Sentences with phrase «enhanced apoptosis»

TRAIL - enhanced apoptosis as measured by cleavage of caspase - 3 (Fig. 4I), and knockdown of ABL kinases increased the sensitivity of 1833 breast cancer cells to the proapoptotic effects of TRAIL (Fig. 4, G to I).

Morphine - enhanced apoptosis in selective brain regions of neonatal rats.

Rasul A, Ding C, Li X, Khan M, Yi F, Ali M and Ma T. Dracorhodin perchlorate inhibits PI3K / Akt and NF - kappaB activation, up - regulates the expression of p53, and enhances apoptosis.

Because elevated COX - 2 has been implicated in enhancing apoptosis resistance (Sheng et al., 1998; Krysan et al., 2004), unphosphorylated STAT6 - mediated apoptosis resistance in NSCLC could be due in part to its direct regulation of COX - 2 expression, though other unidentified targets of unphosphorylated STAT6 may also be involved.

Not exact matches

The research group in Israel showed «that the Spalax p53 suppresses apoptosis (programmed cell death), however enhances cell cycle arrest and DNA repair mechanisms,» he said.

The results were that BES enhanced cell survival and prevented the apoptosis of NPCs caused by growth factor deprivation.

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

Upregulation of retinoic acid receptor - ß reverses drug resistance in cholangiocarcinoma cells by enhancing susceptibility to apoptosis.

IG20 (MADD splice variant - 5), a proapoptotic protein, interacts with DR4 / DR5 and enhances TRAIL - induced apoptosis by increasing recruitment of FADD and caspase - 8 to the DISC.

Enhanced monocyte binding to human cytomegalovirus - infected syncytiotrophoblast results in increased apoptosis via the release of tumour necrosis factor alpha.

Cytotoxicity was enhanced by alterations of the regulators of apoptosis, such as Bcl2 / XIAP, in melanoma, lung cancer and adrenocortical carcinoma [9, 19, 21, 67].

Fas ligand - expressing lymphocytes enhance alveolar macrophage apoptosis in the resolution of acute pulmonary inflammation.

Conversely, they have found that interfering with survivin expression in tumor cells is sufficient to trigger apoptosis, to enhance the efficacy of conventional anti-tumor treatment, and to exert potent anti-tumor activity in vivo.

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.

Li W, Fan JG, Bertino JR: Flavopiridol enhances doxorubicin - induced apoptosis in human sarcoma cells lacking Rb protein.

TGFβ inhibits tumor initiation and progression by inducing cell cycle arrest and apoptosis; however epithelial tumorigenesis may escape this common antitumor mechanism by inducing aberrations in TGFβ signaling resulting in enhanced development and progression of human carcinomas.

Gadd45b mediates Fas - induced apoptosis by enhancing the interaction between p38 and retinoblastoma tumor suppressor

Enhanced amyloidogenic processing of APP by the ß - site APP cleaving enzyme (BACE) and the γ - secretase complex and reduced clearance lead to increased intracellular levels of soluble oligomeric Aß, resulting in cellular dysfunction comprising e.g., synaptic failure, mitochondrial dysfunction, enhanced oxidative stress, neurotransmitter and neurotrophin depletion, inflammation, and apoptosis which is reflected in patients as clinical symptoms such as cognitive deficitsEnhanced amyloidogenic processing of APP by the ß - site APP cleaving enzyme (BACE) and the γ - secretase complex and reduced clearance lead to increased intracellular levels of soluble oligomeric Aß, resulting in cellular dysfunction comprising e.g., synaptic failure, mitochondrial dysfunction, enhanced oxidative stress, neurotransmitter and neurotrophin depletion, inflammation, and apoptosis which is reflected in patients as clinical symptoms such as cognitive deficitsenhanced oxidative stress, neurotransmitter and neurotrophin depletion, inflammation, and apoptosis which is reflected in patients as clinical symptoms such as cognitive deficits [2, 3].

Inecalcitol, an analog of 1,25 D 3, displays enhanced antitumor activity through the induction of apoptosis in a squamous cell carcinoma model system.

One study puts it this way: «Glutamine has protective effects on intestinal mucosa by decreasing bacteremia and epithelial cell apoptosis, enhancing gut barrier function, and influencing gut immune response» [3].

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.

In the same way, whereas NR supplementation increased muscle stem cell number in aged mice, thereby enhancing mitochondrial function and muscle strength, it reduced the expression of cell senescence and apoptosis markers [233]; the state of senescence is important to protect against carcinogenesis [234].

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.