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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, 19 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, 18 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, 14 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, 13 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.
Covalent Labeling Denaturation Mass Spectrometry for Sensitive Localized Higher Order Structure Comparisons.
Anderson et al., In Anal Chem, 11 Feb 2016
UNASSIGNED: Protein higher order structure (HOS) describes the three-dimensional folding arrangement of a given protein, and plays critical roles in structure/function relationships.
The tumor suppressive role of RASSF1A in osteosarcoma through the Wnt signaling pathway.
Zang et al., Changsha, China. In Tumour Biol, 11 Feb 2016
rAd-RASSF1A injection significantly inhibited the growth of xenograft MNNG/HOS tumors in mice.
Novel copy number variants and major limb reduction malformation: Report of three cases.
Alkuraya et al., Riyadh, Saudi Arabia. In Am J Med Genet A, 08 Feb 2016
spanning 20 genes including TBX3 and TBX5, and a third patient with acheiropodia who had a nullizygous deletion of 102 kb on 7q36.3 spanning LMBR1.
Three-Dimensional Cultures of Human Subcutaneous Adipose Tissue-Derived Progenitor Cells Based on RAD16-I Self-Assembling Peptide.
Semino et al., Barcelona, Spain. In Tissue Eng Part C Methods, 07 Feb 2016
Additionally, it has been observed that chemical induction can induce upregulation of cardiac markers, such as TBX5, MEF2C, ACTN1, and GJA1.
A unique TBX5 microdeletion with microinsertion detected in patient with Holt-Oram syndrome.
Imoto et al., Japan. In Am J Med Genet A, 31 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.
A co-culture assay of embryonic zebrafish hearts to assess migration of epicardial cells in vitro.
Heideman et al., Madison, United States. In Bmc Dev Biol, 2014
We demonstrate the utility of this method by showing that epicardial cell migration is significantly delayed or absent when myocardial cells lack contractility and when myocardial cells are deficient in tbx5 expression.
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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