Search engine for discovering works of Art, research articles, and books related to Art and Culture
Javascript must be enabled to continue!
C-Jun N-terminal kinase (JNK) pathway activation is essential for dental papilla cells polarization
View through CrossRef
Abstract
During tooth development, dental papilla cells could develop into odontoblasts with polarized morphology and cell function, c-Jun N-terminal kinase (JNK) signaling could participate in this process. Histological staining, qPCR and Western Blot shown that activation of JNK signaling in polarized mouse dental papilla tissue.
In vitro
cell culture and organ culture method found JNK inhibitor SP600125 postponed tooth germ development and reduced the polarization, migration and differentiation of mouse dental papilla cells (mDPCs)
in vitro
. The expression of polarity-related genes including Prickle3, Golga2, Golga5 and RhoA was consistent with JNK signaling activation, by screening of up-regulated polarity-related genes during the process of dental papilla development and mDPCs or A11 differentiation. Further, constitutively active RhoA mutant (RhoA Q63L) partly rescue the inhibition of SP600125 on cell differentiation and polarity formation of mDPCs. This study suggests that JNK signaling has a positive role in dental papilla cells polarization formation.
Title: C-Jun N-terminal kinase (JNK) pathway activation is essential for dental papilla cells polarization
Description:
Abstract
During tooth development, dental papilla cells could develop into odontoblasts with polarized morphology and cell function, c-Jun N-terminal kinase (JNK) signaling could participate in this process.
Histological staining, qPCR and Western Blot shown that activation of JNK signaling in polarized mouse dental papilla tissue.
In vitro
cell culture and organ culture method found JNK inhibitor SP600125 postponed tooth germ development and reduced the polarization, migration and differentiation of mouse dental papilla cells (mDPCs)
in vitro
.
The expression of polarity-related genes including Prickle3, Golga2, Golga5 and RhoA was consistent with JNK signaling activation, by screening of up-regulated polarity-related genes during the process of dental papilla development and mDPCs or A11 differentiation.
Further, constitutively active RhoA mutant (RhoA Q63L) partly rescue the inhibition of SP600125 on cell differentiation and polarity formation of mDPCs.
This study suggests that JNK signaling has a positive role in dental papilla cells polarization formation.
Related Results
C-Jun N-terminal kinase (JNK) pathway activation is essential for dental papilla cells polarization
C-Jun N-terminal kinase (JNK) pathway activation is essential for dental papilla cells polarization
During tooth development, dental papilla cells differentiate into odontoblasts with polarized morphology and cell function. Our previous study indicated that the C-Jun N-terminal k...
Awareness of Dental Personnel towards Occupational Injury- A Cross Sectional Study
Awareness of Dental Personnel towards Occupational Injury- A Cross Sectional Study
TITLE:
Awareness of dental personnel towards occupational injury- a cross sectional study
ABSTRACT
Objective: To determine the awareness of dental personnel towards dental occup...
Inhibition of c-Jun N-Terminal Kinase Ameliorates Apoptosis Induced by Hydrogen Peroxide in the Kidney Tubule Epithelial Cells (NRK-52E)
Inhibition of c-Jun N-Terminal Kinase Ameliorates Apoptosis Induced by Hydrogen Peroxide in the Kidney Tubule Epithelial Cells (NRK-52E)
<i>Background:</i> Hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-induced apoptosis has been shown to be involved in ischemic and toxic tubular ...
Negative Regulation by p70 S6 Kinase of FGF-2–Stimulated VEGF Release Through Stress-Activated Protein Kinase/c-Jun N-Terminal Kinase in Osteoblasts
Negative Regulation by p70 S6 Kinase of FGF-2–Stimulated VEGF Release Through Stress-Activated Protein Kinase/c-Jun N-Terminal Kinase in Osteoblasts
Abstract
To clarify the mechanism of VEGF release in osteoblasts, we studied whether p70 S6 kinase is involved in basic FGF-2–stimulated VEGF release in osteoblast-l...
JNK, essential for anticancer therapy-induced apoptosis, promotes breast cancer progression.
JNK, essential for anticancer therapy-induced apoptosis, promotes breast cancer progression.
Abstract
Abstract #5075
The c-Jun N-terminal kinase (JNK) is a critical mediator of stress-induced apoptosis and is required for the cytotoxic effect ...
A new c-Jun N-terminal kinase (JNK)-interacting protein, Sab (SH3BP5), associates with mitochondria
A new c-Jun N-terminal kinase (JNK)-interacting protein, Sab (SH3BP5), associates with mitochondria
We have identified a novel c-Jun N-terminal kinase (JNK)-interacting protein, Sab, by yeast two-hybrid screening. Sab binds to and serves as a substrate for JNK in vitro, and was p...
Sustained c-Jun-NH2-Kinase Activity Promotes Epithelial-Mesenchymal Transition, Invasion, and Survival of Breast Cancer Cells by Regulating Extracellular Signal-Regulated Kinase Activation
Sustained c-Jun-NH2-Kinase Activity Promotes Epithelial-Mesenchymal Transition, Invasion, and Survival of Breast Cancer Cells by Regulating Extracellular Signal-Regulated Kinase Activation
Abstract
The c-Jun NH2-terminus kinase (JNK) mediates stress-induced apoptosis and the cytotoxic effect of anticancer therapies. Paradoxically, recent clinical st...
JNK Pathway Is Constitutively Activated and Is Required for Survival in Human Mantle-Cell Lymphoma Fresh Cells and Cell-Lines.
JNK Pathway Is Constitutively Activated and Is Required for Survival in Human Mantle-Cell Lymphoma Fresh Cells and Cell-Lines.
Abstract
We previously reported that GST-pi, a cellular JNK effector and activator, was strongly expressed in MCL patient’s samples (Clin Cancer Res. 2004). Recently...