Literature DB >> 19535566

Regulation of mRNA translation in renal physiology and disease.

Balakuntalam S Kasinath1, Denis Feliers, Kavithalakshmi Sataranatarajan, Goutam Ghosh Choudhury, Myung Ja Lee, Meenalakshmi M Mariappan.   

Abstract

Translation, a process of generating a peptide from the codons present in messenger RNA, can be a site of independent regulation of protein synthesis; it has not been well studied in the kidney. Translation occurs in three stages (initiation, elongation, and termination), each with its own set of regulatory factors. Mechanisms controlling translation include small inhibitory RNAs such as microRNAs, binding proteins, and signaling reactions. Role of translation in renal injury in diabetes, endoplasmic reticulum stress, acute kidney injury, and, in physiological adaptation to loss of nephrons is reviewed here. Contribution of mRNA translation to physiology and disease is not well understood. Because it is involved in such diverse areas as development and cancer, it should prove a fertile field for investigation in renal science.

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Year:  2009        PMID: 19535566      PMCID: PMC2781325          DOI: 10.1152/ajprenal.90748.2008

Source DB:  PubMed          Journal:  Am J Physiol Renal Physiol        ISSN: 1522-1466


  156 in total

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5.  Decay of endoplasmic reticulum-localized mRNAs during the unfolded protein response.

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6.  Albumin induces endoplasmic reticulum stress and apoptosis in renal proximal tubular cells.

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8.  PKCdelta regulates the stimulation of vascular endothelial factor mRNA translation by angiotensin II through hnRNP K.

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  40 in total

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2.  PDGF receptor-β uses Akt/mTORC1 signaling node to promote high glucose-induced renal proximal tubular cell collagen I (α2) expression.

Authors:  Falguni Das; Nandini Ghosh-Choudhury; Balachandar Venkatesan; Balakuntalam S Kasinath; Goutam Ghosh Choudhury
Journal:  Am J Physiol Renal Physiol       Date:  2017-04-19

3.  PRAS40 acts as a nodal regulator of high glucose-induced TORC1 activation in glomerular mesangial cell hypertrophy.

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5.  MicroRNA-21 orchestrates high glucose-induced signals to TOR complex 1, resulting in renal cell pathology in diabetes.

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6.  TGFβ acts through PDGFRβ to activate mTORC1 via the Akt/PRAS40 axis and causes glomerular mesangial cell hypertrophy and matrix protein expression.

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7.  microRNA-181a downregulates deptor for TGFβ-induced glomerular mesangial cell hypertrophy and matrix protein expression.

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Review 8.  Nox4 and diabetic nephropathy: with a friend like this, who needs enemies?

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