Sentences with phrase «promoting apoptosis»

Studies have shown gamma - tocotrienol selectively targets cancer cells, triggering cellular senescence and promoting apoptosis — a type of programmed cell suicide.
RemedyLink Ellagic Acid contains a blend of USP grade ellagic acid and specific herbs which offer many health benefits, some of which include inhibiting fungi and yeast growth, killing bacteria, promoting the apoptosis of certain cells, and more.
Finally the soy isoflavone genistein reduces DNA synthesis in the brain, reducing the birth of new brain cells and promoting apoptosis and cell death.
Their antioxidant activity is known to inhibit cell proliferation and invasion, and promote apoptosis (cell death) in various cancer cells.
When it reaches the brain, Zika virus infects neuronal stem cells, which will generate fewer neurons, and by inducing chronic stress in the endoplasmic reticulum, it promotes apoptosis, i.e. the early death of these neuronal cells.
In a related finding that year, Michael Karin and his collaborators at the University of California, San Diego, found that inhibiting NF - kB in mice engineered to develop colitis, which can lead to colon cancer, also promoted apoptosis.
Caspase - mediated activation of Caenorhabditis elegans CED - 8 promotes apoptosis and phosphatidylserine externalization.
The DEP domain - containing protein TOE - 2 promotes apoptosis in the Q lineage of C. elegans through two distinct mechanisms.
Notably, genes thought to induce and promote apoptosis through the intrinsic mitochondrial apoptotic pathway, such as KLF10 [32], were not altered in differentiated cells or in treated versus untreated cells.
A review of human, animal and test - tube studies, published in 2016 in Critical Reviews in Food Science and Nutrition, found that broccoli glucosinolates promote apoptosis, or cancer cell death.
In cancer therapy, melatonin counteracts chemotherapy toxicity, by acting as an anti-oxidant agent, and promotes apoptosis (programmed cell death) of cancer cells, thus enhancing the toxicity of chemotherapy.
It contains the phytochemical Quercetin, which is known to slow cancer growth and also promote apoptosis (there's that word again).
In a study published this year in Current Drug Targets, a combination of tocotrienols and quercetin induced senescence and promoted apoptosis in many different types of cancer cells, while delaying senescence in healthy cells and rejuvenating formerly healthy senescent cells.
Dr. Lee and Dr. Zava cited research studies which show that progesterone receptors activate genes such as p53 that promote apoptosis.
Pomegranate's antioxidant activity is known to inhibit cell proliferation and invasion, and promote apoptosis (cell death) in various cancer cells.
Their antioxidant activity is known to inhibit cell proliferation and invasion, and promote apoptosis (cell death) in various cancer cells.

