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

T-box 5

HOS, Tbx5
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. This gene is closely linked to related family member T-box 3 (ulnar mammary syndrome) on human chromosome 12. The encoded protein may play a role in heart development and specification of limb identity. Mutations in this gene have been associated with Holt-Oram syndrome, a developmental disorder affecting the heart and upper limbs. Several transcript variants encoding different isoforms have been described for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, HAD, V1a, ACID, Nkx2.5
Papers using HOS antibodies
Beta and gamma oscillations in the olfactory system of the urethane-anesthetized rat
Yoshihara Yoshihiro et al., In Neural Systems & Circuits, 2002
... Double immunofluorescence labelling of OB coronal sections from Tbx5.0gV transgenic mice [line #3(2)] at ...
Papers on HOS
Long non-coding RNA tumor suppressor candidate 7 functions as a tumor suppressor and inhibits proliferation in osteosarcoma.
Li et al., Jinan, China. In Tumour Biol, Feb 2016
Two osteosarcoma cell lines, HOS and MG63, were utilized to investigate biological function of TUSC7.
The Barrett-associated variants at GDF7 and TBX5 also increase esophageal adenocarcinoma risk.
Schumacher et al., Bonn, Germany. In Cancer Med, Feb 2016
In this study we analyzed three most recently identified BE variants at the genes GDF7 (rs3072), TBX5 (rs2701108), and ALDH1A2 (rs3784262) separately in BE and EAC samples in order to determine their risk effects during BE/EAC sequence.
Nitric oxide and iron modulate heme oxygenase activity as a long distance signaling response to salt stress in sunflower seedling cotyledons.
Bhatla et al., Delhi, India. In Nitric Oxide, Feb 2016
Its catabolism is carried out by heme oxygenase (HOs; EC which uses heme both as a prosthetic group and as a substrate.
TBX5 mutations contribute to early-onset atrial fibrillation in Chinese and Caucasians.
Tian et al., Shanghai, China. In Cardiovasc Res, Feb 2016
METHODS AND RESULTS: We screened six candidate genes (CAV1, KCNJ2, KCNQ1, NKX2.5, PITX2, and TBX5) for novel mutations in 139 patients of Chinese descent with early-onset AF and 576 controls.
A unique TBX5 microdeletion with microinsertion detected in patient with Holt-Oram syndrome.
Imoto et al., Japan. In Am J Med Genet A, Dec 2015
Holt-Oram syndrome (HOS) is an autosomal dominant condition characterized by upper limb and congenital heart defects and caused by numerous germline mutations of TBX5 producing preterminal stop codons.
Molecular basis of the clinical features of Holt-Oram syndrome resulting from missense and extended protein mutations of the TBX5 gene as well as TBX5 intragenic duplications.
Abou Al-Shaar et al., Riyadh, Saudi Arabia. In Gene, May 2015
This paper reviews the molecular basis of the clinical features of Holt-Oram syndrome resulting from missense and extended protein mutations of the TBX5 gene as well as TBX5 intragenic duplications.
Biology of MET: a double life between normal tissue repair and tumor progression.
Petrini, Pisa, Italy. In Ann Transl Med, Apr 2015
MNNG HOS transforming gene (MET) is a class IV receptor tyrosine kinase, expressed on the surface of epithelial cells.
The role of transcription factors in atrial fibrillation.
Tu et al., Wuhan, China. In J Thorac Dis, Feb 2015
In this review, we will focus on the potential role of PITX2, PRRX1, ZHFX3, TBX5, and NKX2.5 in AF.
Biology of upper-body and lower-body adipose tissue--link to whole-body phenotypes.
Pinnick et al., Oxford, United Kingdom. In Nat Rev Endocrinol, Feb 2015
New data suggest that the profound functional differences between the upper-body and lower-body tissues are controlled by site-specific sets of developmental genes, such as HOXA6, HOXA5, HOXA3, IRX2 and TBX5 in subcutaneous abdominal adipose tissue and HOTAIR, SHOX2 and HOXC11 in gluteofemoral adipose tissue, which are under epigenetic control.
Inherited progressive cardiac conduction disorders.
Abriel et al., Bern, Switzerland. In Curr Opin Cardiol, 2015
Other genes coding for cardiac transcription factors, such as NKX2.5 and TBX5, are involved in the development of the cardiac conduction system and in the morphogenesis of the heart.
Gibbon genome and the fast karyotype evolution of small apes.
Gibbs et al., Portland, United States. In Nature, 2014
Finally, we identify signatures of positive selection in genes important for forelimb development (TBX5) and connective tissues (COL1A1) that may have been involved in the adaptation of gibbons to their arboreal habitat.
Mending broken hearts: cardiac development as a basis for adult heart regeneration and repair.
Bassel-Duby et al., Dallas, United States. In Nat Rev Mol Cell Biol, 2013
Heart function has been restored in rodents by reprogramming non-myocytes into cardiomyocytes, by expressing transcription factors (GATA4, HAND2, myocyte-specific enhancer factor 2C (MEF2C) and T-box 5 (TBX5)) and microRNAs (miR-1, miR-133, miR-208 and miR-499) that control cardiomyocyte identity.
Blending hippo and WNT: sharing messengers and regulation.
Waterman et al., Irvine, United States. In Cell, 2013
show how β-catenin and YAP1 form a kinase-regulated complex with transcription factor TBX5.
β-Catenin-driven cancers require a YAP1 transcriptional complex for survival and tumorigenesis.
Hahn et al., Boston, United States. In Cell, 2013
Specifically, we found that YAP1 and the transcription factor TBX5 form a complex with β-catenin.
Hox genes regulate the onset of Tbx5 expression in the forelimb.
Logan et al., London, United Kingdom. In Development, 2012
Hox genes act upstream of Tbx5 to control the axial position of forelimb formation.
Functional analysis of the novel sequence variants within TBX5 gene promoter in patients with ventricular septal defects.
Yan et al., Jining, China. In Transl Res, 2012
data will not only deepen our understanding of genetic causes of CHD but also provide insight into designing novel personalized therapy for adult patients with CHD by upregulating TBX5 gene expression with different approache
Tbx5-hedgehog molecular networks are essential in the second heart field for atrial septation.
Moskowitz et al., Chicago, United States. In Dev Cell, 2012
Tbx5 regulated second heart field Gas1 and Osr1 expression, supporting both pathways.
TBX5 drives Scn5a expression to regulate cardiac conduction system function.
Moskowitz et al., Chicago, United States. In J Clin Invest, 2012
a TBX5-responsive enhancer downstream of Scn5a is sufficient to drive ventricular conduction system expression in vivo, dependent on canonical T-box binding sites
Inefficient reprogramming of fibroblasts into cardiomyocytes using Gata4, Mef2c, and Tbx5.
Wu et al., Boston, United States. In Circ Res, 2012
Induction of Gata4/Mef2c/Tbx5 overexpression in fibroblasts is inefficient at inducing molecular and electrophysiological phenotypes of mature cardiomyocytes.
Heart repair by reprogramming non-myocytes with cardiac transcription factors.
Olson et al., Dallas, United States. In Nature, 2012
Here we show that four transcription factors, GATA4, HAND2, MEF2C and TBX5, can cooperatively reprogram adult mouse tail-tip and cardiac fibroblasts into beating cardiac-like myocytes in vitro.
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