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.