Estradiol-17beta regulates mouse uterine epithelial cell proliferation through insulin-like growth factor 1 signaling.

Estradiol-17beta regulates mouse uterine epithelial cell proliferation through insulin-like growth factor 1 signaling. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Estradiol-17beta regulates mouse uterine epithelial cell proliferation through insulin-like growth factor 1 signaling. Abstract Text:

Liyin Zhu,Jeffrey W Pollard,

Estradiol-17beta (E(2)) causes cell proliferation in the uterine epithelium of mice and humans by signaling through its transcription factor receptor alpha (ERalpha). In this work we show that this signaling is mediated by the insulin-like growth factor 1 receptor (IGF1R) expressed in the epithelium, whose activation leads to the stimulation of the phosphoinositide 3-kinase/protein kinase B pathway leading to cyclin D1 nuclear accumulation and engagement with the canonical cell cycle machinery. This cyclin D1 nuclear accumulation results from the inhibition of glycogen synthase kinase 3beta (GSK3beta) activity caused by an inhibitory phosphorylation by protein kinase B. Once the IGF1 pathway is activated, inhibition of ER signaling demonstrates that it is independent of ER. Inhibition of GSK3beta in the absence of E(2) is sufficient to induce uterine epithelial cell proliferation, and GSK3beta is epistatic to IGF1 signaling, indicating a linear pathway from E(2) to cyclin D1. Exposure to E(2) is the major risk factor for endometrial cancer, suggesting that downstream activation of this IGF1-mediated pathway by mutation could be causal in the progression to ER-independent tumors.

Estradiol-17beta regulates mouse uterine epithelial cell proliferation through insulin-like growth factor 1 signaling. Publishing Authors By Initials

L Zhu,JW Pollard,

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

Estradiol-17beta regulates mouse uterine epithelial cell proliferation through insulin-like growth factor 1 signaling. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Proceedings of the National Academy of Sciences of

VOLUME: 104

Page Numbers: 15847-51

Journal Abbreviation: Proc. Natl. Acad. Sci. U.S.A.

ISSN: 0027-8424

DAY: 25

MONTH: 09

YEAR: 2007

Estradiol-17beta regulates mouse uterine epithelial cell proliferation through insulin-like growth factor 1 signaling. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 7505876

Estradiol-17beta regulates mouse uterine epithelial cell proliferation through insulin-like growth factor 1 signaling. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: Estradiol-17beta regulates mouse uterine epithelial cell proliferation through insulin-like growth factor 1 signaling. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Estradiol-17beta regulates mouse uterine epithelial cell proliferation through insulin-like growth factor 1 signaling.

AFFILIATION: Department of Developmental and Molecular Biology, Center of Reproductive Biology and Women's Health, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.

Country: United States

AGENCY: United States NCI

GRANT: R01 CA89617

ACRONYM: CA

MEDLINETA: Proc Natl Acad Sci U S A

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Estradiol-17beta regulates mouse uterine epithelial cell proliferation through insulin-like growth factor 1 signaling Related Publications

• A new combination haemophilus influenzae type B and Neisseria meningitidis serogroup C-tetanus toxoid conjugate vaccine for primary immunization of infants.
• Bayesian analysis of fiber impedance measurements.
• Biased clustered substitutions in the human genome: the footprints of male-driven biased gene conversion.
• Blood transfusion; the indications its technique and dangers.
• Children's participation in vaccine research: parents' views.
• Emerging treatments for viral retinitis.
• Estradiol-17beta regulates mouse uterine epithelial cell proliferation through insulin-like growth factor 1 signaling.
• INJURIES IN AUSTRALIAN RULES FOOTBALL: A Review of the Literature.
• Incorporation of newly synthesized fatty acids into cytosolic glycerolipids in pea leaves occurs via acyl editing.
• MANAGEMENT OF ACHILLES TENDON DISORDERS: A Case Review.
• Macrophages promote collagen fibrillogenesis around terminal end buds of the developing mammary gland.
• Macrophages regulate the angiogenic switch in a mouse model of breast cancer.
• Modern dressings: must do better.
• Optimisation and validation of a medium-throughput electrophysiology-based hNav1.5 assay using IonWorkstrade mark.
• Peptic ulcer following splanchnicectomy; a report of 13 cases.
• Pharmacological validation of a semi-automated in vitro hippocampal brain slice assay for assessment of seizure liability.
• Polymerization kinetics of ADP- and ADP-Pi-actin determined by fluorescence microscopy.
• Progesterone blocks estrogen-induced DNA synthesis through the inhibition of replication licensing.
• Promoting healthy survivorship.
• Reconsideration of the use of meningococcal polysaccharide vaccine.
• Reduced expression of decay-accelerating factor 1 on CD4+ T cells in murine systemic autoimmune disease.
• Regulation of actin filament assembly by Arp2/3 complex and formins.
• SPONDYLOLYSIS IN A PROFESSIONAL FAST BOWLER: A Case Study.
• Single molecule kinetic analysis of actin filament capping. Polyphosphoinositides do not dissociate capping proteins.
• Solastalgia: the distress caused by environmental change.
• Studies of bromine-oxidizable sulfur-containing compounds in mold metabolism.
• The occurrence of gastric neoplasms in youth.
• The virologic, immunologic, and clinical effects of interleukin 2 with potent antiretroviral therapy in patients with moderately advanced human immunodeficiency virus infection: a randomized controlled clinical trial--AIDS Clinical Trials Group 328.
• Tumor-associated macrophages press the angiogenic switch in breast cancer.
• W135 in Africa: origins, problems and perspectives.