NDLI: Thyrocyte-specific Gq/G11 deficiency impairs thyroid function and prevents goiter development

Content Provider	PubMed Central
Author	Kero, Jukka Ahmed, Kashan Nina, Wettschureck Sorin, Tunaru Wintermantel, Tim Greiner, Erich Schütz, Günther Offermanns, Stefan
Copyright Year	2007
Abstract	The function of the adult thyroid is regulated by thyroid-stimulating hormone (TSH), which acts through a G protein–coupled receptor. Overactivation of the TSH receptor results in hyperthyroidism and goiter. The Gs-mediated stimulation of adenylyl cyclase–dependent cAMP formation has been regarded as the principal intracellular signaling mechanism mediating the action of TSH. Here we show that the Gq/G11-mediated signaling pathway plays an unexpected and essential role in the regulation of thyroid function. Mice lacking the α subunits of Gq and G11 specifically in thyroid epithelial cells showed severely reduced iodine organification and thyroid hormone secretion in response to TSH, and many developed hypothyroidism within months after birth. In addition, thyrocyte-specific Gαq/Gα11-deficient mice lacked the normal proliferative thyroid response to TSH or goitrogenic diet, indicating an essential role of this pathway in the adaptive growth of the thyroid gland. Our data suggest that Gq/G11 and their downstream effectors are promising targets to interfere with increased thyroid function and growth.
Related Links	http://dx.doi.org/10.1172/jci30380
Ending Page	2407
Page Count	9
Starting Page	2399
File Format	PDF
ISSN	00219738
Journal	The Journal of Clinical Investigation
Issue Number	9
Volume Number	117
Language	English
Publisher	American Society for Clinical Investigation
Publisher Date	2007-09-04
Access Restriction	Open
Rights Holder	American Society for Clinical Investigation
Subject Keyword	Medicine(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Medicine

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Thyrocyte-Specific Dicer1 Deficiency Alters Thyroid Follicular Organization and Prevents Goiter Development

Thyrocyte-specific inactivation of p53 and Pten results in anaplastic thyroid carcinomas faithfully recapitulating human tumors

The Gq/G11-mediated signaling pathway is critical for autocrine potentiation of insulin secretion in mice

P2Y2 and Gq/G11 control blood pressure by mediating endothelial mechanotransduction

Agonistic anti-CD40 induces thyrocyte proliferation and promotes thyroid autoimmunity by increasing CD40 expression on thyroid epithelial cells1

Pathogenesis of heterogeneity in human multinodular goiter. A study on growth and function of thyroid tissue transplanted onto nude mice.

Primary Hypothyroidism and Thyroid Goiter in an Adult Cat

Gelatinase B deficiency impairs reproduction

A Dominant Negative CREB (cAMP Response Element-Binding Protein) Isoform Inhibits Thyrocyte Growth, Thyroid-Specific Gene Expression, Differentiation, and Function

Thyrocyte-specific Gq/G11 deficiency impairs thyroid function and prevents goiter development

Similar Documents

Thyrocyte-Specific Dicer1 Deficiency Alters Thyroid Follicular Organization and Prevents Goiter Development

Thyrocyte-specific inactivation of p53 and Pten results in anaplastic thyroid carcinomas faithfully recapitulating human tumors

The Gq/G11-mediated signaling pathway is critical for autocrine potentiation of insulin secretion in mice

P2Y2 and Gq/G11 control blood pressure by mediating endothelial mechanotransduction

Agonistic anti-CD40 induces thyrocyte proliferation and promotes thyroid autoimmunity by increasing CD40 expression on thyroid epithelial cells1

Pathogenesis of heterogeneity in human multinodular goiter. A study on growth and function of thyroid tissue transplanted onto nude mice.

Primary Hypothyroidism and Thyroid Goiter in an Adult Cat

Gelatinase B deficiency impairs reproduction

A Dominant Negative CREB (cAMP Response Element-Binding Protein) Isoform Inhibits Thyrocyte Growth, Thyroid-Specific Gene Expression, Differentiation, and Function

Thyrocyte-specific Gq/G11 deficiency impairs thyroid function and prevents goiter development