Not exact matches

«We've long known that NF - kB promotes cancer development by subverting apoptosis, an internal safety mechanism that otherwise would cause cancer cells to self - destruct,» says principal investigator Denis Guttridge, PhD, professor of molecular virology, immunology and medical genetics and of molecular and cellular biochemistry.
Rather, the group speculates that the transplanted cells secreted protective neurotrophins, proteins that promote cell survival by keeping neurons from inducing apoptosis (programmed cell death).
At mitochondria, p53 activates apoptosis - promoting proteins, the investigation suggests.
Gradual increase of p53 levels activates apoptosis promoting protein Bak on the surface of the mitochondria making these cells vulnerable to death.
Importantly, in contrast to p53 - dependent senescence induction, in the absence of p53 or in the presence of MdmX overexpression, FL118 promotes p53 - independent apoptosis.
Moreover; the PI3K / AKT pathway also can contribute to melanoma tumorigenesis through mutations or loss in PTEN and dysregulation in expression of AKT, which positively regulates the G1 / S phase progression in cell cycle, suppresses apoptosis and promotes cellular survival.
Glycogen synthase kinase - 3β phosphorylates Bax and promotes its mitochondrial localization during neuronal apoptosis.
The results suggest that ApoE4 may contribute to AD in part by promoting inflammation and apoptosis, said Rao.
JNK - mediated phosphorylation of DLK suppresses its ubiquitination to promote neuronal apoptosis.
Binding of PD - L1 to the co-stimulatory receptor on T cells, PD - 1, promotes inactivation and apoptosis of activated anti-tumor T cells.
Tumor - associated B7 - H1 promotes T - cell apoptosis: a potential mechanism of immune evasion.
Stem cells affect the infarcted myocardium via neovascularization, reduction of apoptosis and paracrine effect, they are able to increase myocardial perfusion, inhibit synthesis of pro-inflammatory cytokines (IL6 and TNFα) and promote expression of anti-inflammatory cytokines (IL10) minimizing the necrosis damage caused by local inflammatory reaction.
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].
Independent of MMP activity, TIMP - 1 can promote growth and inhibit apoptosis through various pathways, including P13K and PKA [9] and, furthermore, TIMP - 1 is able to provide β cell - specific pro-survival effects [5, 6, 10].
This is in accordance with previous reports that decitabine and 5 - azacytidine produce a marked synergistic effect in combination with suberoylanilide hydroxamic acid and romidepsin in T - lymphoma cell lines by modulating cell cycle arrest and apoptosis.26, 27 As a mechanism of action, KMT2D mutations of B - lymphoma cells promote malignant outgrowth by perturbing methylation of H3K4 that affect the JAK - STAT, Toll - like receptor, or B - cell receptor pathway.28, 29 Here our study indicated that dual treatment with chidamide and decitabine enhanced the interaction of KMT2D with the transcription factor PU.1, thereby inactivating the H3K4me - associated signaling pathway MAPK, which is constitutively activated in T - cell lymphoma.13, 30,31 The transcription factor PU.1 is involved in the development of all hematopoietic lineages32 and regulates lymphoid cell growth and transformation.33 Aberrant PU.1 expression promotes acute myeloid leukemia and is related to the pathogenesis of multiple myeloma via the MAPK pathway.34, 35 On the other hand, PU.1 is also shown to interact with chromatin remodeler and DNA methyltransferease to control hematopoiesis and suppress leukemia.36 Our data thus suggested that the combined action of chidamide and decitabine may interfere with the differentiation and / or viability of PTCL - NOS through a PU.1 - dependent gene expression program.
Melanoma Differentiation Associated Gene - 7 / Interleukin - 24 Promotes Tumor Cell - Specific Apoptosis through Both Secretory and Nonsecretory Pathways
Estradiol promotes the onco (cancer) gene, Bcl - 2, while progesterone promotes the protective gene known as p53 which slows cell apoptosis.
Prosapogenin A, a saponin from Chinese herb Veratrum nigrum (black false hellebore or Li Lu in Chinese herbalism), could inhibit cell growth and promote cell apoptosis.
It promotes tumor cell proliferation and resistance to apoptosis (programmed cell death after a certain number of cell divisions, a good thing when it comes to cancer cells).
Indeed, insulin plays many vital roles in the brain: it mediates neuronal growth and metabolism, neurotransmission, and synaptic plasticity; promotes neuronal survival by inhibiting apoptosis; and regulates cognition and memory.
Instead, they turned on genes that promote the death of cancer cells (known as apoptosis) and the growth of healthy, normal cells!
Included in those is disrupting cancer cell replication, targeting and disrupting cancer stem cell development, and promoting cancer cell apoptosis (cell destruction)(6).
An anti-cancer diet also needs to be low or moderate in complete protein and high - insulemic index foods (to reduce growth promoting IGF - 1), and perhaps low in methionine specifically while high in fiber, phytochemical hormetics (to induce endogenous antioxidant responses and toxin removal), epigenetically active compunds (to reexpress tumor suppressor genes for induce cellular senescence or apoptosis), inflammation inhibitors, and antiangiogenetic compounds.
It is hypothesized that chronic ingestion of a high - carbohydrate diet promotes obesity and increases the demand on β - cells for insulin secretion, thereby predisposing individuals to hyperinsulinemia, apoptosis, β - cell failure, and development of type 2 diabetes (21).
Essential oils can and do still benefit these issues - as they can help the body to remove inflammation, support the body systems in repair, improve immune system function, relieve stress and discomfort, support the surrounding muscle and tissue structures, promote death of abnormal cells (apoptosis of tumor cells), provide antibacterial and antiviral actions, and more.
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