Sentences with phrase «result of apoptosis»

Earlier research had shown that cells surrounding an HIV - infected cell die as a result of apoptosis, or programmed cell suicide, and scientists knew that Nef had a hand in starting that process.

Not exact matches

But any new therapy can also cause undesirable effects: In our experiments, we saw that blocking apoptosis under inflammatory conditions can result in bililary obstruction (cholestasis) in the context of liver inflammation.»
The results were that BES enhanced cell survival and prevented the apoptosis of NPCs caused by growth factor deprivation.
On closer inspection Håkansson noticed the cells had died as a result of a process called apoptosis — programmed cell suicide — which is one of the ways that the body gets rid of unwanted or damaged cells.
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
The results indicated that CD8 − T cells induced significant, albeit weak, apoptosis of allogeneic corneal epithelial cells (Figure 5A).
We have considered the possibility that radiation could directly result in more apoptosis in the thymus of p21 - null mice; however, quantitation of sub -(G0 / G1) thymocytes after acute irradiation (10 Gy; and analysis 3 h after irradiation) has not supported this idea (data not shown).
Enhanced monocyte binding to human cytomegalovirus - infected syncytiotrophoblast results in increased apoptosis via the release of tumour necrosis factor alpha.
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).
The restriction of cellular growth by p53 has been reported to result in cell cycle arrest or apoptosis [6], and targeting p53 and restoring p53 function to limit tumor growth has been intensively researched for cancer therapy [7].
In addition, ActD has been shown to mimic nutlin - 3 in the activation of p53 - dependent transcription, induction of a reversible protective growth arrest in normal cells, and enhancement of the activity of the chemotherapeutic drugs, melphalan and etoposide, resulting in apoptosis of p53 positive human tumor cells [14].
The combined treatment of ActD with leptomycin B, a small molecule nuclear export inhibitor, has been shown to successfully lead to the accumulation of transcriptionally active p53 in the nuclei of human papillomavirus positive cervical carcinoma cells, resulting in apoptosis of the cells [16].
Loss of Daxx, a promiscuously interacting protein, results in extensive apoptosis in early mouse development.
In addition, knockdown of STAT6 by short hairpin RNAs results in apoptosis of human colon cancer HT - 29 cells (Zhang et al., 2005).
Despite the dramatic levels of apoptosis observed in wing primordia subject to CIN, the impact on the size of the resulting adult wing is mild.
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.
Since amiodarone HCL is known to exert its cytotoxic effect through the extrinsic, caspase - 9 independent apoptotic pathway [33] our microarray results confirm that the differential cytotoxic effect seen in NSCs treated with amiodarone HCL is due to specific activation of extrinsic apoptosis pathways resulting from exposure to the drug.
It was initially thought that TNFα - mediated signaling downstream of TNFR1 results in apoptosis, while those downstream of TNFR2 induce proliferation [40].
Microinjection manipulation resulted in the increased apoptosis of spermatocytes in testes from intracytoplasmic sperm injection (ICSI) derived mice
Since TNFα is such a potent inducer of apoptosis through TNFR1 death domain signaling, and amiodarone treatment results in the down regulation of TNFα with concomitant upregulation in TNFR2 signaling in NSC alone, it is possible that amiodarone selectively kills NSCs by lowering the threshold of TNFα required to trigger apoptosis in NSCs via upregulation of TNFR2 pathways in NSCs and not dopaminergic neurons.
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 deficits [2, 3].
So, if the process of apoptosis (a sort of cellular clean - up crew) is impaired, then the result is too much growth, exactly the problems we see in cancer and other metabolic disorders.
Because we have come to expect that autophagy and apoptosis will increase during fasting does the increased loss of N during the first days of fasting result in significant reduction in muscular functionality or is it a result confounded by multiple mechanisms?
Both of these benefits result in apoptosis (cell death) for cancerous and tumorous cells.
a b c d e f g h i j k l m n o p q r s t u v w x y z