Results 51 to 60 of about 229,819 (298)

Somatostatin receptor 4 (SSTR4) is a tumor suppressor in cutaneous and head & neck squamous cell carcinomas

open access: yesMolecular Oncology, EarlyView.
This study identifies somatostatin receptor 4 (Sstr4) as a critical tumor suppressor against skin and head/neck cancers (HNSCC, cSCC, and BCC). The loss of Sstr4 removes a check on cell growth, causing hyperactivation of the MAPK‐ERK signaling pathway (↑).
Ali Taqvi   +6 more
wiley   +1 more source

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

open access: yesMolecular Oncology, EarlyView.
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim   +7 more
wiley   +1 more source

RND2 attenuates apoptosis and autophagy in glioblastoma cells by targeting the p38 MAPK signalling pathway

open access: yesJournal of Experimental & Clinical Cancer Research, 2020
Background Inhibition of p38 MAPK signalling leads to glioblastoma multiform (GBM) tumourigenesis. Nevertheless, the molecular mechanism that induces p38 MAPK signalling pathway silencing during GBM genesis has yet to be determined.
Yang Xu   +9 more
doaj   +1 more source

Inhibition of Nucleoside Transport by p38 MAPK Inhibitors [PDF]

open access: yesJournal of Biological Chemistry, 2002
While investigating the ability of p38 MAPK to regulate cytarabine (Ara C)-dependent differentiation of erythroleukemia K562 cells, we observed effects that indicated that the imidazoline class of p38 MAPK inhibitors prevented nucleoside transport. Incubation of K562 cells with SB203580, SB203580-iodo, or SB202474, an analogue of SB203580 that does not
Min, Huang   +5 more
openaire   +2 more sources

sCD40L induces p38 MAPK phosphorylation in EOCs.

open access: yes, 2013
Total cell lysates of sCD40L (1 μg/mL)-, p38 inhibitor SB203580 (10 μM)-, and both sCD40L- and SB203580-treated EOCs assessed by SDS-PAGE for phospho-p38 MAPK. The p38 MAPK blot is representative of stripped phospho-p38 MAPK membranes.
Younes Zaid (497842)   +5 more
core   +1 more source

Aquaporin‐3 and aquaporin‐5 impact the development of pancreatic ductal adenocarcinoma spheroids

open access: yesFEBS Open Bio, EarlyView.
Schematic representation of the role of aquaporin‐3 (AQP3) and aquaporin‐5 (AQP5) in pancreatic ductal adenocarcinoma (PDAC). Both proteins are upregulated in PDAC and are associated with tumor progression and metastatic potential. Silencing AQP3 or AQP5 in PDAC spheroids results in decreased diameter, area, and overall growth, underscoring their key ...
Catarina Pimpão   +3 more
wiley   +1 more source

A novel cardioprotective p38-MAPK/mTOR pathway [PDF]

open access: yesExperimental Cell Research, 2011
Despite intensive study, the mechanisms regulating activation of mTOR and the consequences of that activation in the ischemic heart remain unclear. This is particularly true for the setting of ischemia/reperfusion (I/R) injury. In a mouse model of I/R injury, we observed robust mTOR activation, and its inhibition by rapamycin increased injury ...
Gonzalo, Hernández   +6 more
openaire   +2 more sources

The protein levels of JNK1/2, P38 MAPK in heart.

open access: yes, 2014
The protein levels of p-JNK1/2, JNK1/2, p-P38 MAPK and P38 MAPK.
Hanpeng Huang (549638)   +6 more
core   +1 more source

Propofol attenuates intermittent hypoxia induced up-regulation of proinflammatory cytokines in microglia through inhibiting the activation of NF-Bκ/p38 MAPK signalling [PDF]

open access: yes, 2017
As immune sentinels of the central nervous system (CNS), microglia is pivotal cellular mediator of neuroinflammatory processes. Activation of microglia might elicit the expression of proinflammatory cytokines involved in the progression of ...
Jin-Yuan Sun   +4 more
core   +1 more source

Type I interferons modulate autophagy to shape gemcitabine response in pancreatic cancer cells

open access: yesFEBS Open Bio, EarlyView.
Type I interferons differentially modulate autophagy and the response of pancreatic cancer cells to gemcitabine. IFNα2b stimulates autophagic flux and protects cells from gemcitabine‐induced cell death, contributing to chemoresistance. In contrast, IFNβ1a inhibits autophagosome formation and enhances gemcitabine‐induced cell death, resulting in ...
Lucy E. Bonilla   +10 more
wiley   +1 more source

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