Literature DB >> 27110666

Cross talk between the cytoplasm and nucleus during development and disease.

Lori L Wallrath1, Jens Bohnekamp2, Thomas M Magin2.   

Abstract

Mechanotransduction is a process whereby mechanical stimuli outside the cell are sensed by components of the plasma membrane and transmitted as signals through the cytoplasm that terminate in the nucleus. The nucleus responds to these signals by altering gene expression. During mechanotransduction, complex networks of proteins are responsible for cross talk between the cytoplasm and the nucleus. These proteins include cell membrane receptors, cytoplasmic filaments, LINC complex members that bridge the nucleus and cytoplasm, and nuclear envelope proteins that connect to the chromatin. Mechanotransduction also plays a critical role in development. Furthermore, it is possible that disrupted mechanotransduction leads to changes in gene expression that underlie the pathogenic mechanisms of disease.
Copyright © 2016. Published by Elsevier Ltd.

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Year:  2016        PMID: 27110666     DOI: 10.1016/j.gde.2016.03.007

Source DB:  PubMed          Journal:  Curr Opin Genet Dev        ISSN: 0959-437X            Impact factor:   5.578


  5 in total

1.  Suppression of myopathic lamin mutations by muscle-specific activation of AMPK and modulation of downstream signaling.

Authors:  Sahaana Chandran; Jennifer A Suggs; Bingyan J Wang; Andrew Han; Shruti Bhide; Diane E Cryderman; Steven A Moore; Sanford I Bernstein; Lori L Wallrath; Girish C Melkani
Journal:  Hum Mol Genet       Date:  2019-02-01       Impact factor: 6.150

Review 2.  The Nuclear Option: Evidence Implicating the Cell Nucleus in Mechanotransduction.

Authors:  Spencer E Szczesny; Robert L Mauck
Journal:  J Biomech Eng       Date:  2017-02-01       Impact factor: 2.097

Review 3.  A meeting at risk: Unrepaired DSBs go for broke.

Authors:  Aude Guénolé; Gaëlle Legube
Journal:  Nucleus       Date:  2017-11-17       Impact factor: 4.197

Review 4.  Laminopathies: what can humans learn from fruit flies.

Authors:  Marta Pałka; Aleksandra Tomczak; Katarzyna Grabowska; Magdalena Machowska; Katarzyna Piekarowicz; Dorota Rzepecka; Ryszard Rzepecki
Journal:  Cell Mol Biol Lett       Date:  2018-07-06       Impact factor: 5.787

5.  Lamin A/C deficiency enables increased myosin-II bipolar filament ensembles that promote divergent actomyosin network anomalies through self-organization.

Authors:  O'Neil Wiggan; Jennifer G DeLuca; Timothy J Stasevich; James R Bamburg
Journal:  Mol Biol Cell       Date:  2020-08-20       Impact factor: 4.138

  5 in total

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