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Träfflista för sökning "WFRF:(Carling T) srt2:(2010-2014)"

Search: WFRF:(Carling T) > (2010-2014)

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1.
  • Björklund, Peyman, et al. (author)
  • Molecular Basis of Primary Hyperparathyroidism
  • 2010
  • In: World Journal of Endocrine Surgery. - 0975-5039. ; 2:2, s. 63-70
  • Journal article (other academic/artistic)abstract
    • During the past decade and a half, studies of genetic predisposition, parathyroid tumorigenesis, and molecular genetics of familialhyperparathyroid disorders have started to unveil the molecular basis of pHPT. Primary HPT is found in several distinct disorders withautosomal dominant inheritance such as in multiple endocrine neoplasia type 1 (MEN1), MEN2A, the HPT-jaw tumor syndrome (HPT-JT),familial isolated hyperparathyroidism (FIHPT), autosomal dominant mild hyperparathyroidism (ADMH), and neonatal severe HPT (NSHPT).
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4.
  • Åkerström, Tobias, et al. (author)
  • Comprehensive Re-Sequencing of Adrenal Aldosterone Producing Lesions Reveal Three Somatic Mutations near the KCNJ5 Potassium Channel Selectivity Filter.
  • 2012
  • In: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 7:7
  • Journal article (peer-reviewed)abstract
    • Aldosterone producing lesions are a common cause of hypertension, but genetic alterations for tumorigenesis have been unclear. Recently, either of two recurrent somatic missense mutations (G151R or L168R) was found in the potassium channel KCNJ5 gene in aldosterone producing adenomas. These mutations alter the channel selectivity filter and result in Na(+) conductance and cell depolarization, stimulating aldosterone production and cell proliferation. Because a similar mutation occurs in a Mendelian form of primary aldosteronism, these mutations appear to be sufficient for cell proliferation and aldosterone production. The prevalence and spectrum of KCNJ5 mutations in different entities of adrenocortical lesions remain to be defined.
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  • Result 1-4 of 4

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