Isolation and Handling of Mouse Embryonic Fibroblasts

2014 ◽  
pp. 247-252 ◽  
Author(s):  
Kanika Jain ◽  
Paul J. Verma ◽  
Jun Liu
Keyword(s):  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts

scholarly journals Regulation of c-Fos Gene Expression by NF-κB: A p65 Homodimer Binding Site in Mouse Embryonic Fibroblasts but Not Human HEK293 Cells

PLoS ONE ◽  
2013 ◽  
Vol 8 (12) ◽  
pp. e84062 ◽  
Author(s):  
Yu-Cheng Tu ◽  
Duen-Yi Huang ◽  
Shine-Gwo Shiah ◽  
Jang-Shiun Wang ◽  
Wan-Wan Lin
Keyword(s):  
Gene Expression ◽  
Binding Site ◽  
Hek293 Cells ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts

scholarly journals Introduction of Mouse Embryonic Fibroblasts into Early Embryos: From Confusion to Constructive Discussion. Comment on Savatier, P. Introduction of Mouse Embryonic Fibroblasts into Early Embryos Causes Reprogramming and (Con)fusion. Cells 2021, 10, 772

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1534
Author(s):  
Krystyna Żyżyńska-Galeńska ◽  
Jolanta Karasiewicz ◽  
Agnieszka Bernat
Keyword(s):  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts ◽  
Early Embryos ◽  
Constructive Discussion

We would like to address the issues raised by Pierre Savatier in “Introduction of Mouse Embryonic Fibroblasts into Early Embryos Causes Reprogramming and (Con)Fusion” [...]

616 Mouse Embryonic Fibroblasts Null for the KrüPpel-Like Factor 4 Alleles Are Genetically Unstable

2008 ◽  
Vol 134 (4) ◽  
pp. A-86
Author(s):  
Engda G. Hagos ◽  
Amr Ghaleb ◽  
W Brian Dalton ◽  
Jonathan P. Katz ◽  
Klaus H. Kaestner ◽  
...  
Keyword(s):  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts

scholarly journals Introduction of Mouse Embryonic Fibroblasts into Early Embryos Causes Reprogramming and (Con)fusion

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 772
Author(s):  
Pierre Savatier
Keyword(s):  
Somatic Cell ◽  
Cell Nuclei ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts ◽  
Early Embryos

The reprogramming of somatic cell nuclei to achieve pluripotency is one of the most important biological discoveries of the last few decades [...]

scholarly journals AMPKα1 deficiency promotes cellular proliferation and DNA damage via p21 reduction in mouse embryonic fibroblasts

2015 ◽  
Vol 1853 (1) ◽  
pp. 65-73 ◽  
Author(s):  
Hairong Xu ◽  
Yanhong Zhou ◽  
Kathleen A. Coughlan ◽  
Ye Ding ◽  
Shaobin Wang ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cellular Proliferation ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts

Hydrogen-rich medium protects mouse embryonic fibroblasts from oxidative stress by activating LKB1-AMPK-FoxO1 signal pathway

2017 ◽  
Vol 491 (3) ◽  
pp. 733-739 ◽  
Author(s):  
Jihyun Lee ◽  
Goowon Yang ◽  
Young-Joo Kim ◽  
Quynh Hoa Tran ◽  
Wonchae Choe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signal Pathway ◽  
Rich Medium ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts

scholarly journals S6K1 Is Indispensible for Stress-Induced Microtubule Acetylation and Autophagic Flux

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 929
Author(s):  
Aleksandra Hać ◽  
Karolina Pierzynowska ◽  
Anna Herman-Antosiewicz
Keyword(s):  
Degradation Process ◽  
Underlying Mechanism ◽  
Stress Conditions ◽  
Autophagic Flux ◽  
Ratiometric Fluorescence ◽  
Mouse Embryonic Fibroblasts ◽  
Double Knockout ◽  
Embryonic Fibroblasts ◽  
Microtubule Network ◽  
Tubulin Acetylation

Autophagy is a specific macromolecule and organelle degradation process. The target macromolecule or organelle is first enclosed in an autophagosome, and then delivered along acetylated microtubules to the lysosome. Autophagy is triggered by stress and largely contributes to cell survival. We have previously shown that S6K1 kinase is essential for autophagic flux under stress conditions. Here, we aimed to elucidate the underlying mechanism of S6K1 involvement in autophagy. We stimulated autophagy in S6K1/2 double-knockout mouse embryonic fibroblasts by exposing them to different stress conditions. Transient gene overexpression or silencing, immunoblotting, immunofluorescence, flow cytometry, and ratiometric fluorescence analyses revealed that the perturbation of autophagic flux in S6K1-deficient cells did not stem from impaired lysosomal function. Instead, the absence of S6K1 abolished stress-induced tubulin acetylation and disrupted the acetylated microtubule network, in turn impairing the autophagosome-lysosome fusion. S6K1 overexpression restored tubulin acetylation and autophagic flux in stressed S6K1/2-deficient cells. Similar effect of S6K1 status was observed in prostate cancer cells. Furthermore, overexpression of an acetylation-mimicking, but not acetylation-resistant, tubulin variant effectively restored autophagic flux in stressed S6K1/2-deficient cells. Collectively, S6K1 controls tubulin acetylation, hence contributing to the autophagic flux induced by different stress conditions and in different cells.

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