Regulation of camp-inducible genes by creb

Montminy, Marc; González, Gustavo; Yamamoto, Karen K.

doi:10.1016/0166-2236(90)90045-c

Cited by 392 publications

(208 citation statements)

References 23 publications

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“…The latter sequence is designated CRE G/A , as the sequence contains the 8-bp core motif of the cAMP response element (CRE: TGACGTCA) identified from mammals (Montminy et al, 1990), with flanking guanine and adenine (G/A) at -5 and ϩ5 (taking the central two nucleotides, C and G flanking the axis of symmetry designated Ϫ1 and ϩ1). However, the regulatory role of the C-box in cAMP responsiveness is not known in plants.…”

Section: Resultsmentioning

confidence: 99%

STF1 is a novel TGACG‐binding factor with a zinc‐finger motif and a bZIP domain which heterodimerizes with GBF proteins

et al. 1998

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SummaryTwo separate nuclear binding activities (B1 and B2) in the soybean apical hypocotyl have been identified that interact with a palindromic C-box sequence (TGACGTCA) and which are developmentally regulated in an inverse manner. The bZIP factors responsible for these two binding activities, B1 and B2, were isolated from a cDNA library and designated STGA1 and STFs (STF1 and STF2), respectively. Sequence analysis shows that the STFs contain both a zinc-finger domain and a bZIP domain. The two zinc finger sequences of Cys 4 -Cys 4 are most related to the RING zincfinger motif carrying a Cys 3 -His-Cys 4 . In addition the bZIP domain of STFs is highly homologous to the HY5 protein of Arabidopsis. DNA binding studies revealed that STF1 binding to the TGACGT sequence requires distinct flanking sequences. Furthermore, STF1 binds to the Hex sequence as a heterodimer with G-box binding factors (GBFs), a feature not observed with STGA1. Since STF1 expression is most prevalent in apical and elongating hypocotyls, it is proposed that STF1 may be a transcription factor involved in the process of hypocotyl elongation.

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Section: Resultsmentioning

confidence: 99%

STF1 is a novel TGACG‐binding factor with a zinc‐finger motif and a bZIP domain which heterodimerizes with GBF proteins

et al. 1998

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“…to phosphorylate cAMP response element binding protein CREB (Montminy et al 1990). CRH promoter contains cis-acting elements among those the cAMP-response element (CRE) is of the highest significance in stress-initiated CRH transcription (Kovacs & Sawchenko 1996b, Seasholtz et al 1991, Seasholtz et al 1988 .…”

Section: Regulation Of Hypothalamic Crh Transcriptionmentioning

confidence: 99%

CRH: The link between hormonal-, metabolic- and behavioral responses to stress

Kovács

2013

Journal of Chemical Neuroanatomy

108

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Two major and mutually interconnected brain systems are recruited during stress reaction. One is the hypothalamic paraventricular nucleus (PVH) and the second is the extended amygdala. PVH governs the neuroendocrine stress response while CeA regulates most of the autonomic and behavioral stress reactions. The common neurohormonal mediator of these responses is the corticotropin-releasing hormone, CRH, which is expressed in both centers. CRH belongs to a larger family of neuropeptides that also includes urocortins 1, 2, and 3 all have different affinity towards the two types of CRHR receptors and have been implicated in regulation of stress and HPA axis activity. One functionally relevant aspect of CRH systems is their differential regulation by glucocorticoids. While corticosterone inhibits CRH transcription in the PVH, stress-induced glucocorticoids stimulate CRH expression in the extended amygdala. This review summarizes past and recent findings related to CRH gene regulation and its involvement in the neuroendocrine, autonomic and behavioral stress reaction.Key words: Corticotropin-releasing hormone, paraventricular nucleus, central amygdala, bed nucleus of stria terminalis, corticosterone, cAMP-response element.

