Sentences with phrase «activates apoptosis»

Ischemia induces nuclear NOX2 expression in cardiomyocytes and subsequently activates apoptosis.

The good news is that we found a small molecule drug being tested in cancers that activates apoptosis and we decided to test it in combination therapy.»

Gradual increase of p53 levels activates apoptosis promoting protein Bak on the surface of the mitochondria making these cells vulnerable to death.

At mitochondria, p53 activates apoptosis - promoting proteins, the investigation suggests.

b. Creating synthetic receptors or signals of cancer, i.e. when cancer related miRNA is activated, you have it also activate a synthetic gene or protein, that is expressed on the membrane surface to activate apoptosis.

Not exact matches

There, depending on what other chemical signals are present, the GAPDH can either stimulate the neuron's growth or activate a self - destruct program — called apoptosis — that will kill the neuron.

They found that the therapy releases and / or activates the pro-apoptotic proteins Bim, Bak and Bax, which help trigger apoptosis.

In addition, they found that epithelial - derived MMP9 suppresses tumors in CAC by activating the MMP9 - Notch1 - ARF - p53 axis pathway, which increases apoptosis, initiates cell cycle arrest and keeps a check on DNA damage.

Those cells escape from the apoptosis process by activating a cell - survival mechanism called autophagy.

Researchers found TRIF signaling is able to eliminate these aberrantly activated astrocytes by apoptosis, a suicide program of the cells.

The NLR family apoptosis inhibitory proteins (NAIPs) bind conserved bacterial ligands, such as the bacterial rod protein PrgJ, and recruit NLR family CARD - containing protein 4 (NLRC4) as the inflammasome adapter to activate innate immunity.

Receptor interacting protein kinase 1 (RIPK1) has important kinase - dependent and kinase - independent scaffolding functions that activate or prevent apoptosis or necroptosis in a cell context — dependent manner.

In fact, KLF4 blocks senescence and apoptosis by repressing transcription of P53, whereas it can activate P21 - dependent cell - cycle arrest, and therefore, KLF4 can function both as a tumor suppressor and an oncogene (33, 34).

Members of a family that includes the apoptosis regulator APAF1 (apoptotic - protease - activating factor 1), mammalian NOD - LRR proteins (also known as NACHT - LRR proteins or CATERPILLERs) and plant disease - resistance gene products.

In addition, consistent with past studies, AAV2 - infected cancer cells produced more Ki - 67, an immunity system activating protein and c - Myc, a protein that helps both to increase cell growth and induce 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.

Transient receptor potential (TRP) protein 7 acts as a G protein - activated Ca 2 + channel mediating angiotensin II - induced myocardial apoptosis.

Busulfan selectively induces cellular senescence but not apoptosis in WI38 fibroblasts via a p53 - independent but extracellular signal - regulated kinase - p38 mitogen - activated protein kinase - dependent mechanism.

Endoplasmic reticulum stress and trophic factor withdrawal activate distinct signaling cascades that induce glycogen synthase kinase - 3β and a caspase -9-dependent apoptosis in cerebellar granule neurons.

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

A myocyte enhancer factor 2D (MEF2D) kinase activated during neuronal apoptosis is a novel target inhibited by lithium.

Ketamine activates cell cycle signaling and apoptosis in the neonatal rat brain.

Binding of PD - L1 to the co-stimulatory receptor on T cells, PD - 1, promotes inactivation and apoptosis of activated anti-tumor T cells.

Activated ERK1 / 2 modulates the functions of several transcription factors, protein kinases, protein phosphatases, cytoskeletal proteins, signaling molecules, apoptosis - related proteins, as well as other types of proteins [32], while activated AKT modulates the function of numerous substrates involved in the regulation of cell survival, cell cycle progression and cellular growth [33, 34], whereas JNK acts as pro-apoptotic as well as anti-apoptotic depending on the conditiActivated ERK1 / 2 modulates the functions of several transcription factors, protein kinases, protein phosphatases, cytoskeletal proteins, signaling molecules, apoptosis - related proteins, as well as other types of proteins [32], while activated AKT modulates the function of numerous substrates involved in the regulation of cell survival, cell cycle progression and cellular growth [33, 34], whereas JNK acts as pro-apoptotic as well as anti-apoptotic depending on the conditiactivated AKT modulates the function of numerous substrates involved in the regulation of cell survival, cell cycle progression and cellular growth [33, 34], whereas JNK acts as pro-apoptotic as well as anti-apoptotic depending on the conditions [35].

25: Radaeva S, Sun R, Jaruga B, Nguyen VT, Tian Z, Gao B. Natural killer cells ameliorate liver fibrosis by killing activated stellate cells in NKG2D - dependent and tumor necrosis factor - related apoptosis - inducing ligand - dependent manners.

When BubR1H / H; INK - ATTAC mouse bone marrow cells were pushed into senescence in vitro by the PPAR - γ - activating drug rosiglitazone, a subpopulation of the cells exhibited high levels of INK - ATTAC expression and GFP, coupled with SAβ - gal staining; subsequent to treatment with the INK - ATTAC activating drug, these cells rapidly entered into apoptosis, and within 48 h were either destroyed or in the cell death process.

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].

It was shown that VPA could induce the apoptosis of activated T cells and maintain immune homeostasis through the caspase - 8 / caspase - 3 pathway (28).

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.

Abbreviations: ASC, apoptosis - associated speck - like protein containing a caspase - recruitment domain; ATM, adipose - tissue - resident macrophage; BAT, brown adipose tissue; CCR2, CC chemokine receptor 2; CHOP, C / EBP (CCAAT / enhancer - binding protein)- homologous protein; DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; ER, endoplasmic reticulum; GPCR, G - protein - coupled receptor; HIF, hypoxia - inducible factor; IFNγ, interferon γ; IKK, inhibitor of nuclear factor κB kinase; IL, interleukin; IRS - 1, insulin receptor substrate - 1; JNK, c - Jun N - terminal kinase; LDL, low - density lipoprotein; Ldlr, LDL receptor; LXR, liver X receptor; MCP - 1, monocyte chemoattractant protein 1; miRNA, microRNA; mTOR, mammalian target of rapamycin; NAFLD, non-alcoholic fatty liver disease; NF - κB, nuclear factor κB; NLRP3, NLR (nucleotide - binding - domain - and leucine - rich - repeat - containing) family, pyrin - domain - containing 3; oxLDL, oxidized LDL; PKR, double - stranded RNA - dependent protein kinase; PPAR, peroxisome - proliferator - activated receptor; STAT6, signal transducer and activator of transcription 6; SVF, stromal vascular fraction; TLR, Toll - like receptor; TNFα, tumour necrosis factor α; UPR, unfolded protein response; WAT, white adipose tissue

It has been shown that the MAP kinases including JNKs, ERKs, and p38 phosphorylate p53 in response to different stressful stimuli, and in turn, activate a p53 response leading to cell cycle arrest and apoptosis [24].

Oncogenes — whose protein products, when activated, cause uncontrolled cell proliferation or prevent cells from undergoing apoptosis.

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].

Induction of IL17 following S. aureus bioparticle challenge was compromised in mice lacking the ASC (Apoptosis - associated speck - like protein containing a CARD) inflammasome subunit (Figure 1G), consistent with a role for IL1β in activating IL7RαhiCcr6 + cells during the response to these bacteria.

Estrogen does this by activating a gene known as Bcl - 2 that slows the process of cell death, known as apoptosis.

Dr. Lee and Dr. Zava cited research studies which show that progesterone receptors activate genes such as p53 that promote apoptosis.

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.