1 ssue architecture and extensive necrosis and apoptosis.
2 , hyperproliferative vascular cells after EC apoptosis.
3 l outer membrane permeabilization (MOMP) and apoptosis.
4 increased pStat3 or total Stat3, and induced apoptosis.
5 mphoma (CTCL) characterized by resistance to apoptosis.
6 arrested during the cell cycle or cleared by apoptosis.
7 hagic degradation of NBK/Bik, culminating in apoptosis.
8 in a significant increase of epithelial cell apoptosis.
9 size in dictating BAX activation, MOMP, and apoptosis.
10 n of ferroptosis, necrosis and AIF-dependent apoptosis.
11 ct cellular features that are different than apoptosis.
12 a high proliferative rate and resistance to apoptosis.
13 n by decreasing proliferation and increasing apoptosis.
14 BiP/GRP78, leading to ER stress, and induces apoptosis.
15 arget gene, suggesting a mechanism involving apoptosis.
16 e exons are linked to pathways of stress and apoptosis.
17 luding cellular survival, proliferation, and apoptosis.
18 evels, concurrent with complete loss through apoptosis.
19 nal kinase, inhibit proliferation and induce apoptosis.
20 nhibitory activities in different setting of apoptosis.
21 ion and exhibited abnormal proliferation and apoptosis.
22 is associated with cell and tissue-specific apoptosis.
23 resulting in end-stage maturation arrest and apoptosis.
24 and either cell cycle arrest or induction of apoptosis.
25 ction of intracellular K(+) that facilitates apoptosis.
26 strict regulation of cell proliferation and apoptosis.
27 ls in regulating cellular disassembly during apoptosis.
28 cell proliferation and migration and blocked apoptosis.
29 us, including those linked to interferon and apoptosis.
30 1beta and IFN-gamma contributes to beta-cell apoptosis.
31 promotes Bax-dependent but not Bak-dependent apoptosis.
32 ignaling proteins, which can lead to myocyte apoptosis.
33 g that ERbeta1 promotes EnR stress-regulated apoptosis.
34 tein IRE1alpha promotes either adaptation or apoptosis.
35 he cell to either resolve stress or initiate apoptosis.
36 ation of cell proliferation and induction of apoptosis.
37 by inhibiting inflammatory cascades and SMCs apoptosis.
38 duction by cells undergoing Bak/Bax-mediated apoptosis.
39 g cell cycle progression, but did not induce apoptosis.
40 invasion, proliferation, tumorigenesis, and apoptosis.
41 including maintenance of the cell cycle and apoptosis.
42 (UPR) is triggered, leading to adaptation or apoptosis.
43 omoted lethal RIPK1- and caspase-8-dependent apoptosis.
44 ile becoming less sensitive to CD95-mediated apoptosis.
45 r mitochondrial membrane and commit cells to apoptosis.
46 ayed greater sensitivity to DR4/DR5-mediated apoptosis.
47 thymocytes, and leads to RORgammat-dependent apoptosis.
48 CD28(null) T cells to regain sensitivity to apoptosis.
49 d causing most late spermatogonia to undergo apoptosis.
50 rising, concentration-dependent induction of apoptosis.
51 educed myocardial fibrosis, inflammation and apoptosis.
52 is able to inhibit mitochondrial fission and apoptosis.
53 multiple proteins and increased incidence of apoptosis.
54 ct of HBx activation of AKT is inhibition of apoptosis.
55 r-related apoptosis-inducing ligand-mediated apoptosis.
56 m that mediated proNT-dependent Schwann cell apoptosis.
57 7/T479 phosphorylation and elevated cellular apoptosis.
58 DKN1A and CDKN1B, G(1) cell cycle arrest and apoptosis.
59 g agents, and triggers cell-cycle arrest and apoptosis.
60 ovascular endothelial cell proliferation and apoptosis.
61 damage, misoriented divisions, and eventual apoptosis.
62 thal permeabilization process that initiates apoptosis.
63 4(+) T cells and protects the latter against apoptosis.
64 nscriptase and the latter may play a role in apoptosis.
65 regulation of UPR target genes and increased apoptosis.
66 , migration, viral endocytosis, survival, or apoptosis.
