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Reversible HuR‐microRNA binding controls extracellular export of miR‐122 and augments stress response
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Kamalika Mukherjee Bartika Ghoshal Souvik Ghosh Yogaditya Chakrabarty Shivaprasad Shwetha Saumitra Das Suvendra N Bhattacharyya 《EMBO reports》2016,17(8):1184-1203
microRNAs (miRNAs), the tiny but stable regulatory RNAs in metazoan cells, can undergo selective turnover in presence of specific internal and external cues to control cellular response against the changing environment. We have observed reduction in cellular miR‐122 content, due to their accelerated extracellular export in human hepatic cells starved for small metabolites including amino acids. In this context, a new role of human ELAV protein HuR has been identified. HuR, a negative regulator of miRNA function, accelerates extracellular vesicle (EV)‐mediated export of miRNAs in human cells. In stressed cells, HuR replaces miRNPs from target messages and is both necessary and sufficient for the extracellular export of corresponding miRNAs. HuR could reversibly bind miRNAs to replace them from Ago2 and subsequently itself gets freed from bound miRNAs upon ubiquitination. The ubiquitinated form of HuR is predominantly associated with multivesicular bodies (MVB) where HuR‐unbound miRNAs also reside. These MVB‐associated pool of miRNAs get exported out via EVs thereby delimiting cellular miR‐122 level during starvation. Therefore, by modulating extracellular export of miR‐122, HuR could control stress response in starved human hepatic cells. 相似文献
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Soumen Chandra Dipranjan Laha Arindam Pramanik Angshuman Ray Chowdhuri Parimal Karmakar Sumanta Kumar Sahu 《Luminescence》2016,31(1):81-87
Highly fluorescent nitrogen and phosphorus‐doped carbon dots with a quantum yield 59% have been successfully synthesized from citric acid and di‐ammonium hydrogen phosphate by single step hydrothermal method. The synthesized carbon dots have high solubility as well as stability in aqueous medium. The as‐obtained carbon dots are well monodispersed with particle sizes 1.5–4 nm. Owing to a good tunable fluorescence property and biocompatibility, the carbon dots were applied for intercellular sensing of Fe3+ ions as well as cancer cell imaging. Copyright © 2015 John Wiley & Sons, Ltd. 相似文献
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Habacuc Flores‐Moreno Farideh Fazayeli Arindam Banerjee Abhirup Datta Jens Kattge Ethan E. Butler Owen K. Atkin Kirk Wythers Ming Chen Madhur Anand Michael Bahn Chaeho Byun J. Hans C. Cornelissen Joseph Craine Andres Gonzalez‐Melo Wesley N. Hattingh Steven Jansen Nathan J. B. Kraft Koen Kramer Daniel C. Laughlin Vanessa Minden Ülo Niinemets Vladimir Onipchenko Josep Peuelas Nadejda A. Soudzilovskaia Rhiannon L. Dalrymple Peter B. Reich 《Global Ecology and Biogeography》2019,28(12):1806-1826
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We present a new approach for estimation of the population-scaled mutation rate, , from microsatellite genotype data, using the recently introduced "product of approximate conditionals" framework. Comparisons with other methods on simulated data demonstrate that this new approach is attractive in terms of both accuracy and speed of computation. Our simulation experiments also demonstrate that, despite the theoretical advantages of full-likelihood-based methods, methods based on certain summary statistics (specifically, the sample homozygosity) can perform very competitively in practice. 相似文献
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Fragile X syndrome (FX), the most common heritable cause of mental retardation and autism, is a developmental disorder characterized by physical, cognitive, and behavioral deficits. FX results from a trinucleotide expansion mutation in the fmr1 gene that reduces levels of fragile X mental retardation protein (FMRP). Although research efforts have focused on FMRP's impact on mGluR signaling, how the loss of FMRP leads to the individual symptoms of FX is not known. Previous studies on human FX blood cells revealed alterations in the cyclic adenosine 3', 5'-monophosphate (cAMP) cascade. We tested the hypothesis that cAMP signaling is altered in the FX nervous system using three different model systems. Induced levels of cAMP in platelets and in brains of fmr1 knockout mice are substantially reduced. Cyclic AMP induction is also significantly reduced in human FX neural cells. Furthermore, cAMP production is decreased in the heads of FX Drosophila and this defect can be rescued by reintroduction of the dfmr gene. Our results indicate that a robust defect in cAMP production in FX is conserved across species and suggest that cAMP metabolism may serve as a useful biomarker in the human disease population. Reduced cAMP induction has implications for the underlying causes of FX and autism spectrum disorders. Pharmacological agents known to modulate the cAMP cascade may be therapeutic in FX patients and can be tested in these models, thus supplementing current efforts centered on mGluR signaling. 相似文献
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Debasish Haldar Arindam Banerjee 《International journal of peptide research and therapeutics》2007,13(3):439-446
The terminally protected peptide Boc-Leu-Val-Phe-Phe-Ala-OMe bearing sequence similarity with the central hydrophobic cluster
(CHC) of Alzheimer’s Aβ17–21 peptide self-assembles to produce amyloid-like straight unbranched fibrils from organic solvents. The fibrils readily bind
with a physiological dye Congo red (CR) and exhibits green gold birefringence under polarized light, a characteristic feature
of amyloid plaque obtained from many neurodegenerative diseases. FTIR spectroscopy and in silico energy minimization study shed some light on the antiparallel supramolecular β-sheet aggregation of the peptide. 相似文献