Potentiation of Estrogen Receptor Activation Function 1 (AF-1) by Src/JNK through a Serine 118-Independent Pathway

Feng, Wendy

doi:10.1210/me.15.1.32

Cited by 54 publications

(36 citation statements)

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“…However, our results showing that c-Src mRNA and protein expression increased proportionally with c-Jun and JNK expression suggest that METH might mediate JNK activation via Src because Src can stimulate JNK activity (Feng et al, 2001). This is supported by the recent demonstration that adenoviral transfection of a dominantnegative form of Src can abrogate H 2 O 2 -induced JNK activation (Chen et al, 2001).…”

Section: Downloaded Fromsupporting

confidence: 61%

Methamphetamine Causes Coordinate Regulation of Src, Cas, Crk, and the Jun N-Terminal Kinase–Jun Pathway

et al. 2002

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The clinical abuse of methamphetamine (METH) is a major concern because it can cause long-lasting neurodegenerative effects in humans. Current concepts of the molecular mechanisms underlying these complications have centered on the formation of reactive oxygen species. Herein, we provide cDNA microarray evidence that METH administration caused the induction of c-Jun and of other members involved in the pathway leading to c-Jun activation [stress-activated protein kinase/Jun N-terminal kinase (JNK3), Crk-associated substrate-Cas and c-Src] after environmental stresses or cytokine stimulation. Reverse transcription-polymerase chain reaction analysis confirmed these increases and also showed that the expression of JNK1 and JNK3 but not JNK2 was also increased in the METHtreated mice. Western blot analysis showed that METH increased the expression of c-Jun phosphorylated at serine-63 and serine-73 residues. Other upstream members of the JNK pathway, including phosphorylated JNKs, mitogen-activated protein kinase kinase 4, mitogen-activated protein kinase kinase 7, Crk II, Cas, and c-Src were also increased at the protein level. These values returned to baseline by 1 week after drug treatment. These results are discussed in terms of their support for a possible role of the activation of the JNK/Jun pathway in the pathophysiological effects of METH.

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Section: Downloaded Fromsupporting

confidence: 61%

Methamphetamine Causes Coordinate Regulation of Src, Cas, Crk, and the Jun N-Terminal Kinase–Jun Pathway

et al. 2002

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“…The actions of nonliganded ER␣ have been demonstrated to affect many different transcriptional systems through direct binding of DNA after phosphorylation (49). It has also been postulated that certain phosphorylation events of nonliganded ERs may alter the activity of coactivators that bind ER␣ (50). In addition, nonliganded ER␣ has been reported to suppress NF-B activity in the transfected osteoblastic U2-OS cell line (51).…”

Section: Discussionmentioning

confidence: 99%

Estrogen Receptor α (ERα) Deficiency in Macrophages Results in Increased Stimulation of CD4+ T Cells while 17β-Estradiol Acts through ERα to Increase IL-4 and GATA-3 Expression in CD4+ T Cells Independent of Antigen Presentation

Lambert

Curran

Judy

et al. 2005

The Journal of Immunology

125

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The effects of 17β-estradiol (E2) on immune function have been extensively reported. The effects are dependent on concentration and duration of exposure and potential differences in signaling between the known E2 receptors, estrogen receptors (ER) α and ERβ. Through the use of ER-deficient mice, we and others have begun to demonstrate the role of the two known receptors in modulating immune functional activities. Previous studies have shown that cells of the innate immune system have altered function (bactericidal capacity) and patterns of cytokine expression (increased proinflammatory cytokine expression) through amelioration of ERα signaling. In this study, we extend these studies to analysis of T cell differentiation and proliferation in APC-dependent and APC-independent in vitro assay systems. Our results demonstrate that ERα deficiency in splenic macrophages, but not CD11c+ splenic dendritic cells pulsed with OVA significantly enhances proliferative responses and IFN-γ production by transgenic OVA peptide-specific (OT-II) CD4+ T cells when compared with Ag-pulsed APC from wild-type littermates. The addition of E2 in this culture system did not significantly affect the production of IFN-γ. In addition, when purified CD4+ T cells from ERα-deficient and wild-type littermates were stimulated with anti-CD3/CD28 Ab in the absence of E2, there were no significant differences in IFN-γ or IL-4 production. However, the addition of E2 significantly increased IL-4 secretion, as well as increased GATA-3 mRNA levels from ERα-replete CD4+ T cells, while this effect was abrogated in ERα-deficient CD4+ T cells.

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“…Among the known intracellular mediators of unliganded ER activation, it is worth mentioning also cyclins [66,67], Src/JNK pathway [68], Protein kinase C␦ [69], and Protein kinase B [70].…”

Section: Ligand-independent Signalingmentioning

confidence: 99%

The “busy life” of unliganded estrogen receptors

et al. 2015

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Understanding of the role of estrogen receptors (ERα and ERβ) in the pathophysiology of breast cancer (BC) has considerably increased in last decades. Despite sharing a similar structure, these two transcription factors often exert opposite roles in BC. In addition, it has been shown that their transcriptional activity is not strictly associated to ligand activation and that unliganded ERs are able to "have a life on their own." This appears to be mainly due to ligand-independent mechanisms leading to ERs PTMs or to their recruitment to specific protein complexes, dependent on cellular context. Furthermore, a significant unliganded ER activity, probably independent by the activation of other pathways, has been recently reported to affect gene transcription, microRNA expression, and downstream proteome. In this review, we describe recent findings on nuclear and cytoplasmic unliganded ERα and ERβ activity. We focus on functional genomics, epigenomics, and interaction proteomics data, including PTM induced by ERs-modulated miRNAs in the BC context. A better comprehension of the molecular events controlled by unliganded ERs activity in BC pathogenesis is crucial since it may impact the therapeutic approach to the initial or acquired resistance to endocrine therapies, frequently experienced in the treatment of BC.

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Potentiation of Estrogen Receptor Activation Function 1 (AF-1) by Src/JNK through a Serine 118-Independent Pathway

Cited by 54 publications

References 0 publications

Methamphetamine Causes Coordinate Regulation of Src, Cas, Crk, and the Jun N-Terminal Kinase–Jun Pathway

Methamphetamine Causes Coordinate Regulation of Src, Cas, Crk, and the Jun N-Terminal Kinase–Jun Pathway

Estrogen Receptor α (ERα) Deficiency in Macrophages Results in Increased Stimulation of CD4+ T Cells while 17β-Estradiol Acts through ERα to Increase IL-4 and GATA-3 Expression in CD4+ T Cells Independent of Antigen Presentation

The “busy life” of unliganded estrogen receptors

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