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Wolf-Hirschhorn syndrome candidate 2

WHSC2, NELF-A, Negative elongation factor
This gene is expressed ubiquitously with higher levels in fetal than in adult tissues. It encodes a protein sharing 93% sequence identity with the mouse protein. Wolf-Hirschhorn syndrome (WHS) is a malformation syndrome associated with a hemizygous deletion of the distal short arm of chromosome 4. This gene is mapped to the 165 kb WHS critical region, and may play a role in the phenotype of the WHS or Pitt-Rogers-Danks syndrome. The encoded protein is found to be capable of reacting with HLA-A2-restricted and tumor-specific cytotoxic T lymphocytes, suggesting a target for use in specific immunotherapy for a large number of cancer patients. This protein has also been shown to be a member of the NELF (negative elongation factor) protein complex that participates in the regulation of RNA polymerase II transcription elongation. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: NELF, POLYMERASE, WHS, Histone, ACID
Papers on WHSC2
Systematic analysis of copy number variants of a large cohort of orofacial cleft patients identifies candidate genes for orofacial clefts.
Zhou et al., Nijmegen, Netherlands. In Hum Genet, Jan 2016
Our analyses of these overlapping CNVs identified two genes known to be causative for human OFCs, SATB2 and MEIS2, and 12 genes (DGCR6, FGF2, FRZB, LETM1, MAPK3, SPRY1, THBS1, TSHZ1, TTC28, TULP4, WHSC1, WHSC2) that are associated with OFC or orofacial development.
Translational Initiation at a Non-AUG Start Codon for Human and Mouse Negative Elongation Factor-B.
Li et al., San Antonio, United States. In Plos One, 2014
Negative elongation factor (NELF), a four-subunit protein complex in metazoan, plays an important role in regulating promoter-proximal pausing of RNA polymerase II (RNAPII).
Negative elongation factor controls energy homeostasis in cardiomyocytes.
Li et al., San Antonio, United States. In Cell Rep, 2014
Negative elongation factor (NELF) is known to enforce promoter-proximal pausing of RNA polymerase II (Pol II), a pervasive phenomenon observed across multicellular genomes.
A kinase-independent activity of Cdk9 modulates glucocorticoid receptor-mediated gene induction.
Simons et al., Bethesda, United States. In Biochemistry, 2014
A gene induction competition assay has recently uncovered new inhibitory activities of two transcriptional cofactors, NELF-A and NELF-B, in glucocorticoid-regulated transactivation.
A conserved protein motif is required for full modulatory activity of negative elongation factor subunits NELF-A and NELF-B in modifying glucocorticoid receptor-regulated gene induction properties.
Simons et al., Bethesda, United States. In J Biol Chem, 2013
NELF-B is a BRCA1-interacting protein and subunit (with NELF-A, -C/D, and -E) of the human negative elongation factor (NELF) complex, which participates in RNA polymerase II pausing shortly after transcription initiation, especially for synchronized gene expression.
Circulating levels of miR-133a predict the regression potential of left ventricular hypertrophy after valve replacement surgery in patients with aortic stenosis.
Nistal et al., In J Am Heart Assoc, 2013
Multiple linear regression analysis revealed plasma miR-133a and its myocardial target Wolf-Hirschhorn syndrome candidate 2/Negative elongation factor A as opposite predictors of the LV mass loss (g) after AVR.
Identification of location and kinetically defined mechanism of cofactors and reporter genes in the cascade of steroid-regulated transactivation.
Simons et al., Bethesda, United States. In J Biol Chem, 2012
glucocorticoid receptor (GR), reporter, TIF2, NCoR, NELF-A, sSMRT, and STAMP) using our recently developed competition assay.
Characterizing the functional consequences of haploinsufficiency of NELF-A (WHSC2) and SLBP identifies novel cellular phenotypes in Wolf-Hirschhorn syndrome.
O'Driscoll et al., Brighton, United Kingdom. In Hum Mol Genet, 2012
haploinsufficiency of SLBP and/or WHSC2 (NELF-A) contributes to several novel cellular phenotypes of WHS.