67 increases cell sensitivity to TRAIL-mediated apoptosis, acting as a key regulator of the cellular res
68 Recent studies show that apoptosis affects surrounding tissue, playing a role in
69 more, silencing of TCTP expression increased apoptosis and abrogated the hyperproliferative phenotype
70 ses that promote tumour suppression, such as apoptosis and autophagy, thus a clear understanding of t
71 hibition of USP15 may both induce tumor cell apoptosis and boost antitumor T cell responses.
72 Fingolimod significantly decreased edema, apoptosis and brain atrophy.
73 as well as downstream effectors that induce apoptosis and cell cycle arrest.
74 f Sp1 alone by RNA interference also induced apoptosis and decreased pancreatic cancer cell growth an
75 essel function per se, but induces increased apoptosis and decreased proliferation within perivascula
76 differential sensitivities to CD95-mediated apoptosis and DICE, and that killing of cancer cells can
77 However, while the apoptosis and differentiation markers remained unchanged
78 erized by increased proliferation, decreased apoptosis and elevated oestrogen receptor alpha (ERalpha
79 tumours, Ppp2r2d knockdown inhibited T-cell apoptosis and enhanced T-cell proliferation as well as c
80 related, we investigated UV-induced sunburn apoptosis and erythema in mouse skin as a function of ci
81 otein synthesis renders cells susceptible to apoptosis and functions to eliminate suboptimal germ cel
82 ar localization accompanied by resistance to apoptosis and induction of migration in both papillary a
83 have been shown to be signaling centers for apoptosis and inflammation.
84 NA-BGL3 sensitized leukemic cells to undergo apoptosis and inhibited Bcr-Abl-induced tumorigenesis.
85 ptor sensitized them to chemotherapy-induced apoptosis and inhibited their growth in vivo by augmenti
86 important role in degrading IRF3 to prevent apoptosis and interferon production during infection, th
87 dence that lumen expansion is independent of apoptosis and involves the cystic fibrosis transmembrane
88 ssor p53 is a central regulatory molecule of apoptosis and is commonly mutated in tumors.
89 Many novel ways of inhibiting apoptosis and necrosis, including blockage of the Fas re
90 on but also inhibits death of neutrophils by apoptosis and NETosis.
91 Both constitutive apoptosis and oxidative stress-induced apoptosis were po
92 trophil life span by inhibiting constitutive apoptosis and preventing apoptosis induced by exposure t
93 e to IL-7 mediated signalling, more prone to apoptosis and produce less IL-22 due to a defect in IL-2
94 ers of the placenta with an increase in both apoptosis and proliferation in the maternal decidua, a d
95 vIL-6 is able to prevent apoptosis and promote proinflammatory signaling, angioge
96 lpha-dependent pathways, of the induction of apoptosis and reduction of autophagy by SubAB.
97 inhibition reduces proliferation, increases apoptosis and remarkably, elicits the formation of multi
98 shown to have key roles in oncogene-induced apoptosis and senescence, but the mechanism regulating t
99 h CD4 and CD8 coreceptors, a balance between apoptosis and survival signals results in outcomes as di
100 o to limit caspase-8-dependent, TNFR-induced apoptosis, and animals lacking RIPK1, RIPK3, and TNFR1 s
101 feron-induced activation of innate immunity, apoptosis, and antigen presentation in the early phase o
102 ulation of genes related to innate immunity, apoptosis, and antigen processing/presentation in the ea
103 racterized differential monocyte activation, apoptosis, and apoptosis-related gene expression in low-
104 ased inflammation, organ damage, immune cell apoptosis, and bacterial load.
105 cell lines reduced their adhesion, increased apoptosis, and decreased production of phosphatidylinosi
106 ubiquitin-binding mice show increased liver apoptosis, and enlarged spleen and lymph nodes, respecti
107 species displayed rapid virus accumulation, apoptosis, and extensive cellular damage.
108 ation and colony-forming capability, induced apoptosis, and inhibited melanoma tumor growth in vivo.
109 notype of increased proliferation, decreased apoptosis, and metastatic potential by conservation of p
110 IL15RA established its role in cell growth, apoptosis, and migration, whereas expression of the IL15
111 viors, including migration, differentiation, apoptosis, and proliferation [1, 2].
112 in15+ epithelial progenitor cells, increased apoptosis, and reduced proliferation.
