Expression of Nuclear Lamin Proteins in Endothelial Cells is Sensitive to Cell Passage and Fluid Shear Stress (Q63304701)

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:31719878 AND SRC:MED&resulttype=core&format=json

20 April 2020

title

Expression of Nuclear Lamin Proteins in Endothelial Cells is Sensitive to Cell Passage and Fluid Shear Stress (English)

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:31719878 AND SRC:MED&resulttype=core&format=json

20 April 2020

2

Julie Y. Ji

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author name string

Yizhi Jiang

series ordinal

1

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https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:31719878 AND SRC:MED&resulttype=core&format=json

20 April 2020

Julie Y Ji

series ordinal

2

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https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:31719878 AND SRC:MED&resulttype=core&format=json

20 April 2020

publication date

16 November 2017

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Cellular and Molecular Bioengineering

20 April 2020

published in

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volume

11

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issue

1

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page(s)

53-64

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describes a project that uses

20 April 2020

ImageJ

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11 June 2022

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inferred from PubMed Central ID database lookup

cites work

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12 December 2020

The nuclear envelope lamina is reversibly depolymerized during mitosis

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Flow-mediated endothelial mechanotransduction

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Laminar shear stress: mechanisms by which endothelial cells transduce an atheroprotective force

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Vascular endothelial cells minimize the total force on their nuclei

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Recurrent de novo point mutations in lamin A cause Hutchinson–Gilford progeria syndrome

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Differential responsiveness of vascular endothelial cells to different types of fluid mechanical shear stress

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Lamin A/C deficiency causes defective nuclear mechanics and mechanotransduction.

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Aging and nuclear organization: lamins and progeria

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Hutchinson-Gilford progeria syndrome

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A mechanosensory complex that mediates the endothelial cell response to fluid shear stress

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Hutchinson-Gilford progeria mutant lamin A primarily targets human vascular cells as detected by an anti-Lamin A G608G antibody

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Lamin A-dependent nuclear defects in human aging

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Mutant nuclear lamin A leads to progressive alterations of epigenetic control in premature aging

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Lamins A and C but not lamin B1 regulate nuclear mechanics.

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Cell nuclei spin in the absence of lamin b1.

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Laminar shear stress acts as a switch to regulate divergent functions of NF-kappaB in endothelial cells

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The mutant form of lamin A that causes Hutchinson-Gilford progeria is a biomarker of cellular aging in human skin

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Prelamin A acts to accelerate smooth muscle cell senescence and is a novel biomarker of human vascular aging

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Premature senescence of vascular cells is induced by HIV protease inhibitors: implication of prelamin A and reversion by statin

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Oxidative stress induces an ATM-independent senescence pathway through p38 MAPK-mediated lamin B1 accumulation

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LBR and lamin A/C sequentially tether peripheral heterochromatin and inversely regulate differentiation.

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Nuclear lamin-A scales with tissue stiffness and enhances matrix-directed differentiation

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Human iPSC-based modeling of late-onset disease via progerin-induced aging

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Isolated nuclei adapt to force and reveal a mechanotransduction pathway in the nucleus.

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Prelamin A accumulation and stress conditions induce impaired Oct-1 activity and autophagy in prematurely aged human mesenchymal stem cell

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Matrix elasticity regulates lamin-A,C phosphorylation and turnover with feedback to actomyosin.

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Nuclear envelope proteins Nesprin2 and LaminA regulate proliferation and apoptosis of vascular endothelial cells in response to shear stress

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12 December 2020

Differential basal-to-apical accessibility of lamin A/C epitopes in the nuclear lamina regulated by changes in cytoskeletal tension

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Heart Disease and Stroke Statistics-2016 Update: A Report From the American Heart Association

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10.1007/S12195-017-0513-8

Identifiers

DOI

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:31719878 AND SRC:MED&resulttype=core&format=json

Dimensions Publication ID

20 April 2020

0 references

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https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:31719878 AND SRC:MED&resulttype=core&format=json

20 April 2020

PubMed publication ID

31719878

1 reference