Results 41 to 50 of about 25,432,439 (260)

Western blot analysis of Bcl-xl, Bcl-2, Bax, truncated Bid (t-Bid), c-jun N-terminal kinase (JNK), phospho-JNK (p-JNK), extracellular signal-regulated protein kinase (ERK1/2), phospho-ERK1/2 (p-ERK1/2), CD95 and CD95L

open access: yes, 2011
(A) Sodium dodecyl sulphate-polyacrilamide gel electrophoresis of HSC cell lysates at days 2 and 7 of control cultures and cultures treated over 6 and 20 h with atorvastatin 10 mol/L, with and without U0126.
Isabella Aprigliano (45681)   +3 more
core   +1 more source

Proto-oncogene c-jun expression is induced by AML1-ETO in a JNK dependent manner:possible role in the pathogenesis of acute myeloid leukemia [PDF]

open access: yes, 2003
Overexpression of proto-oncogene c-jun and constitutive activation of the Jun NH2-terminal kinase (JNK) signaling pathway have been implicated in the leukemic transformation process.
Elsaesser, Annika
core   +1 more source

C-Jun N-terminal kinases/c-Jun and p38 pathways cooperate in ceramide-induced neuronal apoptosis [PDF]

open access: yes, 2003
Understanding the regulation of the apoptotic program in neurons by intracellular pathways is currently a subject of great interest. Recent results suggest that c-Jun N-terminal kinases (JNK), mitogen-activated protein kinases and the transcription ...
Brugg, B.   +4 more
core   +1 more source

Molecular marker identification for relapse prediction in 5-FU-based adjuvant chemotherapy in gastric and colorectal cancers. [PDF]

open access: yesPLoS ONE, 2012
To confirm the clinical significance of NF-κB and JNK protein expression from experimentally identified candidates for predicting prognosis for patients with 5-FU treatment, we evaluated the protein expression of surgically removed specimens.
Kazushige Ishida   +20 more
doaj   +1 more source

Activation of non-canonical TGFβ pathway through p-JNK.

open access: yes, 2015
DBA iPSCs, the corrected DBA cells and the GFP cells were cultured, and RNA, total protein and the protein from nuclear and cytoplasmic fraction were extracted from iPSCs for analysis. Fibrillarin were used as loading controls.
Monica Bessler (508914)   +7 more
core   +1 more source

Neutralization of the PTX3/CD44 axis suppresses TGF‐β1 signaling in kidney fibrosis

open access: yesFEBS Letters, EarlyView.
This study investigates how the PTX3/CD44 axis promotes kidney fibrosis by activating TGF‐β1 signaling. We demonstrate that the neutralizing antibody WHC‐001 effectively inhibits this pathway, suppressing myofibroblast activation and partial epithelial–mesenchymal transition (EMT).
Chao‐Chun Cheng   +8 more
wiley   +1 more source

Participation of JNK in TMZ-induced autophagy.

open access: yes, 2012
(A) U87 MG cells were treated with 400 µM TMZ for the indicated time periods and then analyzed using immunoblotting with anti-p-JNK and anti-t-JNK antibodies. The amount of protein applied in each lane was normalized by t-JNK internal control. (B) U87 MG
Chien-Huang Lin (156191)   +6 more
core   +1 more source

Tumour–host interactions in Drosophila: mechanisms in the tumour micro‐ and macroenvironment

open access: yesMolecular Oncology, EarlyView.
This review examines how tumour–host crosstalk takes place at multiple levels of biological organisation, from local cell competition and immune crosstalk to organism‐wide metabolic and physiological collapse. Here, we integrate findings from Drosophila melanogaster studies that reveal conserved mechanisms through which tumours hijack host systems to ...
José Teles‐Reis, Tor Erik Rusten
wiley   +1 more source

Activation of c-jun N-terminal kinase in spinal cord contributes to breast cancer induced bone pain in rats

open access: yesMolecular Brain, 2012
Background The most frequent pain in patients with metastatic breast and prostate cancer is bone pain, which can be severe and difficult to treat. The mechanisms underlying this pain remain unclear.
Wang Xiao-Wei   +8 more
doaj   +1 more source

SPARC overexpression activates JNK and JNK in turn activates PTEN.

open access: yes, 2012
SK-N-AS, NB1691 and IMR-32 cells were transfected for 24 hours with mock (PBS control), empty vector (pEV) or with pSPARC and treated with or without JNK activation inhibitor (JNK-I) for another 12 hours.
G. S. Sailaja (167091)   +6 more
core   +1 more source

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