「apoptosis」の共起表現(1語右で並び替え)

「apoptosis」の共起表現一覧(1語右で並び替え)

apoptosis

1語右で並び替え

該当件数:141件

Apoptosis, a major form of cell death, is an efficient
ich protects cells against TNF-alpha induced apoptosis, a lack of IKBKG (and hence a lack of active
Often at late stages of apoptosis, adherent cells are known to detach or “pop”
urs mainly as a result of necrosis, while in apoptosis after karyorrhexis the nucleus usually disso
AD thus do not show DNA fragmentation during apoptosis, although they do exhibit some other feature
Since it can block apoptosis, and thereby promote cell survival, Akt1 has
to increased survival due to lower rates of apoptosis and increased proliferation due to the activ
domain (CARD), and has been shown to induce apoptosis and to activate NF-kappaB.
lular processes, such as cell proliferation, apoptosis, and differentiation.
hown to be genotoxic in human cells, causing apoptosis and also decreased DNA production and shorte
l signaling and in the regulation of growth, apoptosis, and differentiation of a variety of cell ty
such as cell proliferation, differentiation, apoptosis and immunoresponses.
ls to isoflurane has been reported to induce apoptosis and accumulation and aggregation of amyloid
eventual outcome of cell death (through both apoptosis and necrosis, depending on concentration).
utation also results in muscle cell death by apoptosis and necrosis.
eractions, it has roles in the regulation of apoptosis and the suppression of poly(Q) toxicity.
differentiation, homeostasis, osteogenesis, apoptosis and many other functions.
tion of Thrombospondin-1 protein involved in apoptosis and angiogenesis.
therefore it is a useful tool in determining apoptosis and distinguishing between dead cells and li
ase play a key role in T cell proliferation, apoptosis and differentiation.
ecies (ROS), resulting in cell death through apoptosis and/or necrosis.
the cell cycle, cell growth, cell survival, apoptosis, angiogenesis and oncogenesis.
een shown to interact with POLR2C, SATB1 and Apoptosis antagonizing transcription factor.
ition of cell proliferation and induction of apoptosis are the likely mechanisms responsible for ma
its activation appears to drive neurons into apoptosis by initiating cell cycle reentry.
d no mechanism for the putative induction of apoptosis by fucoidan has been identified.
ses have found a way of countering defensive apoptosis by encoding their own anti-apoptosis genes p
This way, the cell can quickly undergo apoptosis by activating the protein that is already th
t to prevent infected cells from under-going apoptosis by down-regulating the genes ERCC1 and IER3.
e vesicle surface and into the cell, causing apoptosis by various pathways.
inhibition of angiogenesis and activation of apoptosis by the combination of natural and artificial
This receptor is capable of inducing apoptosis by a caspase-independent mechanism, and it i
During apoptosis, caspase 3 inhibits ICAD, thereby freeing CA
When cells are induced to undergo apoptosis, caspases-in particular caspase 3-cleave ICA
cells, and the regulation of transcription, apoptosis, cell division, and enucleation during eryth
Its re-expression induced apoptosis, cell cycle arrest and results in a mesenchy
It was however shown that apoptosis could be blocked by the caspase inhibitor (Z
Apoptosis DNA fragmentation is a natural fragmentation
XIAP is a member of the inhibitor of apoptosis family of proteins (IAP).
including cell division, cell proliferation, apoptosis, fertilization, development, behavior, learn
ore become a sensitive method to distinguish apoptosis from ischemic or toxic cell death.
atories are genetically modified to suppress apoptosis however maintain this phenomenon.
e responsible for the untimely initiation of apoptosis in myelocytes, producing their premature des
ingham suggests capsaicin is able to trigger apoptosis in human lung cancer cells as well.
It has been found to stimulate cell death ( apoptosis) in animal models of prostate and breast can
sosomal cystine appears to amplify and alter apoptosis in such a way that cells die inappropriately
n be treated by stimulating TNF-α to trigger apoptosis in autoimmune T cells.
sorption of the septum during the process of apoptosis in order to form the foramen secundum.
It has been found to induce apoptosis in HL60 leukemia cells in vitro at a concent
A23187 also induces apoptosis in some cells (e.g.
Apoptosis in lens epithelial cells (LEC) is linked to
tine reduced immune function and could cause apoptosis in the long term.
hen overexpressed, the mouse protein induced apoptosis in cell lines growing in vitro.
to be activated rapidly during Fas-mediated apoptosis in Jurkat cells.
attern was observed as a specific feature of apoptosis in 1978/1980 and became as a hallmark of pro
gy includes a high rate of cell division and apoptosis in malignant compared with a low rate of apo
wn that alpha-toxin plays a role in inducing apoptosis in certain human immune cells.
Hopwood, J.A., et al., Malaria-induced apoptosis in mosquito ovaries: a mechanism to control
den KH. (2001) Proliferation, cell cycle and apoptosis in cancer Nature 411: 342-348 (PMID 11357141
t evidence has shown that CTX III may induce apoptosis in K562 cells via the release of cytochrome
thiocyanate (PEITC) has been shown to induce apoptosis in certain cancer cell lines, and, in some c
Survival factors can suppress apoptosis in a transcription-independent manner by act
It is speculated that AFP may induce apoptosis in pre-malignant breast tissue cells which w
It is possible that the difference in apoptosis in vitro is connected to the degradation of
-34 suppression of SIRT1 ultimately leads to apoptosis in WT human colon cancer cells but not in hu
peutic agents that can differentially induce apoptosis in tumor cells and spare normal cells.
ll growth and induces chemosensitization and apoptosis, indicating that miR-34 may restore p53 func
It blocks β-cell apoptosis, induced by fatty acids (lipoapoptosis) in a
