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

Thyroid hormone responsive

p31, S14, RPS14
expression is induced by dietary sucrose and by thyroid hormone [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: HAD, CAN, ACID, CYP1A1, p53
Papers using p31 antibodies
Primer3 on the WWW for general users and for biological programmers.
Mansvelder Huibert D., In PLoS ONE, 1999
... T14, S14, B14, and SB14 peptides were custom synthesized by AnaSpec (San Jose, CA., USA) ...
Papers on p31
TRIP13PCH-2 promotes Mad2 localization to unattached kinetochores in the spindle checkpoint response.
Bhalla et al., Santa Cruz, United States. In J Cell Biol, Dec 2015
Furthermore, we show that the C. elegans orthologue of the Mad2 inhibitor p31(comet)(CMT-1) interacts with TRIP13(PCH-2) and is required for its localization to unattached kinetochores.
Are Synonymous Substitutions in Flowering Plant Mitochondria Neutral?
Christensen et al., Lincoln, United States. In J Mol Evol, Oct 2015
Rps14 is co-transcribed with cob and rpl5 in most plant mitochondrial genomes, but in some genomes, rps14 has been duplicated to the nucleus leaving a pseudogene in the mitochondria.
Differential expression of ribosomal proteins in myelodysplastic syndromes.
Kim et al., New Orleans, United States. In J Clin Pathol, Oct 2015
Recent studies have identified haploinsufficiency of RPS14 in the acquired bone marrow disease isolated 5q minus syndrome, a subtype of myelodysplastic syndromes (MDS).
Pch2(TRIP13): controlling cell division through regulation of HORMA domains.
Vader, Dortmund, Germany. In Chromosoma, Sep 2015
For several of these functions, the Hop1, Rev7, and Mad2 (HORMA) domain-containing proteins Hop1(HORMAD), Mad2, and p31(COMET) are important downstream clients or cofactors of Pch2(TRIP13).
The molecular pathogenesis of the myelodysplastic syndromes.
Boultwood et al., Oxford, United Kingdom. In Eur J Haematol, Jul 2015
Haploinsufficiency of the ribosomal protein gene RPS14 plays a critical role in the development of anemia in the 5q- syndrome, and haploinsufficiency of CUX1 is important in some patients with MDS and AML with complete or partial loss of chromosome 7. Gene expression profiling has identified key deregulated genes and pathways and new prognostic gene signatures in MDS.
The S6K protein family in health and disease.
Simabuco et al., Limeira, Brazil. In Life Sci, Jul 2015
A third isoform, named p31-S6K1, has been characterized as a truncated type of the protein due to alternative splicing, and reports have shown its important role in cancer.
Reference Genes in the Pathosystem Phakopsora pachyrhizi/ Soybean Suitable for Normalization in Transcript Profiling.
Link et al., Stuttgart, Germany. In Int J Mol Sci, 2014
Here, RPS14 and UbcE2 are ranked best by geNorm and NormFinder.
Recent Advances in the 5q- Syndrome.
Boultwood et al., Oxford, United Kingdom. In Mediterr J Hematol Infect Dis, 2014
Haploinsufficiency of the ribosomal gene RPS14 has been shown to cause the erythroid defect in the 5q- syndrome.
Defective sister chromatid cohesion is synthetically lethal with impaired APC/C function.
Wolthuis et al., Amsterdam, Netherlands. In Nat Commun, 2014
Here, a paired genome-wide siRNA screen in patient-derived cell lines reveals that WABS cells do not tolerate partial depletion of individual APC/C subunits or the spindle checkpoint inhibitor p31(comet).
PP2A: The Achilles Heal in MDS with 5q Deletion.
List et al., Tampa, United States. In Front Oncol, 2013
Ineffective erythropoiesis in del(5q) MDS arises from allelic deletion of the ribosomal processing S-14 (RPS14) gene, which leads to MDM2 sequestration with consequent p53 activation and erythroid cell death.
Effects of L-leucine in 5q- syndrome and other RPS14-deficient erythroblasts.
Boultwood et al., In Leukemia, 2012
Loss of RPS14 is associated with 5q-syndrome.
Structure of the mitotic checkpoint complex.
Barford et al., London, United Kingdom. In Nature, 2012
Mad3 and p31(comet) (also known as MAD2L1-binding protein) compete for the same C-Mad2 interface, which explains how p31(comet) disrupts MCC assembly to antagonize the SAC.
Differential expression of cyclophilin A and EMMPRIN in developing molars of rats.
Kim et al., Kwangju, South Korea. In Anat Rec (hoboken), 2012
Cyclophilin-A and EMMPRIN play roles in the maturation of dental hard tissue and the formation of a molar eruption pathway.
Coordinate loss of a microRNA and protein-coding gene cooperate in the pathogenesis of 5q- syndrome.
Ebert et al., United States. In Blood, 2011
Combined loss of miR-145 and RPS14 cooperates to alter erythroid-megakaryocytic differentiation in a manner similar to the 5q- syndrome.
Expression, purification and preliminary crystallographic analysis of human thyroid hormone responsive protein.
Bartlam et al., Tianjin, China. In Acta Crystallogr Sect F Struct Biol Cryst Commun, 2011
N-terminally truncated human Thrsp and its selenomethionyl derivative were collected to 4.0, 3.0 and 3.6 A resolution
Cyclophilin A promotes cardiac hypertrophy in apolipoprotein E-deficient mice.
Berk et al., Rochester, United States. In Arterioscler Thromb Vasc Biol, 2011
CyPA is required for Ang II-mediated cardiac hypertrophy by directly potentiating ROS production, stimulating the proliferation and migration of cardiac fibroblasts, and promoting cardiac myocyte hypertrophy.
Identification of RPS14 as a 5q- syndrome gene by RNA interference screen.
Golub et al., Cambridge, United States. In Nature, 2008
results indicate that the 5q- syndrome is caused by a defect in RPS14 ribosomal protein function
p31comet blocks Mad2 activation through structural mimicry.
Luo et al., Dallas, United States. In Cell, 2007
p31(comet) inactivates the checkpoint through binding to Mad1- or Cdc20-bound Mad2, thereby preventing Mad2 activation and promoting the dissociation of the Mad2-Cdc20 complex.
A direct role for NKG2D/MICA interaction in villous atrophy during celiac disease.
Caillat-Zucman et al., Paris, France. In Immunity, 2004
We show that MICA is strongly expressed at epithelial cell surface in patients with active disease and is induced by gliadin or its p31-49 derived peptide upon in vitro challenge, an effect relayed by IL-15.
Association between innate response to gliadin and activation of pathogenic T cells in coeliac disease.
Londei et al., London, United Kingdom. In Lancet, 2003
METHODS: Duodenal biopsy samples from 42 patients with untreated coeliac disease, 37 treated patients, and 18 controls, were cultured in vitro for 3 h or 24 h, in the presence of either immunodominant gliadin epitopes (p(alpha)-2 and p(alpha)-9) or a non-immunodominant peptide (p31-43) known to induce small intestine damage in coeliac disease.
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