotie protease CPP32 by cytotoxic T-cell-derived granzyme B显示文摘	Darmon AJ Nicholson DW Bleackley RC	1995	J Nature1995，377，6548：	1
16	Aspergillosis of the sphenoid sinus: presentation as a pituitary mass and postoperative gallium-67 imaging 显示文摘	Parker KM Nicholson JK Cezayirli RC	1996	Surg Neurol1996，45，4：	1
17	Aspergillosis of the sphenoid sinus: presentation as a pituitary mass and postoperative gallium-67 imaging显示文摘	Parker KM Nicholson JK Cezayidi RC	1996	Surg Neurol1996，45，4：	1
18	Microdeletionsdetected using chromosome microarray in children with suspectedgenetic movement disorders: a single-centre study显示文摘	Dale RC Grattan-Smith P Nicholson M	2012	Dev MedChild Neurol2012，54，：	1
19	Estrogen receptor-mediated down-regulation of corticotropin-releasing hormone gene expression is dependent on a cyclic adenosine 3’,5’-monophosphate regulatory element in human placental syncytiotrophoblast cells显示文摘Placental CRH plays a major role in the mechanisms controlling human pregnancy and parturition. Understanding how placental CRH production is regulated is therefore of importance. Previously we have shown that placental expression of CRH peptide and mRNA are inhibited by estrogens, in contrast to the stimulatory effects of estrogen on hypothalamic CRH production. Our current study found that in placental cells cotransfected with a CRH promoter construct and an estrogen receptor-alpha expression vector results in a differential regulation whereby 17beta-estradiol (E2) decreased and the putative pure estrogen antagonist, ICI 182780, increased CRH promoter activity. Sequential deletion of the CRH promoter indicated that the region between -248 and -213 bp was essential for the effect of both E2 and ICI 182780. This region contains a consensus cAMP regulatory element (CRE) that is a requirement for E2- and ICI 182780-mediated activity because the CRE motif can confer E2 inhibition on a heterologous promoter such as rabbit beta-globin. Mutation of the CRE resulted in a complete reversal of E2 and ICI 182780 regulatory effects. In summary, our results demonstrate that a consensus CRE is required for the action of estrogen receptor ligands in human placental syncytiotrophoblast cells.	Read MA Smith R Nicholson RC	2005	第二军医大学学报2005，26，4：	0
20	Progesterone receptors A and B differentially modulate corticotropin-releasing hormone gene expression through a cAMP regulatory element显示文摘Corticotrophin-releasing hormone (CRH) plays a major role in mechanisms controlling human pregnancy and parturition. Gene regulation by progesterone may be a key point in the control of placental CRH production. Studies in primary placental cells show that antagonism of progesterone activity or production by RU486 or trilostane leads to an increase in CRH promoter activity. This effect can be reversed by the addition of progesterone. Overexpression of progesterone receptor A (PR-A) or glucocorticoid receptor resulted in a decrease in CRH promoter activity following progesterone treatment, whereas an increase in promoter activity was observed with overexpressed PR-B. Studies including mutation of the cAMP regulatory element (CRE) confirm this site to be essential for the progesterone-mediated effects. In summary, our results demonstrate that progesterone regulates CRH gene transcription via a CRE in the CRH promoter and that PR-A and PR-B exhibit different actions in the regulation of CRH gene expression.	Smith R Nicholson RC	2005	第二军医大学学报2005，26，4：	0

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