Results 11 to 20 of about 317,110 (186)

Non-phosphorylatable mutants of Ser184 lead to incomplete activation of Bax

open access: yesFrontiers in Oncology, 2023
The S184 residue of Bax is the target of several protein kinases regulating cell fate, including AKT. It is well-established that, in cellulo, the substitution of S184 by a non-phosphorylatable residue stimulates both the mitochondrial localization of ...
Lilit Simonyan   +10 more
doaj   +1 more source

Accumulation of tissue factor in endothelial cells induces cell apoptosis, mediated through p38 and p53 activation [PDF]

open access: yes, 2015
We previously reported that high levels of tissue factor (TF) can induce cellular apoptosis in endothelial. In this study, TF-mediated mechanisms of induction of apoptosis were explored.
Collier, Mary E. W.   +3 more
core   +1 more source

Pharmacological inhibition of Bax-induced cell death: Bax-inhibiting peptides and small compounds inhibiting Bax [PDF]

open access: yesExperimental Biology and Medicine, 2019
Bax is an essential mediator of mitochondria-dependent programed cell death. Bax belongs to the Bcl-2 family of proteins and its activities are regulated through interaction with other member proteins in the Bcl-2 family. To date, several apoptosis-inducing drugs activating Bax have been developed, and some of them are already in the market as ...
Kelsey, Jensen   +4 more
openaire   +2 more sources

Effect of N-acetyl cysteine on oxidative stress and Bax and Bcl2 expression in the kidney tissue of rats exposed to lead [PDF]

open access: yesThe Ukrainian Biochemical Journal, 2021
This study aimed to consider the lead-induced oxidative damage of the kidney of male rats and the role of antioxidant N-acetylcysteine (NAC) in preserving cells against Pb toxicity.
M. Gholami   +4 more
doaj   +1 more source

RelA/NF-kappaB recruitment on the bax gene promoter antagonizes p73-dependent apoptosis in costimulated T cells [PDF]

open access: yes, 2008
The balance between antiapoptotic and proapoptotic proteins of the Bcl-2 family is critical in determining the fate of T cells in response to death stimuli.
A., Annibaldi   +7 more
core   +1 more source

Circulating Cell-Free DNA in Dogs with Mammary Tumors: Short and Long Fragments and Integrity Index [PDF]

open access: yes, 2017
Circulating cell-free DNA (cfDNA) has been considered an interesting diagnostic/prognostic plasma biomarker in tumor-bearing subjects. In cancer patients, cfDNA can hypothetically derive from tumor necrosis/apoptosis, lysed circulating cells, and some ...
A Asmarinah   +79 more
core   +8 more sources

Inhibition of c-Jun N-terminal kinase (JNK) suppresses porcine oocyte ageing in vitro

open access: yesCzech Journal of Animal Science, 2013
Oocyte ageing is a complex of processes that occur when matured in vitro oocytes are, after reaching the metaphase II stage, exposed to further in vitro culture.
M. Sedmíková   +7 more
doaj   +1 more source

Two Targets, One Hit: new Anticancer Therapeutics to Prevent Tumorigenesis Without Cardiotoxicity

open access: yesFrontiers in Pharmacology, 2021
A serious adverse effect of cancer therapies is cardiovascular toxicity, which significantly limits the widespread use of antineoplastic agents. The promising new field of cardio-oncology offers the identification of potent anti-cancer therapeutics that ...
Zoltán Szabó   +4 more
doaj   +1 more source

Metformin alters signaling induced crosstalk and homeostasis in the carcinogenesis paradigm “Epistemology of the origin of cancer”

open access: yes4 open, 2019
The anti-hyperglycemic drug, Metformin, is effective in treating early stages of diabetes and has been associated with a 37% decrease in cancer incidence. While the precise mechanisms for the anti-cancer effects of Metformin remain to be elucidated, this
Brücher Björn L.D.M., Jamall Ijaz S.
doaj   +1 more source

Apoptosis status and proliferative activity in mucopolysaccharidosis type I mice tongue mucosa cells

open access: yesDental Research Journal, 2012
Background: Mucopolysaccharidosis type I (MPS I) is caused by a deficiency of alfa-iduronidase (IDUA), which leads to intralysosomal accumulation of glysosaminoglycans.
Juliana Noguti   +5 more
doaj   +1 more source

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