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

ATPase, Ca++ transporting, plasma membrane 3

member of a family of plasma membrane calmodulin sensitive ATPases [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: ATPase, PMCA2, PMCA, PMCA1, PMCA4
Papers on PMCA3
Molecular Heterogeneity in Aldosterone-Producing Adenomas.
Rainey et al., Ann Arbor, United States. In J Clin Endocrinol Metab, Feb 2016
Of the six adrenocortical adenomas with CYP11B2 heterogeneity, three had aldosterone-regulating mutations (CACNA1D p.F747C, KCNJ5 p.L168R, ATP1A1 p.L104R) only in CYP11B2 positive regions, and one had two different mutations localized to two histologically distinct CYP11B2 positive regions (ATP2B3 p.L424_V425del, KCNJ5 p.G151R).
GNAS mutations in adrenal aldosterone-producing adenomas.
Yamada et al., Maebashi, Japan. In Endocr J, Feb 2016
Our results suggest that these mutations, in addition to mutations in the KCNJ5 gene and other genes such as ATP1A1, ATP2B3 and CACNA1D, may be responsible for the tumorigenesis of APAs and CPAs with subclinical Cushing's syndrome.
ENDOCRINE TUMOURS: The genomics of adrenocortical tumors.
Assie et al., Paris, France. In Eur J Endocrinol, Feb 2016
Exome sequencing identified new major drivers in all tumor types, including KCNJ5, ATP1A1, ATP2B3 and CACNA1D mutations in aldosterone producing adenomas (APA), PRKACA mutations in cortisol producing adenomas (CPA), ARMC5 mutations in primary bilateral macronodular adrenocortical hyperplasia (PBMAH), and ZNRF3 mutations in adrenocortical carcinomas (ACC).
Genotype-Specific Steroid Profiles Associated With Aldosterone-Producing Adenomas.
Reincke et al., München, Germany. In Hypertension, Jan 2016
Somatic APA mutations have been described in other genes (CACNA1D, ATP1A1, and ATP2B3) albeit at a lower frequency.
Novel somatic mutations in primary hyperaldosteronism are related to the clinical, radiological and pathological phenotype.
Carling et al., New Haven, United States. In Clin Endocrinol (oxf), Dec 2015
Somatic mutations in KCNJ5, CACNA1D, ATP1A1, ATP2B3 and CTNNB1 have been described in APAs.
Clinical and Steroidogenic characteristics of Aldosterone-producing Adenomas with ATPase or CACNA1D gene mutations.
Nishikawa et al., Yokohama, Japan. In J Clin Endocrinol Metab, Dec 2015
RESULTS: ATP1A1, ATP2B3, and CACNA1D mutations were detected in 1, 4, and 4 patients, respectively.
Different Somatic Mutations in Multinodular Adrenals With Aldosterone-Producing Adenoma.
Zennaro et al., Paris, France. In Hypertension, Nov 2015
Somatic mutations in KCNJ5, ATP1A1, ATP2B3, and CACNA1D are found in aldosterone-producing adenoma.
A Novel Somatic Deletion Mutation of ATP2B3 in Aldosterone-Producing Adenoma.
Ogawa et al., Tokyo, Japan. In Endocr Pathol, Nov 2015
Recent studies suggested that somatic mutations in the KCNJ5, ATP1A1, ATP2B3, and CACNA1D genes are involved in the pathogenesis of APA.
Novel somatic mutations and distinct molecular signature in aldosterone-producing adenomas.
Hellman et al., Uppsala, Sweden. In Endocr Relat Cancer, Oct 2015
More recently, somatic mutations in CACNA1D, ATP1A1 and ATP2B3, also important for membrane potential/intracellular Ca(2) (+) regulation, were observed in APAs.
Clinicopathologic Correlates of Primary Aldosteronism.
Mete et al., In Arch Pathol Lab Med, Jul 2015
Recently, the molecular basis of primary aldosteronism has begun to be unraveled, with the discovery of mutations in potassium channel (KCNJ5), ATPases (ATP1A1, ATP2B3), and calcium channel (CACNA1D), and aberrant Wnt/β-catenin signaling.
An update on novel mechanisms of primary aldosteronism.
Fernandes-Rosa et al., Paris, France. In J Endocrinol, Feb 2015
Recurrent somatic mutations in genes coding for ion channels (KCNJ5 and CACNA1D) and ATPases (ATP1A1 and ATP2B3) regulating intracellular ionic homeostasis and cell membrane potential have been identified in APA.
Prevalence and clinical correlates of somatic mutation in aldosterone producing adenoma-Taiwanese population.
Wu et al., Taiwan. In Sci Rep, 2014
A high rate of somatic mutation in APA was found (n=91, 61.5%); including mutations in KCNJ5 (n=88, 59.5%), ATP1A1 (n=2, 1.4%), and ATP2B3 (n=1, 0.7%); however, no mutations in CACNA1D were identified.
Molecular and Cellular Mechanisms of Aldosterone Producing Adenoma Development.
Zennaro et al., Paris, France. In Front Endocrinol (lausanne), 2014
The identification of recurrent and somatic mutations in genes coding for ion channels (KCNJ5 and CACNA1D) and ATPases (ATP1A1 and ATP2B3) allowed highlighting the central role of calcium signaling in autonomous aldosterone production by the adrenal.
Overview of the genetic determinants of primary aldosteronism.
Desailloud et al., Creil, France. In Appl Clin Genet, 2013
Somatic mutations in the KCNJ5, ATP1A1, ATP2B3 or CACNA1D genes are present in more than half of all cases of aldosterone-producing adenoma (~40%, ~6%, ~1% and ~8%, respectively).
Somatic mutations in ATP1A1 and ATP2B3 lead to aldosterone-producing adenomas and secondary hypertension.
Reincke et al., München, Germany. In Nat Genet, 2013
We identified somatic hotspot mutations in the ATP1A1 (encoding an Na(+)/K(+) ATPase α subunit) and ATP2B3 (encoding a Ca(2+) ATPase) genes in three and two of the nine APAs, respectively.
GABA-shunt enzymes activity in GH3 cells with reduced level of PMCA2 or PMCA3 isoform.
Rębas et al., Łódź, Poland. In Biochem Biophys Res Commun, 2011
Results suggest that PMCA2 and PMCA3 function is rather related to regulation of GABA synthesis and degradation than supplying cells with metabolites, which can be potentially energetic source.
Changes in islet plasma membrane calcium-ATPase activity and isoform expression induced by insulin resistance.
Flores et al., La Plata, Argentina. In Arch Biochem Biophys, 2009
Changes in islet plasma membrane calcium-ATPase activity and Atp2b3 protein isoform expression induced by insulin resistance are reported.
Placental calcium transporter (PMCA3) gene expression predicts intrauterine bone mineral accrual.
SWS Study Group et al., Southampton, United Kingdom. In Bone, 2007
Expression of the placental calcium transporter PMCA3 mRNA predicts neonatal whole body bone mineral content
Perisynaptic organization of plasma membrane calcium pumps in cerebellar cortex.
Weinberg et al., Chapel Hill, United States. In J Comp Neurol, 2007
PMCA3 is targeted to distinct compartments within the plasma membrane. In the molecular layer, this isoform was at highest levels within presynaptic profiles of the cerebellar cortex.
Expression and role of calcium-ATPase pump and sodium-calcium exchanger in differentiated trophoblasts from human term placenta.
Lafond et al., Montréal, Canada. In Mol Reprod Dev, 2003
role in the intracellular Ca(2+) extrusion of syncytiotrophoblast-like structure originating from the differentiation of cultured trophoblast cells isolated from human term placenta
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