Molecular Mechanisms of Thyroid Disorders: from Human Diseases to Mouse Models

​Description of Research

The aim of our study is to provide novel information with respect to the etiology and mechanism of thyroid diseases. The main objectives are: 1) to identify gene mutations (novel and known) from patients with familial thyroid diseases, using congenital hypothyroidism as main model, 2) to generate in vitro and in vivo tools to study the function of novel genes in the thyroid, 3) to characterize and generate mouse models for human thyroid diseases (e.g. hyperthyroidism) to understand the molecular mechanisms underlying these diseases, and use them for in vivo drug testing and 4) to evaluate the epidemiology of CH in Finland using national population-based health registers.

List of Personnel

Holger Jäschke, Dos
Christoffer Löf, FT
Henriette Undeutsch, MSc
Konrad Patyra, MSc
Meeri Jännäri, LK

Selected Publications

Undeutsch H, Löf C, Pakarinen P, Poutanen M, Ahmed K, Kero J.
Thyrocyte-specific Dicer1 deficiency impairs thyroid follicular structure, function and growth. Endocrinology. 2015 Apr;156(4):1590-601. doi: 10.1210/en.2014-1767.

Undeutsch H, Löf C, Offermanns S, Kero J.
Genesis. 2014 Apr;52(4):333-40. doi: 10.1002/dvg.22740. Epub 2014 Jan 15.
A mouse model with tamoxifen-inducible thyrocyte-specific cre recombinase activity.

Kero J, Ahmed K, Wettschureck N, Tunaru S, Wintermantel T, Greiner E, Schutz G, Offer-manns S. Thyrocyte-specific Gq/G11 deficiency impairs thyroid function and prevents goiter development. J Clin Invest 117, 2399-407 (2007).

Tunaru, S*., Kero, J*., Schaub, A., Wufka, C., Blaukat, A., Pfeffer, K. & Offermanns, S. PUMA-G and HM74 are receptors for nicotinic acid and mediate its anti-lipolytic effect. Nat Med 9, 352-5 (2003)

Kero, J., Poutanen, M., Zhang, F.P., Rahman, N., McNicol, A.M., Nilson, J.H., Keri, R.A. & Huhtaniemi, I.T. Elevated luteinizing hormone induces expression of its receptor and promotes steroidogenesis in the adrenal cortex. J Clin Invest 105, 633-41 (2000).