113 scent LSCs due to enhanced proliferation and apoptosis, and results in defective corneal differentiat
114 l-2 proteins leads to effective induction of apoptosis, and strongly support the concept that targeti
115 ha expression is associated with hippocampal apoptosis, and suggest that HIF-1alpha is an important f
116 ial for the manifestation of oxidant-induced apoptosis, and thereby reveal a potential new direction
117 gy was important for inhibition of host cell apoptosis, and this feature seemed to be a strain-indepe
118 ld type, the expression of differentiation-, apoptosis- and axon guidance-related genes was changed i
119 Proliferation and apoptosis are differentially altered in the layers of th
120 While chemotherapy effectively induces apoptosis, associated prostaglandin E2 (PGE2) release pa
121 cle response to DXR includes upregulation of apoptosis-associated markers, as well as substantial reo
122 macromolecular complex with an outer ring of apoptosis-associated speck-like protein containing a cas
123 Apoptosis-associated speck-like protein containing a cas
124 like 1 and inflammasome activation involving apoptosis-associated Speck-like protein containing a cas
125 e prosurvival molecules, preventing cellular apoptosis at a much lower (<5-fold) concentration.
126 arison of proliferation, differentiation and apoptosis between diploid and aneuploid hPSCs shows that
127 Apoptosis block also results in ectopic lineages suggest
128 ng both EsxA and EsxB also induced increased apoptosis but, remarkably, was unable to escape from cel
129 required for PV expansion and prevention of apoptosis, but little else is known about the role of th
130 In cancer, EMT suppresses apoptosis, but the mechanisms remain unclear.
131 duced p53 activation and resveratrol-induced apoptosis by direct targeting of G3BP1.
132 ne attack (beta-cell homicide) and beta-cell apoptosis by endoplasmic reticulum stress (beta-cell sui
133 After induction of apoptosis by H. pylori or camptothecin, there was a 5-fo
134 g that E. faecalis protects macrophages from apoptosis by inhibiting caspase 3 activation.
135 and reducing Bcl-2, but otherwise inhibiting apoptosis by reduction of caspase-3 and cytochrome c.
136 1 potently suppresses lung tumour growth via apoptosis by selectively activating Bax in vivo without
137 ARL), can suppress mitochondrial fission and apoptosis by targeting miR-539 and PHB2.
138 hts a common mechanism unveiling RHIM-driven apoptosis by therapeutic or genetic perturbation of RIP3
139 Cell apoptosis can cause hippocampal neuronal loss after epil
140 e suppression (PD-L1, NFKB1B, TNFAIP3, CGB), apoptosis (CASP9, FAS, IL-24), and cell growth and fibro
141 aling also protects cells from JNK-dependent apoptosis caused by epithelial disruption.
142 noid cultures sensitized them to TNF-induced apoptosis, confirming the in vivo observations.
143 in mice, we found that cells are lost due to apoptosis, consistent with increase in expression of cel
144 Differences in proliferation rates and apoptosis could be explained by defective signalling dow
145 ne expression to induce cell cycle arrest or apoptosis depending on the extent of DNA damage.
146 However, inhibiting apoptosis does not completely prevent retinal cell death
147 premature entry into (aborted) HF cycling by apoptosis-driven HF regression (catagen).
148 ells, uninfected CD4(+) T cells also undergo apoptosis due to ongoing toxic inflammation in the regio
149 ans, gastric epithelial cells (GECs) undergo apoptosis due to stimulation by the bacteria or inflamma
150 othesis that dying melanoma cells undergoing apoptosis during cytotoxic treatment activate paracrine
151 tion of Hh/Ptch1-regulated cell survival and apoptosis during embryogenesis.
152 <0.05) HIF-1alpha expression and hippocampal apoptosis during epileptogenesis in comparison with the
153 proliferation-effector genes, and when not, apoptosis effector genes have silenced chromatin structu
154 mining analyses that indicate that copies of apoptosis-effector genes are commonly lost in cancer dev
155 protein (PUMA, p53 upregulated modulator of apoptosis) folds to an alpha-helix when bound to a groov
156 Induction of cell-autonomous apoptosis following oncogene-induced overproliferation i
157 sis, whereas MafB/cJun heterodimers promoted apoptosis for sculpting the shape of the limbs.
158 t proximo-distal patterning, they succumb to apoptosis from embryonic day 9.75 onwards.
159 ll proliferation and survival and inhibiting apoptosis, GRP78 may promote the pulmonary microvascular
160 on of survivin, a member of the inhibitor of apoptosis (IAP) family.
