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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 08 Nov 2015.

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
Time-resolved studies of IsdG identify molecular signposts along the non-canonical heme oxygenase pathway.
DuBois et al., United States. In J Biol Chem, 03 Dec 2015
An apparent meso -(hydr)oxyheme (forming with k = 0.6 min(-1), pH 7.4, 10 mM ascorbate, 10 μM IsdG-heme, 22 °C) was identified as a likely common intermediate with the canonical heme oxygenases (HOs).
Genetic mutation analysis in Japanese patients with non-syndromic congenital heart disease.
Morisaki et al., Suita, Japan. In J Hum Genet, 22 Nov 2015
We conducted sequence analysis of the coding regions of NKX2.5, GATA4, TBX1, TBX5, TBX20, CFC1 and ZIC3 in 111 Japanese patients with non-syndromic CHD and 9 of their relatives.
MiR-542-5p is a negative prognostic factor and promotes osteosarcoma tumorigenesis by targeting HUWE1.
Yang et al., Shanghai, China. In Oncotarget, 20 Nov 2015
We used isobaric tags for relative and absolute quantitation (iTRAQ) and nanoscale liquid chromatography-mass spectrometry (NanoLC-MS/MS) to identify differentially expressed proteins in MNNG/HOS and U2OS osteosarcoma cell lines transfected with miR-542-5p; in both cell lines, seven proteins were downregulated, and nine were upregulated.
Eradication of osteosarcoma by fluorescence-guided surgery with tumor labeling by a killer-reporter adenovirus.
Hoffman et al., Okayama, Japan. In J Orthop Res, 19 Nov 2015
OBP-401-illuminated human osteosarcoma cell lines, 143B and MNNG/HOS cells in vitro and in vivo.
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.
Inherited progressive cardiac conduction disorders.
Abriel et al., Bern, Switzerland. In Curr Opin Cardiol, Jan 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.
A new high-throughput screening-compatible gap junctional intercellular communication assay.
Lee et al., Inch'ŏn, South Korea. In Bmc Biotechnol, Dec 2014
This assay system also worked well in HOS osteosarcoma cells with a Z' factor at 10 s of 0.70.
Morphogenesis and molecular considerations on congenital cardiac septal defects.
Jongbloed et al., Leiden, Netherlands. In Ann Med, Dec 2014
TBX5), it can explain a variety of atrial septal defects.
Gibbon genome and the fast karyotype evolution of small apes.
Gibbs et al., Portland, United States. In Nature, Oct 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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