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Cell Adhesion and Spreading Affect Adipogenesis from Embryonic Stem Cells: The Role of Calreticulin

2009· article· en· 37 citations· W1984480602 on OpenAlex· 10.1002/stem.137

Why is this work in the frame?

A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.

Canadian affiliationAn author listed a Canadian institution. This is the only route the usual frame has.
Canadian funderA Canadian agency funded it. The work may carry no Canadian affiliation at all.

Post-publication record

Nature
Retraction
Reason
Cites Retracted Work;Duplication of/in Article;Investigation by Company/Institution;
Date
2/6/2020 0:00
Flagged by OpenAlex?
Yes

Source: Retraction Watch, joined by DOI. OpenAlex records retraction as is_retracted, a boolean over a state space with at least four values, so it cannot express an expression of concern, a correction or a reinstatement — it reports them as false, which reads as “fine”.

Abstract

Calreticulin is an endoplasmic reticulum-resident multifunctional protein, which has been shown to influence numerous cellular processes, including cell adhesion. In this study, we characterized the adhesive properties of embryonic stem cells (ESCs) lacking calreticulin and showed that adipogenesis from ESCs is directly and reciprocally controlled by the adhesive status of a cell, which in turn is modulated by calreticulin. Calreticulin-deficient ESCs are not only highly adipogenic but also show elevated calmodulin/CaMKII signaling and poor adhesiveness compared with the wild-type ESCs. Calreticulin deficiency leads to a disorganized cytoskeleton and low levels of focal adhesion-related proteins, such as vinculin, paxillin, and phosphorylated focal adhesion kinase, which cause limited focal adhesion formation and limited fibronectin deposition. Moreover, differentiation on nonadhesive substrata, which hinder cell spreading, promoted adipogenesis in the wild-type ESCs that normally have low adipogenic potential, causing a decrease in focal adhesion protein expression and an increase in calmodulin/CaMKII signaling. In contrast, inhibition of CaMKII effectively increased focal adhesion protein levels and inhibited adipogenesis in calreticulin-deficient ESCs, causing them to behave like the low adipogenic, wild-type ESCs. Thus, the adipogenic potential of ESCs is proportional to their calmodulin/CaMKII activity but is inversely related to their focal adhesion protein levels and degree of adhesiveness/spreading.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

The record

Venue
Stem Cells
Topic
Endoplasmic Reticulum Stress and Disease
Field
Biochemistry, Genetics and Molecular Biology
Canadian institutions
University of Toronto
Funders
Canadian Institutes of Health ResearchHeart and Stroke Foundation of Canada
Keywords
CalreticulinFocal adhesionCell biologyBiologyAdipogenesisPaxillinVinculinCell adhesionStem cellEmbryonic stem cellEndoplasmic reticulumSignal transductionCellBiochemistry
Has abstract in OpenAlex
yes