161 ays of interest, including stress responses, apoptosis, immunity, and protein trafficking.
162 lts in irreversible oxidative DNA damage and apoptosis, impairing skeletal muscle development.
163 OXA protected cells from combination-induced apoptosis, implicating the role of NOXA in the drug syne
164 rther identified to be due to TIPE1-inducing apoptosis in a caspase-independent, necrostatin-1 (Nec-1
165 owth in vivo and induced variable degrees of apoptosis in a panel of melanoma cells.
166 Although imatinib induces apoptosis in a subset of gastrointestinal stromal tumor
167 tored sensitivity of adrenocortical cells to apoptosis in AdKO but not in wild-type mice.
168 tein Bax by itself is sufficient to initiate apoptosis in almost all apoptotic paradigms.
169 epithelium in mice and inhibits Leydig cell apoptosis in both adult mice and patients with CAIS, pos
170 stress response and provides protection from apoptosis in both hippocampal neurons in vitro and in an
171 ) or treatment with ERbeta agonists enhanced apoptosis in breast cancer cells in the presence of phar
172 s5 lincRNA interaction, altering Gas5-driven apoptosis in cancer cell lines.
173 f utility in the promotion of E2F1-dependent apoptosis in cancer cells, in avoiding metastatic pathwa
174 synthase kinase 3 (GSK3) causes synergistic apoptosis in CTCL cell lines and patient cells.
175 BINDI induces apoptosis in EBV-infected cancer lines, and when deliver
176 , such as hair follicles, and causes massive apoptosis in hair matrix keratinocytes followed by hair
177 IFN) play an important role in memory B cell apoptosis in HIV infection.
178 The latter leads to cytochrome c release and apoptosis in human lung cancer cells, which occurs in a
179 s, demonstrating selective ability to induce apoptosis in macrophages.
180 th the activation of ER stress, the UPR, and apoptosis in OSCC cells.
181 HED transplantation induces activated T-cell apoptosis in OVX mice via Fas ligand (FasL)-mediated Fas
182 oliferation in glomerular tuft and increased apoptosis in perivascular mesenchyme were observed in Tb
183 Depletion of Fezf2 induces apoptosis in postmitotic neural progenitors, with concom
184 Jun N-terminal kinase (JNK) often mediates apoptosis in response to cellular stress.
185 erexpression of Ash2L enhanced P53-dependent apoptosis in response to chemotherapy, associated with i
186 All three genes inhibited p53-mediated apoptosis in response to Nutlin-3 treatment in non-infec
187 iated with telomeric DNA damage response and apoptosis in stem cells and basal cells.
188 te that these stem-like chondrocytes undergo apoptosis in the absence of the receptor (PPR) for parat
189 emonstrate that dMyc-induced cell-autonomous apoptosis in the fruit fly Drosophila melanogaster relie
190 a decrease in proliferation and increase in apoptosis in the labyrinth layer and both unchanged in t
191 cords of ActB-deficient Inhbb(-/-) embryos, apoptosis in the oligodendrocyte lineage is increased an
192 endogenous RET protein levels and increased apoptosis in these cells.
193 low YAP1 levels prevent nuclear ABL1-induced apoptosis in these hematologic malignancies.
194 that could inhibit proliferation and induce apoptosis in TKI-resistant lines.
195 of transplanted tumors, probably by inducing apoptosis in tumors.
196 tutive and oxidative stress-induced monocyte apoptosis in uninfected and HIV(+) individuals across a
197 and sensitizes the epidermis to UVB-induced apoptosis in vivo, while heterozygous SIRT1 deletion has
198 epair proteins NBN and MRE11A, regulators of apoptosis, including BIRC6, and the proteasome.
199 e one hand activating the initial cascade of apoptosis, increasing Bax and reducing Bcl-2, but otherw
200 kinase-dead D161N mutant induces spontaneous apoptosis independent of compound, whereas D161G, D143N,
201 rdiomyocyte maturation by activating a novel apoptosis-independent function of Caspases.
202 wever, the molecular mechanism(s) underlying apoptosis induced by Cdc20 abrogation remains poorly und
203 Hair follicle apoptosis induced by DXR was significantly inhibited by
204 f the ERbeta1-expressing cells prevented the apoptosis induced by EnR stress but not by non-EnR stres
205 biting constitutive apoptosis and preventing apoptosis induced by exposure to live B. pertussis.
