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NK2 homeobox 5

Nkx2.5, Nkx2-5, Csx
This gene encodes a homeobox-containing transcription factor. This transcription factor functions in heart formation and development. Mutations in this gene cause atrial septal defect with atrioventricular conduction defect, and also tetralogy of Fallot, which are both heart malformation diseases. Mutations in this gene can also cause congenital hypothyroidism non-goitrous type 5, a non-autoimmune condition. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Oct 2009] (from NCBI)
Top mentioned proteins: GATA4, CAN, HAD, Chordin, HOS
Papers using Nkx2.5 antibodies
The neural progenitor-specifying activity of FoxG1 is antagonistically regulated by CKI and FGF.
Alberola-Ila Jose, In PLoS ONE, 2006
... Nkx2-5, a cDNA plasmid clone was generated by RT-PCR using E11-day mouse total RNA (Clontech).
A novel LIM protein Cal promotes cardiac differentiation by association with CSX/NKX2-5
Komuro Issei et al., In The Journal of Cell Biology, 1998
... The plasmid pGBT9-CSX, which encodes the GAL4 DNA-binding domain fused to the human CSX/NKX2-5, was used as a bait in screening of a human heart MATCHMAKER cDNA Library (CLONTECH Laboratories, Inc.) ...
Papers on Nkx2.5
Desmin enters the nucleus of cardiac stem cells and modulates Nkx2.5 expression by participating in transcription factor complexes that interact with the nkx2.5 gene.
Weitzer et al., Vienna, Austria. In Biol Open, Feb 2016
UNASSIGNED: The transcription factor Nkx2.5 and the intermediate filament protein desmin are simultaneously expressed in cardiac progenitor cells during commitment of primitive mesoderm to the cardiomyogenic lineage.
Apelin: An Endogenous Peptide Essential for Cardiomyogenic Differentiation of Mesenchymal Stem Cells via Activating Extracellular Signal-Regulated Kinase 1/2 and 5.
Gao et al., Beijing, China. In Cell Biol Int, Feb 2016
The silencing expression of apelin in Wharton's jelly-derived mesenchymal stem cells decreased the expression of several critical cardiac progenitor transcription factors (Mesp1, Mef2c, NKX2.5) and cardiac phenotypes (cardiac α-actin, β-MHC, cTnT and connexin-43).
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.
Recognition of a Pseudo-Symmetric RNA Tetranucleotide by Csx3, a New Member of the CRISPR Associated Rossmann Fold Superfamily.
Lawrence et al., Bozeman, United States. In Rna Biol, Feb 2016
Such proteins have traditionally been designated as CRISPR subtype x (Csx).
A comprehensive gene expression analysis at sequential stages of in vitro cardiac differentiation from isolated MESP1-expressing-mesoderm progenitors.
Passier et al., Leiden, Netherlands. In Sci Rep, Dec 2015
We recently generated the dual cardiac fluorescent reporter MESP1(mCherry/w)NKX2-5(eGFP/w) line in human embryonic stem cells (hESCs), allowing the visualization of pre-cardiac MESP1+ mesoderm and their further commitment towards the cardiac lineage, marked by activation of the cardiac transcription factor NKX2-5.
Fractal heterogeneity in minimal matrix models of scars modulates stiff-niche stem-cell responses via nuclear exit of a mechanorepressor.
Discher et al., Philadelphia, United States. In Nat Mater, Sep 2015
Such differences from bulk-average responses arise because a strong SMA repressor, NKX2.5, slowly exits the nucleus on rigid matrices.
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, 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.
Genetic Defects in Thyroid Hormone Supply
Macchia et al., Madagascar. In Unknown Journal, 2015
Several genes have been associated to TD, including PAX8, NKX2-5, FOXE1, NKX2-5 and TSH-receptor genes.
Insights into the genetic structure of congenital heart disease from human and murine studies on monogenic disorders.
Pu et al., Cambridge, United States. In Cold Spring Harb Perspect Med, 2014
In this review, we discuss monogenic CHD caused by mutations of the cardiac transcription factor genes NKX2-5 and GATA4.
Clinical genetics of congenital hypothyroidism.
Szinnai, Basel, Switzerland. In Endocr Dev, 2013
Five monogenetic forms due to mutations in TSHR, PAX8, NKX2-1, FOXE1 and NKX2-5 have been identified so far.
Heart field origin of great vessel precursors relies on nkx2.5-mediated vasculogenesis.
Burns et al., United States. In Nat Cell Biol, 2013
Here, we identify the embryonic source of PAA endothelium as nkx2.5(+)
Genetic analysis of an enhancer of the NKX2-5 gene in ventricular septal defects.
Yan et al., Jining, China. In Gene, 2012
Variants within the cardiac enhancer in the NKX2-5 gene is not associated with ventricular septal defects.
Crystal structure of the human NKX2.5 homeodomain in complex with DNA target.
Nam et al., Richardson, United States. In Biochemistry, 2012
The high resolution crystal structure of NKX2.5 protein provides a detailed picture of protein and DNA interactions, which allows to predict DNA binding of mutants identified in human patients.
Epistatic rescue of Nkx2.5 adult cardiac conduction disease phenotypes by prospero-related homeobox protein 1 and HDAC3.
Riley et al., London, United Kingdom. In Circ Res, 2012
Rescue of Nkx2.5 phenotype establishes a model for ensuring electrophysiological function within the adult heart.
Complex trait analysis of ventricular septal defects caused by Nkx2-5 mutation.
Jay et al., Saint Louis, United States. In Circ Cardiovasc Genet, 2012
Multiple logistic regression analysis for environmental variables revealed that maternal age is correlated with the risk of membranous and muscular VSD in Nkx2-5(+/-) but not wild-type animals.
Congenital asplenia in mice and humans with mutations in a Pbx/Nkx2-5/p15 module.
Selleri et al., New York City, United States. In Dev Cell, 2012
Genetic data suggest that a heterozygous missense mutation (P236H) in NKX2-5 is associated with isolated congenital asplenia (ICA).
Common variants near MBNL1 and NKX2-5 are associated with infantile hypertrophic pyloric stenosis.
Melbye et al., Copenhagen, Denmark. In Nat Genet, 2012
Common variants near MBNL1 and NKX2-5 are associated with infantile hypertrophic pyloric stenosis.
NKX2-5(eGFP/w) hESCs for isolation of human cardiac progenitors and cardiomyocytes.
Stanley et al., Australia. In Nat Methods, 2011
NKX2-5 is expressed in the heart throughout life.
Latent TGF-β binding protein 3 identifies a second heart field in zebrafish.
Burns et al., United States. In Nature, 2011
In addition to expressing Ltbp3, a protein that regulates the bioavailability of TGF-β ligands, zebrafish SHF cells co-express nkx2.5, an evolutionarily conserved marker of cardiac progenitor cells in both fields.
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