is thought to play an important role in the apoptosis induced by this receptor.
eukaryotic cells and in some viruses and an apoptosis inducer in HeLa cells.
e activated by tumor necrosis factor-related apoptosis inducing ligand (TNFSF10/TRAIL/APO-2L), and
s activated by tumor necrosis factor-related apoptosis inducing ligand (TNFSF10/TRAIL), and thus tr
Apoptosis is a form of cell death that is used by the
es, but the main cellular "switch" to induce apoptosis is the p53 protein.
Apoptosis is also encouraged by the blocking of apopto
Apoptosis is the process of normal cell death.
UVB-induced apoptosis is the programmed cell death of cells that b
Active cell suicide ( apoptosis) is induced by events such as growth factor
Cell suicide, or apoptosis, is the body's way of controlling cell death
mally, the balance between cell division and apoptosis is rigorously regulated to keep the integrit
ockout studies in mice suggest that blocking apoptosis is an essential function of this protein dur
Not only does the LTBR help trigger apoptosis, it can lead to the release of the cytokine
Through his studies of apoptosis, Korsmeyer helped develop the concepts of th
production of other proteins involved in the apoptosis mechanism, including proteins caspase-8 and
taining adaptor protein, is required for the apoptosis mediated by this protein.
Cell death ( apoptosis, necrosis)
ld only identify cells in the last phase of apoptosis.. New methods incorporate the dUTPs modified
s which are apoptotic (ie. in the process of apoptosis) no longer actively manage the distribution
I receptors, includes programmed cell death ( apoptosis) of the target tissue (the fetal mullerian d
te for the induction of growth arrest and/or apoptosis of myeloid precursor cells
nducing localised inflammation that leads to apoptosis of tumour cells as well as recruitment of th
The DNA damage leads to apoptosis of the affected cells.
PCGEM1 inhibits doxorubicin-induced apoptosis of cells, via delayed induction of p53 and p
on induces caspase-9 and caspase-3-dependent apoptosis of cultured human endothelial cells.
deacetylase enzymes, a mechanism leading to apoptosis of malignant cells via multiple pathways.
at it has anti-cancer potential as it causes apoptosis of murine lung-cancer cells.
nse response to oxidative stress, preventing apoptosis of the cell.
ous system, resulting in the protection from apoptosis or degradation of brain neurons.
s known in molecular and cellular biology as apoptosis or programmed cell death.
s cytokine assays, caspase assays to measure apoptosis, or reporter assays to measure a gene or a p
conditions, TNF-α causes T cells to undergo apoptosis, or programmed cell death.
31 does not cause arrest in cell cycle, cell apoptosis or caspase activation.
tive pathway, ultimately forcing a cell into apoptosis or necrosis.
The problem lies when one part of the apoptosis pathway is broken.
Examples of broken apoptosis pathways occur in many cancers.
BP), proteasome, and Drosophila inhibitor of apoptosis protein 1 (DIAP1).
f proteins, subnuclear location of proteins, apoptosis protein subcellular localization, submitocho
ct with the X chromosome-linked inhibitor of apoptosis protein, and this interaction enhances the a
d Omi/HtrA2 (which suppress the inhibitor of apoptosis proteins(IAPs)), among other proteins.
In contrast to apoptosis, pyroptosis requires the function of caspase
this process and causes the cell to undergo apoptosis quickly.
dominant mode of cell death turned out to be apoptosis rather than necrosis.
s the founding member of the Bcl-2 family of apoptosis regulator proteins encoded by the BCL2 gene.
gets of p53 that regulate the cell cycle and apoptosis, respectively.
continues to develop, frenulum cells undergo apoptosis, retracting away from the tip of the tongue,
hibition of the stress sensor enzyme MAP3K5 ( APOPTOSIS SIGNAL-REGULATING KINASE 1, ASK1).
In many tumor cells it causes selective apoptosis, sparing healthy cells.
ing of phosphatidyl serine followed by rapid apoptosis specifically in human lymphoma cells.
li1 include regulators of the cell cycle and apoptosis such as cyclin D2 and plakoglobin respective
effective inhibitation of cell division and apoptosis than curcumin.
troduce DNA breaks in the wires that lead to apoptosis, then inhibiting the catalytic activity of t
ut insert into the plasma membrane and cause apoptosis through influencing several signal pathways.
Its effects apoptosis through IRES mediated translation of the BAG
luteolin to inhibit angiogenesis, to induce apoptosis, to affect carcinogenesis in animal models,
h as glucose metabolism, cell proliferation, apoptosis, transcription and cell migration.
rgets tumor cells, leading to cell death and apoptosis via inhibition of thioredoxin reductase and
eus cell lysate resulted in the induction of apoptosis via the intrinsic death pathway.
Arsenic trioxide induced apoptosis was not enhanced by ascorbic acid in normal
hat the characteristic structural changes of apoptosis were present in cells that died in order to
e 3 (DAPK3) induces morphological changes in apoptosis when overexpressed in mammalian cells.
-repair, or inability of the cell to undergo apoptosis when it ought to have done so.
express androgen receptors, MDV3100 induced apoptosis whereas bicalutamide did not.
Overexpression of this protein induces apoptosis, which can be suppressed by co-expression of
ergo astrogliosis (proliferation followed by apoptosis), which may contribute to neurodysfunction.
ase is also involved in UV radiation-induced apoptosis, which is thought to be related to the cytoc
do not survive, and undergo caspases induced apoptosis, while other proteases participate in the de
CIAPIN1 is a cytokine-induced inhibitor of apoptosis with no relation to apoptosis regulatory mol
Their purpose is to induce apoptosis within virus-infected cells, thus destroying
cleave many of the chemicals responsible for apoptosis without the aid of caspase, as proven by exp