206 in DG75 B-lymphoma cells protects cells from apoptosis induced by oxidative or genotoxic stress by st
207 titutively active Rac1 partially rescued the apoptosis induced by TIPE1, and Rac1 knockdown significa
208 endent apoptotic pathway associated with the apoptosis-inducing factor.
209 crosis factor alpha (TNF-alpha), TNF-related apoptosis-inducing ligand (TRAIL), and interleukin-6 (IL
210 h" facilitates tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis.
211 We then linked z13 with an apoptosis-inducing peptide and with an endosome-escaping
212 transcriptional network and contributing to apoptosis induction by DNA damage.
213 se to replication stress, a major pathway of apoptosis induction by many chemotherapeutic agents.
214 CD28(null) T cells in ACS were resistant to apoptosis induction via Fas-ligation or ceramide.
215 us IkappaBalpha mutants, we demonstrate that apoptosis inhibition and NF-kappaB inhibition can be fun
216 3)-linked polyubiquitination mediated by the apoptosis inhibitor cIAP2 that was enhanced by the bioac
217 Cytochrome c (Cyt c) is an apoptosis-initiating protein when released into the cyto
218 and current models propose that induction of apoptosis is a key p53 tumor suppressive function.
219 demonstrate that TolC-mediated inhibition of apoptosis is an active process and not due to defects in
220 Evasion of apoptosis is critical in Myc-induced tumor progression.
221 Apoptosis is generally considered the main pathway by wh
222 metabolism, muscle cell atrophy, and myocyte apoptosis is increasingly clear.
223 effect of K13 against death receptor-induced apoptosis is not clear.
224 Neuronal apoptosis is one of the major causes of poststroke neuro
225 e how complex cellular susceptibility toward apoptosis is regulated in a developing organ.
226 going DNA damage and the mechanisms by which apoptosis is suppressed are largely unknown.
227 These precursor cells commit to apoptosis-like death under the toxic conditions.
228 is initiated by the calcium-binding protein-apoptosis-linked gene (ALG)-2.
229 lasmic reticulum (ER) stress and cancer cell apoptosis mediated through C/EBP homologous protein (CHO
230 fundamental carcinogenic processes including apoptosis, mitogen-activated protein kinase signalling a
231 P include the control of cell proliferation, apoptosis, movement and fate.
232 However, Skp2 deletion induced apoptosis, not proliferation arrest, in Rb1-deficient pi
233 ly associated with CD4, with an elevation in apoptosis occurring in patients with more than 40,000 (4
234 d the Hippo pathway in the proliferation and apoptosis of a murine hemangioendothelioma (EOMA) cell.
235 one marrow of adult mice resulted in massive apoptosis of all hematopoietic cell types.
236 rate that targeting ATase1/ATase2 results in apoptosis of CD133 expressing acute lymphoblastic leukem
237 fects of HIV and lipopolysaccharide (LPS) on apoptosis of CD27+ IgD- memory B (mB) cells from healthy
238 totic and neurotrophic molecules and reduced apoptosis of cortical neurons following injury.
239 Because apoptosis of infected cells can limit virus production a
240 of enterocyte apicobasal polarity, increased apoptosis of intestinal cells, decreased proliferation o
241 apid, and cost-effective method for inducing apoptosis of primary normal human dermal fibroblasts wit
242 The macrophages infiltration and apoptosis of smooth muscle cells (SMCs) were examined im
243 ress and promotes mitochondrial division and apoptosis of the cell.
244 a significant decrease in proliferation and apoptosis of tubular epithelial cells.
245 This increased resistance to apoptosis of virus-specific CD8+ T cells in nonlymphoid
246 AnkG inhibits pathogen-induced apoptosis, possibly by binding to the host cell mitochon
247 While HIV induces apoptosis (programmed cell death) by directly entering a
248 Apoptosis, programmed necrosis, and pyroptosis each serv
249 we demonstrate that the X-linked inhibitory apoptosis protein (XIAP) associates with the C terminus
250 The X-linked inhibitor of apoptosis protein (XIAP) is a potent caspase inhibitor,
251 iremic HIV-1 patients, suggesting a shift in apoptosis regulation that may be associated with disease
252 optosis through regulating the expression of apoptosis related pathways.
