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Cited by 42

The DOI matches its Crossref record; 56 of the 56 references it cites were found in a registry or an index.

FSH stimulates IRS-2 expression in human granulosa cells through cAMP/SP1, an inoperative FSH action in PCOS patients

Anjali, G., Kaur, Surleen, Lakra, Ruchi, Taneja, Jyoti, Kalsey, Gaganjot S., Nagendra, Anjali, Shrivastav, T.G., Gouri Devi, M., Malhotra, Neena, Kriplani, Alka, Singh, Rita·2015·Cellular Signalling
DOI 10.1016/j.cellsig.2015.09.011
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Abstract

Follicle stimulating hormone (FSH) plays a central role in growth and differentiation of ovarian follicles. A plethora of information exists on molecular aspects of FSH responses but little is known about the mechanisms involved in its cross-talk with insulin/IGF-1 pathways implicated in the coordination of energy homeostasis in preovulatory granulosa cells (GCs). In this study, we hypothesized that FSH may regulate IRS-2 expression and thereby maintain the energy balance in GCs. We demonstrate here that FSH specifically increases IRS-2 expression in human and rat GCs. FSH-stimulated IRS-2 expression was inhibited by actinomycin D or cycloheximide. Furthermore, FSH decreases IRS-2 mRNA degradation indicating post-transcriptional stabilization. Herein, we demonstrate a role of cAMP pathway in the activation of IRS-2 expression by FSH. Scan and activity analysis of IRS-2 promoter demonstrated that FSH regulates IRS-2 expression through SP1 binding sites. FSH stimulates SP1 translocation into nucleus and its binding to IRS-2 promoter. These results are corroborated by the fact that siRNA mediated knockdown of IRS-2 decreased the FSH-stimulated PI3K activity, p-Akt levels, GLUT4 translocation and glucose uptake. However, FSH was not able to increase IRS-2 expression in GCs from PCOS women undergoing IVF. Interestingly, IRS-2 mRNA expression was downregulated in GCs from the PCOS rat model. Taken together, our findings establish that FSH induces IRS-2 expression and thereby activa…

Overview

Integrity signals

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Crossref · 10.1016/j.cellsig.2015.09.011

Cites

56 of 56 references verified0 citation errors · 0 not checkable

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Citations

Cites

1 retracted

Research works printed but not linked: 4

  1. Richards, 2002, Endocrinology, 14, 1283
  2. Gonzalez-Robayna, 2000, Mol. Endocrinol., 14, 1283, 10.1210/mend.14.8.0500 · DOI · Paper page
  3. Jakimiuk, 2001, Clin. Endocrinol. Metab., 86, 1318
  4. Stilley, 2014, Biol. Reprod., 91, 1

Cited by

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Metadata

Authors
Anjali, G., Kaur, S., Lakra, R., Taneja, J., Kalsey, G. S., Nagendra, A., Shrivastav, T. G., Gouri Devi, M., Malhotra, N., Kriplani, A., & Singh, R.
Venue
Cellular Signalling
Publisher
Elsevier BV
Published
2015-12
Volume
27
Issue
12
Pages
2452-2466
ISSN
0898-6568
DOI
10.1016/j.cellsig.2015.09.011
Cited by
42
References
56
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Funders
  • Department of Biotechnology (DBT) (BT/PR 5379/MED/14/631/2004, BT/PR 8330/AAQ/01/313/2006)
  • Council of Scientific and Industrial Research (CSIR) (37/1217/05-EMRII/2009)
  • Delhi University
  • Central Instrumentation Facility (CIF) (Dean(R)/R&D/2011/423)

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.