Mechanism of glycyrrhizic acid inhibition of Kaposi's sarcoma-associated herpesvirus: disruption of CTCF-cohesin-mediated RNA polymerase II pausing and sister chromatid cohesion.
Lieberman et al., Philadelphia, United States. In J Virol, 2011
GA altered the enrichment of the RNAPII pausing complex, along with pausing factors SPT5 and NELF-A, at the intragenic CTCF-cohesin binding sites.
A novel 4p16.3 microduplication distal to WHSC1 and WHSC2 characterized by oligonucleotide array with new phenotypic features.
Shchelochkov et al., Iowa City, United States. In Am J Med Genet A, 2011
The microduplication did not involve WHSC1 and WHSC2 which are considered in the critical region for WHS and trisomy 4p.
Myocardial gene expression of microRNA-133a and myosin heavy and light chains, in conjunction with clinical parameters, predict regression of left ventricular hypertrophy after valve replacement in patients with aortic stenosis.
Nistal et al., Spain. In Heart, 2011
Using multiple linear regression analysis, an equation was developed (adjusted R²=0.73; p<0.0001) that included positive [preoperative LVM, microRNA-133a, serum response factor (SRF, which is known to be a transactivator of miR-133) and age] and negative [body mass index (BMI), Wolf-Hirschhorn syndrome candidate-2 (WHSC2, which is a target for repression by miR-133a), β-myosin heavy chain, myosin light chain-2, diabetes mellitus, and male gender] independent predictors of LVM reduction.
Human negative elongation factor activates transcription and regulates alternative transcription initiation.
Li et al., San Antonio, United States. In J Biol Chem, 2010
The human negative elongation factor (NELF) is a four-subunit protein complex that inhibits the movement of RNA polymerase II (RNAPII) at an early elongation stage in vitro.
Cellular dynamics of the negative transcription elongation factor NELF.
Handa et al., Yokohama, Japan. In Exp Cell Res, 2009
data show that NELF subunits exhibit highly specific subcellular localizations, such as in NELF bodies or in midbodies, and some shuttle actively between the nucleus and cytoplasm; loss of NELF from cells can lead to enlarged and/or multiple nuclei
NELF interacts with CBC and participates in 3' end processing of replication-dependent histone mRNAs.
Handa et al., Yokohama, Japan. In Mol Cell, 2007
Negative elongation factor (NELF) is a four subunit transcription factor. Our results point to a surprising role of NELF in the 3' end processing of histone mRNAs and suggest that NELF is a new factor that coordinates mRNA processing in transcription
MicroRNA-133 controls cardiac hypertrophy.
Condorelli et al., Roma, Italy. In Nat Med, 2007
We identified specific targets of miR-133: RhoA, a GDP-GTP exchange protein regulating cardiac hypertrophy; Cdc42, a signal transduction kinase implicated in hypertrophy; and Nelf-A/WHSC2, a nuclear factor involved in cardiogenesis.
Human transcription elongation factor NELF: identification of novel subunits and reconstitution of the functionally active complex.
Handa et al., Yokohama, Japan. In Mol Cell Biol, 2003
NELF-C and NELF-D are highly related or identical to the protein called TH1, of unknown function. NELF-B and NELF-C or NELF-D are integral subunits that bring NELF-A and NELF-E together. [NELF-B] [NELF-C]
[Genetic determination of Wolf-Hirschhorn syndrome ].
Rokicka et al., Laizhou, China. In Wiad Lek, 2001
connection between the syndrome phenotype and cytogenetic abnormalities, through gradual shortening of the length of the critical region WHSCR (finally up to 165 kb), and sequencing it, at least 2 genes (WHSC1 and WHSC2) were identified.
Stimulation of RNA polymerase II elongation by hepatitis delta antigen.
Handa et al., Yokohama, Japan. In Science, 2001
Transcription elongation by RNA polymerase II (RNAPII) is negatively regulated by the human factors DRB-sensitivity inducing factor (DSIF) and negative elongation factor (NELF).
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