253 erential monocyte activation, apoptosis, and apoptosis-related gene expression in low- versus high-le
254 Here we report that a lncRNA, named cardiac apoptosis-related lncRNA (CARL), can suppress mitochondr
255 characterized by increased proliferation and apoptosis resistance of pulmonary artery smooth muscle c
256 ures of cancer including cancer cell growth, apoptosis resistance, DNA damage response, metastasis, i
257 rtical cells and its possible involvement in apoptosis resistance.
258 omote migration, invasion, metastization and apoptosis resistance.
259 ment the pre-existing therapies to eliminate apoptosis-resistant cancer stem cells by necrosis.
260 tissues along with preferential migration of apoptosis-resistant CD8+ T cells into peripheral sites a
261 Furthermore, apoptosis-resistant CD8+ T cells preferentially migrated
262 that TCTP may be a link in the emergence of apoptosis-resistant, hyperproliferative vascular cells a
263 Understanding monocyte apoptosis response may inform HIV immunopathogenesis, re
264 Senescence or apoptosis result, forming a barrier against tumour progr
265 n of the mechanisms by which eEF2K regulates apoptosis shows that eEF2K senses oxidative stress and q
266 ent activation of intestinal epithelial cell apoptosis signaling and progressive monolayer destructio
267 Studies have shown a relationship between apoptosis signaling pathways and psychiatric disorders,
268 Here, we identify apoptosis-stimulating protein of p53 with signature sequ
269 n important role for APC(Cdc20) in governing apoptosis, strengthening the rationale for developing sp
270 ting that other factors were determinants of apoptosis, such as downregulation of antiapoptotic prote
271 that Treg cells were much more resistant to apoptosis than CD44hi CD8 and CD4 T cells at days 2 to 3
272 ible to endoplasmic reticulum stress-induced apoptosis than control cells.
273 he nonlymphoid tissues are more resistant to apoptosis than those in lymphoid organs during the resol
274 ty, which results in increased resistance to apoptosis that contributes to the tumorigenic process.
275 e report that unmitigated ER stress promoted apoptosis through cell-autonomous, UPR-controlled activa
276 ancer activity exhibited as the induction of apoptosis through p53 activation.
277 TLs contributed to KBD excessive chondrocyte apoptosis through regulating the expression of apoptosis
278 Inhibition of FGFR3 increased target cell apoptosis through the suppression of Bcl-xL expression,
279 erial pathogens frequently inhibit host cell apoptosis to ensure survival of their host, thereby allo
280 n of phospho-gammaH2AX and p53, and elevated apoptosis together with reduced cell proliferation.
281 aused by pathogenic autoreactive T-cells and apoptosis triggered by endoplasmic reticulum stress.
282 These cells then either undergo apoptosis triggered by the intrinsic mitochondrial pathw
283 ggers cell-cycle checkpoints, DNA repair and apoptosis using multiple post-translational modification
284 In summary, SHED-mediated T-cell apoptosis via a FasL/Fas pathway results in immune toler
285 se of cytochrome c from the mitochondria and apoptosis via caspase activation.
286 nly proteins termed sensitizers can initiate apoptosis via this mechanism in response to diverse sign
287 Apoptosis was caspase dependent and associated with G1 c
288 Apoptosis was dependent on BIM in some but not all cell
289 naling on activation of the mTOR pathway and apoptosis was measured in a mouse model of PPNAD (AdKO m
290 nd in ovarian cancer ascites, AMG655-induced apoptosis was not enabled to any significant degree, ind
291 en the HIF-1alpha expression and hippocampal apoptosis were investigated by histological confirmation
292 Both CDKN1A accumulation and apoptosis were partially dependent on activation of the
293 utive apoptosis and oxidative stress-induced apoptosis were positively associated with viral load and
294 d K51A mutants, like wild-type, only trigger apoptosis when compound is present.
295 Balpha(-/-) cells also become protected from apoptosis when IkappaBalpha is specifically reconstitute
296 b buds, and MafB/cFos heterodimers repressed apoptosis, whereas MafB/cJun heterodimers promoted apopt
297 progressive islet dysfunction, and beta-cell apoptosis, which interact variably to cause the differen
298 that activates Bax and induces Bax-dependent apoptosis, which may lead to the development of new ther
299 opic expression of SOX30 induces cancer cell apoptosis with inhibiting proliferation in vitro and rep
300 During apoptosis, XIAP is antagonized by SMAC, which is release
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