about
GPR109A (PUMA-G/HM74A) mediates nicotinic acid-induced flushingPUMA-G and HM74 are receptors for nicotinic acid and mediate its anti-lipolytic effectElevated luteinizing hormone induces expression of its receptor and promotes steroidogenesis in the adrenal cortexTransgenic and knockout mouse models for the study of luteinizing hormone and luteinizing hormone receptor function.Nicotinic acid inhibits progression of atherosclerosis in mice through its receptor GPR109A expressed by immune cells.Thyrocyte-specific Gq/G11 deficiency impairs thyroid function and prevents goiter development.Adrenocortical tumorigenesis in transgenic mice expressing the inhibin alpha-subunit promoter/simian virus 40 T-antigen transgene: relationship between ectopic expression of luteinizing hormone receptor and transcription factor GATA-4.Human homologs of the putative G protein-coupled membrane progestin receptors (mPRalpha, beta, and gamma) localize to the endoplasmic reticulum and are not activated by progesterone.(D)-beta-Hydroxybutyrate inhibits adipocyte lipolysis via the nicotinic acid receptor PUMA-G.Long-term testosterone treatment prevents gonadal and adrenal tumorigenesis of mice transgenic for the mouse inhibin-alpha subunit promoter/simian virus 40 T-antigen fusion gene.Thyrocyte-specific Dicer1 deficiency alters thyroid follicular organization and prevents goiter development.Experimental cryptorchidism induces a change in the pattern of expression of LH receptor mRNA in rat testis after selective Leydig cell destruction by ethylene dimethane sulfonate.Virus shedding after human rhinovirus infection in children, adults and patients with hypogammaglobulinaemia.Characterization of determinants of ligand binding to the nicotinic acid receptor GPR109A (HM74A/PUMA-G).A mouse model with tamoxifen-inducible thyrocyte-specific cre recombinase activity.Transgenic mice harboring murine luteinizing hormone receptor promoter/beta-galactosidase fusion genes: different structural and hormonal requirements of expression in the testis, ovary, and adrenal gland.Homozygous loss-of-function mutations in SLC26A7 cause goitrous congenital hypothyroidismStem cell factor functions as a survival factor for mature Leydig cells and a growth factor for precursor Leydig cells after ethylene dimethane sulfonate treatment: implication of a role of the stem cell factor/c-Kit system in Leydig cell developmenObesity in transgenic female mice with constitutively elevated luteinizing hormone secretionCould TH1 and TH2 diseases coexist? Evaluation of asthma incidence in children with coeliac disease, type 1 diabetes, or rheumatoid arthritis: a register study
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description
onderzoeker
@nl
researcher ORCID ID = 0000-0001-8767-7222
@en
name
Jukka Kero
@ast
Jukka Kero
@en
Jukka Kero
@es
Jukka Kero
@nl
type
label
Jukka Kero
@ast
Jukka Kero
@en
Jukka Kero
@es
Jukka Kero
@nl
prefLabel
Jukka Kero
@ast
Jukka Kero
@en
Jukka Kero
@es
Jukka Kero
@nl
P106
P21
P31
P496
0000-0001-8767-7222