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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

T-box 19

Tpit, TBX19, T-box 19
This gene is a member of a phylogenetically conserved family of genes that share a common DNA-binding domain, the T-box. T-box genes encode transcription factors involved in the regulation of developmental processes. Mutations in this gene were found in patients with isolated deficiency of pituitary POMC-derived ACTH, suggesting an essential role for this gene in differentiation of the pituitary POMC lineage. ACTH deficiency is characterized by adrenal insufficiency symptoms such as weight loss, lack of appetite (anorexia), weakness, nausea, vomiting, and low blood pressure. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Pit-1, proopiomelanocortin, CAN, SF-1, Pitx1
Papers on Tpit
The Complementary Role of Transcription Factors in the Accurate Diagnosis of Clinically Nonfunctioning Pituitary Adenomas.
Yamada et al., Tokyo, Japan. In Endocr Pathol, Nov 2015
The 119 hormone-negative adenomas were further evaluated for expression of transcription factors including steroidogenic factor-1 (SF-1), estrogen receptor-α (ERα), pituitary-specific transcription factor 1 (Pit-1), and t-box transcription factor (Tpit).
Cyclin E-Mediated Human Proopiomelanocortin Regulation as a Therapeutic Target for Cushing Disease.
Melmed et al., Los Angeles, United States. In J Clin Endocrinol Metab, Jul 2015
RESULTS: R-roscovitine inhibits human corticotroph tumor POMC and Tpit/Tbx19 transcription with decreased ACTH expression.
Characterization of murine pituitary-derived cell lines Tpit/F1, Tpit/E and TtT/GF.
Kato et al., Kawasaki, Japan. In J Reprod Dev, 2013
In this study, we compared gene expression profiles by microarray analysis and real-time PCR for murine pituitary tumor-derived non-hormone-producing cell lines TtT/GF, Tpit/F1 and Tpit/E.
Retinoic acid receptor-α up-regulates proopiomelanocortin gene expression in AtT20 corticotroph cells.
Sugawara et al., Sendai, Japan. In Endocr J, 2013
Pomc promoter mutation analysis revealed that both Tpit and NeuroD1 binding elements were responsible for the Am80-mediated effect.
Characterization of a pituitary-tumor-derived cell line, TtT/GF, that expresses Hoechst efflux ABC transporter subfamily G2 and stem cell antigen 1.
Kato et al., Kawasaki, Japan. In Cell Tissue Res, 2013
Real-time polymerase chain reaction (PCR) for ABC transporters demonstrated that Abcb1a, Abcb1b and Abcg2, regarded as stem cell markers, were characteristically expressed in TtT/GF cells but not in Tpit/F1 and LβT2 cells.
PROP1 overexpression in corticotrophinomas: evidence for the role of PROP1 in the maintenance of cells committed to corticotrophic differentiation.
Carvalho et al., São Paulo, Brazil. In Clinics (sao Paulo), 2013
In this study, we sought to characterize the transcriptional profiles of PROP1, POU1F1, and TBX19 in functioning and nonfunctioning pituitary adenomas in an attempt to identify their roles in tumorigenesis and hormone hypersecretion.
The side population phenomenon enriches for designated adrenocortical progenitor cells in mice.
Beuschlein et al., München, Germany. In J Endocrinol, 2012
By contrast, the subcapsular zone of ACTH-deficient Tpit(-/-) mice was significantly wider compared with wild-type adrenals (Tpit(-/-) 259±10.7 vs Tpit(+/-) 100±12.3%;
The selector gene Pax7 dictates alternate pituitary cell fates through its pioneer action on chromatin remodeling.
Drouin et al., Montréal, Canada. In Genes Dev, 2012
The T-box transcription factor Tpit controls terminal differentiation of both lineages.
Phenotypic homogeneity and genotypic variability in a large series of congenital isolated ACTH-deficiency patients with TPIT gene mutations.
Vallette et al., Montréal, Canada. In J Clin Endocrinol Metab, 2012
Identification of nine new TPIT mutations in a large series of congenital isolated ACTH-deficiency patients.
Identification of TPIT and other novel autoantigens in lymphocytic hypophysitis: immunoscreening of a pituitary cDNA library and development of immunoprecipitation assays.
Crock et al., Newcastle, Australia. In Eur J Endocrinol, 2012
TPIT is identified as a target autoantigen in 10.5% of patients with lymphocytic hypophysitis.
The Ets factor Etv1 interacts with Tpit protein for pituitary pro-opiomelanocortin (POMC) gene transcription.
Drouin et al., Montréal, Canada. In J Biol Chem, 2011
The coordinate expression of Etv1 with POMC cell differentiation and its interaction with the highly cell-restricted Tpit factor indicate that Etv1 participates in a combinatorial code for pituitary cell-specific gene expression.
The human POMC gene promoter: where do we stand?
Cavagnini et al., Milano, Italy. In J Endocrinol Invest, 2011
This increased knowledge benefits the clinician as it allows genetic testing and early recognition of patients with congenital ACTH deficiency due to mutations in TPIT and paves the way to new medical treatments in Cushing's disease.
Molecular mechanisms of pituitary organogenesis: In search of novel regulatory genes.
Camper et al., Ann Arbor, United States. In Mol Cell Endocrinol, 2010
A few later-acting transcription factors have pituitary-specific effects, including PROP1, POU1F1 (PIT1), and TPIT (TBX19), while others, such as NeuroD1 and NR5A1 (SF1), are syndromic, influencing development of other endocrine organs.
Growth hormone deficiency (GHD) and small for gestational age (SGA): genetic alterations.
Pop-Jordanova et al., In Prilozi, 2009
In animal models and in humans the importance of the transcription factors HESX1, PROP1, POU1F1, LHX3, LHX4, TBX19, SOX2 and SOX3 has been extensively studied.
Adrenal gland development and defects.
Flück et al., Bern, Switzerland. In Best Pract Res Clin Endocrinol Metab, 2008
Adrenal differentiation seems to depend on adrenocorticotropic hormone (ACTH) stimulation and signalling, including biosynthesis and action of POMC, PC1, TPIT, MC2R, MRAP and ALADIN, all of which cause adrenocortical hypoplasia when mutated in humans.
Disorders of adrenal development.
Achermann et al., London, United Kingdom. In Endocr Dev, 2007
HESX1, LHX4, SOX3, TPIT, pituitary POMC, PC1); (2) as part of several ACTH resistance syndromes (e.g.
The TPIT gene mutation M86R associated with isolated adrenocorticotropin deficiency interferes with protein: protein interactions.
Drouin et al., Montréal, Canada. In J Clin Endocrinol Metab, 2007
the M86R TPIT mutation is defining an important surface of the T domain for multiple protein interactions and for transcription
Genetic variation in the hypothalamic-pituitary-adrenocortical axis regulatory factor, T-box 19, and the angry/hostility personality trait.
Wasserman et al., Stockholm, Sweden. In Genes Brain Behav, 2007
Overtransmission of a haplotype GAC at the TBX19 locus was associated with increased angry/hostility scores among suicide attempters.
A pituitary cell-restricted T box factor, Tpit, activates POMC transcription in cooperation with Pitx homeoproteins.
Drouin et al., Montréal, Canada. In Cell, 2001
We identified Tpit, a novel T box factor only present in the two pituitary POMC-expressing lineages, the corticotrophs and melanotrophs, and apparently in no other tissue, including hypothalamic POMC neurons.
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