Sentences with phrase «apoptosis inhibition»

Background: Citicoline can have beneficial effects both in degenerative and in vascular cognitive decline in a variety of ways (apoptosis inhibition, neuroplasticity potentiation, phospholipid, and acetylcholine (ACh) synthesis).

Not exact matches

The protein encoded by the PIK3C2G gene belongs to the phosphatidylinositol -4,5-bisphosphonate 3 - kinase (PI3K) family, which plays a critical role in cancer.28 Experimental evidence suggests that activation of PI3K signaling enhances production of COX - 2 and PGE2, which results in inhibition of apoptosis in colon cancer cell lines that can be restored with NSAID - mediated blockade of PI3K.29

MicroRNA - 15a inhibition protects against hypoxia / reoxygenation - induced apoptosis of cardiomyocytes by targeting mothers against decapentaplegic homolog 7.

Inhibition of raf - 1 alters multiple downstream pathways to induce pancreatic β - cell apoptosis.

Neuronal apoptosis induced by selective inhibition of Rac GTPase versus global suppression of Rho family GTPases is mediated by alterations in distinct mitogen - activated protein kinase signaling cascades.

NF - κB: Inhibition of this gene extends life modestly in a number of lower species, though given its involvement in immunity, inflammation, apoptosis, and other fundamental processes, there is an embarrassment of riches when it comes to trying to explain the roots of the effect.

Furthermore, niclosamide inhibited not only signal transduction, but also targeted mitochondria in cancer cells resulting in cell cycle arrest, growth inhibition and apoptosis [49 - 51].

Signal Transducer and Activator of Transcription - 5 Mediates Neuronal Apoptosis Induced by Inhibition of Rac GTPase Activity.

Oxidant - mediated mitochondrial injury in eosinophil apoptosis: enhancement by glucocorticoids and inhibition by granulocyte - macrophage colony - stimulating factor.

Signal transducer and activator of transcription - 5 mediates neuronal apoptosis induced by the inhibition of Rac GTPase activity.

Inhibition of c - Abl with STI571 attenuates stress - activated protein kinase activation and apoptosis in the cellular response to 1 - β - d - arabinofuranosylcytosine.

Apoptosis following inhibition of mTOR expression or function was associated with down - regulation of antiapoptotic proteins, including c - FLIP, MCL - 1, and BCL - 2.

Previous studies have shown that inhibition of PI3K using LY294002 or wortmannin resulted in decreased cell growth and apoptosis of ALCL cells (5).

As reported previously, inhibition of PI3K resulted in increased apoptosis of ALCL cells (5).

Inhibition of mTOR expression or function induces apoptosis in ALCL cells.

Inhibition of mTOR induces apoptosis in ALK + ALCL cells.

We also show that inhibition of mTOR with rapamycin, as well as silencing mTOR gene product expression using mTOR - specific small interfering RNA, decreased phosphorylation of mTOR signaling proteins and induced cell cycle arrest and apoptosis in ALK + ALCL cells.

Activation of ERK1 / 2 triggers G2 checkpoint which is considered protective from radiation - induced cell death [8, 9], while activated AKT is known to promote DNA repair and inhibition of apoptosis induction [10].

These pathways function in the inhibition of apoptosis as well as cell differentiation and cell cycle.

Thioredoxin - 1 (Trx1) is an endogenous antioxidant protein important for redox regulation and participates in the regulation of apoptosis through the inhibition of apoptosis signal - regulating kinase - 1 (Ask - 1).

Our data raise the possibility that inhibition of ABL kinases can increase apoptosis of breast cancer cells and block osteoclast activation, which is required for osteolytic metastasis.

Moreover, annexin V / propidium iodide staining showed that VPA only marginally decreased the viability of in vitro — differentiated Th1 and Th17 cells at a relatively high concentration (1 mM)(Supplemental Fig. 4A, 4B), whereas VPA readily inhibited the differentiation of Th1 and Th17 cells at a low concentration (0.2 — 0.5 mM), indicating that apoptosis induction was not the primary mechanism for Th1 and Th17 cell differentiation inhibition (28, 29).

These biochemical mechanisms influence four different actions, which are cellular apoptosis, the inhibition of cell proliferation, the suppression of cytokine production and the reduction of white blood cells or leukocytes.

In response to cellular stress such as DNA damage, oncogene activation, transcriptional inhibition, and hypoxia, tumor suppressor p53 is activated and expressed, and acts as a transcription factor to induce its target genes [1], thereby playing a central role in the regulation of DNA repair, cell cycle, apoptosis, senescence, and angiogenesis [2 - 4].

ONC201 induced caspase - dependent apoptosis that involved activation of the integrated stress response (ATF4 / CHOP) pathway, inhibition of Akt phosphorylation, Foxo3a activation, downregulation of cyclin D1, IAP and Bcl - 2 family members.

«Programmed cell death, or apoptosis, is very important, particularly in the hematopoietic (blood forming) system, where inhibition of cell death leads to leukemias,» says Whitehead Institute Founding Member Harvey Lodish, who is also a professor of biology and a professor of bioengineering at MIT.

Targeting autophagy potentiates chemotherapy - induced apoptosis and proliferation inhibition in hepatocarcinoma cells.

Liu J, Bai J, Jiang G, Li X, Wang J, Wu D, Owusu L, Zhang E, Li W. Anti-tumor Effect of Pinus Massoniana Bark Proanthocyanidins on Ovarian Cancer Through Induction of Cell Apoptosis and Inhibition of Cell Migration.

We have initiated studies regarding the hypothesis that the benzamides and nicotinamides could inhibit the production of tumor necrosis factor alpha (TNFalpha) and the inflammatory response as well as induce apoptosis via inhibition of NF - kappaB.

For example, KBs were recently reported to act as neuroprotective agents by raising ATP levels and reducing the production of reactive oxygen species in neurological tissues, 80 together with increased mitochondrial biogenesis, which may help to enhance the regulation of synaptic function.80 Moreover, the increased synthesis of polyunsaturated fatty acids stimulated by a KD may have a role in the regulation of neuronal membrane excitability: it has been demonstrated, for example, that polyunsaturated fatty acids modulate the excitability of neurons by blocking voltage-gated sodium channels.81 Another possibility is that by reducing glucose metabolism, ketogenic diets may activate anticonvulsant mechanisms, as has been reported in a rat model.82 In addition, caloric restriction per se has been suggested to exert neuroprotective effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits of ketogenic diets in most neurological diseases remain largely speculative and uncertain, with the significant exception of its use in the treatment of convulsion diseases.