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“…One such postreceptor target that can be influenced by either 5HT or NE as well as by drugs that affect these systems is the nuclear transcription factor cAMP response element binding protein (CREB) (Montminy, et al 1990;Meyer and Habener 1993;Nibuya et al 1996;Duman et al 1997Duman et al , 1999Thome et al 2000). A role for the cAMP cascade in the long-term ac- (Nestler et al 1989) and that the activity of CREB is enhanced following its phosphorylation by PKA (Meyer and Habener 1993;Ghosh and Greenberg 1995).…”

Section: Abstract : Creb; Antidepressant Drugs; Glucocorticoid Recepmentioning

confidence: 99%

Altered Regulation of CREB by Chronic Antidepressant Administration in the Brain of Transgenic Mice with Impaired Glucocorticoid Receptor Function

Blom

Tascedda

Carra

et al. 2002

Neuropsychopharmacology

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Various effects of antidepressant drugs on gene transcription have been described and altered gene expression has been proposed as being a common biological basis underlying depressive illness. One target for the common action of antidepressants is a modifying effect on the regulation of postreceptor pathways and genes related to the cAMP cascade. Recent studies have demonstrated that long-term antidepressant treatment resulted in sustained activation of the cyclic adenosine 3 Ј ,5 Ј -monophosphate system and in increased expression of the transcription factor cAMP response element binding protein (CREB). KEY WORDS : CREB; Antidepressant drugs; Glucocorticoid receptor; Transgenic miceWhile the regulation of monoamine levels and their receptors or the restoration of hypothalamus-pituitaryadrenal (HPA) system feedback may represent initial effects of antidepressant drugs, their therapeutic action could be related to subsequent action on genes involved in postreceptor mechanisms. One such postreceptor target that can be influenced by either 5HT or NE as well as by drugs that affect these systems is the nuclear transcription factor cAMP response element binding protein (CREB) (Montminy, et al. 1990;Meyer and Habener 1993;Nibuya et al. 1996;Duman et al. 1997Duman et al. , 1999Thome et al. 2000). A role for the cAMP cascade in the long-term ac- (Nestler et al. 1989) and that the activity of CREB is enhanced following its phosphorylation by PKA (Meyer and Habener 1993;Ghosh and Greenberg 1995). Furthermore, viral mediated over-expression of CREB in two animal models of depression produced an antidepressant effect and resulted in improved behavioral performance in both models (Chen et al. 2001).Based on the hypothesis that the apparent lack of sensitivity to corticosteroids observed in major depression is causally linked to the pathogenesis of depression (Holsboer and Barden 1996;Holsboer 2000;Pariante and Miller 2001) as well as to the therapeutic effectiveness of antidepressant drugs (Barden 1996), a transgenic animal model of neuroendocrine changes associated with depression was developed (Pepin et al. 1992a). Insertion into the mouse genome of a transgene expressing antisense RNA complementary to a fragment of the glucocorticoid receptor (GR) cDNA produced an animal with a defect in the neuronal glucocorticoid receptors that mediate the effects of high "stress" levels of glucocorticoids on the negative feedback of the HPA system. These transgenic mice displayed impaired endogenous GR function and were characterized by dysfunctional glucocorticoid inhibitory feedback and disturbed ACTH and corticosterone secretory responses Karanth et al. 1997;Dijkstra et al. 1998). Long-term treatment of the transgenic mice with antidepressant drugs caused an increase in GR gene expression and produced significant normalization of the HPA system hyperactivity through restoration of functional glucocorticoid inhibitory feedback (Pepin et al. 1992b;Barden et al. 1995;Barden et al. 1997).Because the second messenger cyclic AMP plays a...

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Regulation of camp-inducible genes by creb

Cited by 392 publications

References 23 publications

STF1 is a novel TGACG‐binding factor with a zinc‐finger motif and a bZIP domain which heterodimerizes with GBF proteins

STF1 is a novel TGACG‐binding factor with a zinc‐finger motif and a bZIP domain which heterodimerizes with GBF proteins

CRH: The link between hormonal-, metabolic- and behavioral responses to stress

Altered Regulation of CREB by Chronic Antidepressant Administration in the Brain of Transgenic Mice with Impaired Glucocorticoid Receptor Function

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