Results 21 to 30 of about 83,967 (245)

Intracellular S1P generation is essential for S1P-induced motility of human lung endothelial cells : role of sphingosine kinase 1 and S1P lyase [PDF]

open access: yes, 2011
Earlier we have shown that extracellular sphingosine-1-phosphate (S1P) induces migration of human pulmonary artery endothelial cells (HPAECs) through the activation of S1P(1) receptor, PKCε, and PLD2-PKCζ-Rac1 signaling cascade.
Gorshkova, Irina   +9 more
core   +4 more sources

Dual Lineages of Langerhans Cells Cooperate to Restore the Immune Barrier after Skin Injury. [PDF]

open access: yesAdv Sci (Weinh)
After skin injury, the epidermal immune barrier is rebuilt by two sources of Langerhans cells. Resident Langerhans cells first move into the wound during re‐epithelialization, guided by CXCR2 signaling. Later, recruited monocytes become long‐lived Langerhans cells.
Schmitter-Sánchez AD   +8 more
europepmc   +2 more sources

Modulation of the Pol II CTD Phosphorylation Code by Rac1 and Cdc42 Small GTPases in Cultured Human Cancer Cells and Its Implication for Developing a Synthetic-Lethal Cancer Therapy

open access: yesCells, 2020
Rho GTPases, including Rho, Cdc42, Rac and ROP subfamilies, are key signaling molecules in RNA polymerase II (Pol II) transcriptional control.
Bo Zhang   +4 more
doaj   +1 more source

The E3 ubiquitin ligase MG53 inhibits hepatocellular carcinoma by targeting RAC1 signaling

open access: yesOncogenesis, 2022
Ras-related C3 botulinum toxin substrate 1 (RAC1) overexpressiosn and hyperactivation are correlated with aggressive growth and other malignant characteristics in a wide variety of cancers including hepatocellular carcinoma (HCC). However, the regulatory
Xiaomin Ma   +9 more
doaj   +1 more source

RAC1 and Melanoma [PDF]

open access: yesClinical Therapeutics, 2015
RAC1 is a GTPase member of the RAS superfamily, and RAC1(P29S) was recently identified as the third most common recurrent mutation in melanomas, affecting 4-7% of the patients. This is an oncogenic mutation, because the mutant protein remains mostly in its active GTP-bound form, and its ectopic expression increases the rate of normal melanocytes ...
openaire   +2 more sources

Role of rac1 protein in the acquisition and mainteinance of epithelial cell polarity [PDF]

open access: yes, 2009
: The acquisition of cell polarity, which includes the establishment of the tight junction barrier, the polarized assembly of the cytoskeleton and the appropriate organization of membrane traffic, requires external cues, that in epithelial cells are ...
Santoriello, Margherita
core   +2 more sources

Tyrosine phosphorylation of Rac1: a role in regulation of cell spreading. [PDF]

open access: yesPLoS ONE, 2011
Rac1 influences a multiplicity of vital cellular- and tissue-level control functions, making it an important candidate for targeted therapeutics. The activity of the Rho family member Cdc42 has been shown to be modulated by tyrosine phosphorylation at ...
Fumin Chang   +4 more
doaj   +1 more source

K-Ras mediated murine epidermal tumorigenesis Is dependent upon and associated with elevated Rac1 activity [PDF]

open access: yes, 2011
A common goal for potential cancer therapies is the identification of differences in protein expression or activity that would allow for the selective targeting of tumor vs. normal cells. The Ras proto-oncogene family (K-Ras, H-Ras and N-Ras) are amongst
Samuel, M.   +14 more
core   +2 more sources

Nucleophosmin1 is a negative regulator of the small GTPase Rac1. [PDF]

open access: yesPLoS ONE, 2013
The Rac1 GTPase is a critical regulator of cytoskeletal dynamics and controls many biological processes, such as cell migration, cell-cell contacts, cellular growth and cell division.
Younes Zoughlami   +3 more
doaj   +1 more source

Chronic inflammation evoked by pathogenic stimulus during carcinogenesis

open access: yes4 open, 2019
A pathogenic (biological or chemical) stimulus is the earliest information received by a cell that can result in the disruption of homeostasis with consequent development of disease.
Brücher Björn L.D.M., Jamall Ijaz S.
doaj   +1 more source

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