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1. |
Studies create an important conclusion that PUMA promotes Bax translocation both by directly interacting with Bax and by competitive binding to Bcl-X(L) in UV-induced apoptosis. |
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2. |
Results suggest that an increased transcription of pro-apoptotic genes (p53 and Bcl-x(S)) in eutopic endometrium is significantly associated with endometriosis, which indicates dysregulation of apoptotic gene transcription associated with disease. |
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3. |
Na+/H+ exchanger mediates TNF-alpha-induced hepatocyte apoptosis via the calpain-dependent degradation of Bcl-xL. |
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4. |
hnRNP K has a role in preventing the production of the pro-apoptotic Bcl-x(S) splice isoform |
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5. |
Inhibition of host gene expression by the VSV M protein resulted in the degradation of Mcl-1 but not Bcl-X(L); inactivation of both Mcl-1 and Bcl-X(L) was required for cells to undergo apoptosis |
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6. |
Results demonstrated that the inhibition of spontaneous B cell apoptosis by CpG DNA was correlated to up-regulation of Bcl-xL, IAP and down-regulation of p53 and caspase 3 mediated through PI3K/AKT signaling. |
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7. |
Characterization of binding thermodynamics reveals that the interaction of BID with BCL-XL is driven by enthalpy but disfavored by the entropy associated with the conformational order induced in BID upon binding BCL-XL. |
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8. |
Data show that TGF-beta1 correlated with Bcl-xL and Bax in all colorectal cancers. |
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9. |
DAPk phosphorylates Beclin 1 on T119, a critical residue within its BH3 domain, and thus promotes Beclin 1 dissociation from Bcl-X(L) and autophagy induction. |
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10. |
Vacuolar H+-ATPase inhibitors overcome Bcl-X-mediated chemoresistance through restroration of a caspase-independent apoptotic pathway. |
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11. |
bcl-xL, through its antiapoptotic effect, might contribute to tumor cell survival in primary cutaneous follicule center lymphomas |
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12. |
Data show that DAPK phosphorylates beclin 1 on Thr 119 located at a crucial position within its BH3 domain, and thus promotes the dissociation of beclin 1 from Bcl-XL and the induction of autophagy. |
|
13. |
Nucleotide excision repair may protect against cisplatin-induced apoptosis by activating NF-kappaB, which further induces transcription & accumulation of BCL-XL, and activation of the cell survival pathway. |
|
14. |
up-regulation of BCL-XL and BCL2A1 induces approximately 1000-fold resistance to ABT-737 in chronic lymphocytic leukemia. |
|
15. |
HIF-1alpha-dependent BCL-xL overexpression may be an important mechanism by which HIF-1alpha protects prostate cancer cells from apoptosis and leads to treatment resistance |
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16. |
expression of Bcl-XL protein was decreased by proteasome-mediated degradation prior to change of mRNA level in UVB-induced apoptotic basal cell carcinoma cell lines |
|
17. |
two lesions differed significantly in expression of Bcl-xL which was present in 84% of the squamous cell carcinoma compared with only 15% in the keratoacanthoma |
|
18. |
These results suggest that Bim, Bcl-xL, FAK and endonuclease G are involved in safingol-induced apoptosis of detached oral squamous cell carcinoma. |
|
19. |
Beclin-1/Bcl-xl complexes in cells is decreased by increased expression of ARF, thereby providing a basis for ARF-induced autophagy |
|
20. |
C/EBPbeta regulates bcl-xl gene expression in human breast cancer cells in response to cigarette smoke condensate treatment |
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21. |
Clinical trial of gene-disease association, gene-environment interaction, and pharmacogenomic / toxicogenomic. (HuGE Navigator) |
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22. |
Bcl-xL phosphorylation induced by microtubule inhibitors plays a key pro-apoptotic role at least in part by disabling the ability of Bcl-xL to bind Bax. |
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23. |
Bcl-2 and bcl-xL have roles in cell death rates in transitional cell carcinoma cell lines |
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24. |
BCL2 and BCL-xL facilitation of G0 quiescence requires BAX, BAK, and p27 phosphorylation by Mirk |
|
25. |
JAK2 promotes cell survival by signaling through the Pim/BAD/BCL-xL pathway |
|
26. |
These observations suggest that Plk1 is a regulator of Bcl-x(L) phosphorylation and controls the anti-apoptotic activity of Bcl-x(L) during pironetin-induced apoptosis. |
|
27. |
Results show that 072RB, a novel BH3-Bim-derived peptide inhibitor of Bcl-XL, inhibits leukemic cell growth. |
|
28. |
Therefore, over-expression of Bcl-x(L) has a potential for amelioration of SMA, and Bcl-x(L) may be another attractive therapeutic target other than survival motor neuron (SMN) protein for use in future drug screening for SMA. |
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29. |
Results indicate that HBSP interacts with Bcl-2/Bcl-xl in vitro and induces apoptosis in HepG2 cells. |
|
30. |
our results demonstrate the role of NF-kB as the mediator of bcl-xL-induced CXCL8 up-regulation in glioblastoma cells. |
|
31. |
IL-3 up-regulates the expression of the antiapoptotic proteins cIAP2, Mcl-1, and Bcl-X(L) and induces a rapid and sustained de novo expression of the serine/threonine kinase Pim1 that closely correlates with cytokine-enhanced survival. |
|
32. |
Bcl-x(L) and, to a lower extent, Mcl-1, are important anti-apoptotic factors in colorectal carcinoma. |
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33. |
Expressed in most dysmorphic neurons in focal cortical dysplasia type II. |
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34. |
VEGF, hTERT and Bcl-xl have roles in laryngeal squamous carcinoma |
|
35. |
preoperative chemoradiotherapy (CRT) reduced Bcl-X(L) expression, and this decrease closely correlated with the prolonged survival of advanced esophageal cancer patients treated with preoperative CRT |
|
36. |
Data show that the worm protein EGL-1 binds mammalian pro-survival proteins very poorly, but can be converted into a high-affinity ligand for Bcl-2 and Bcl-x(L) by mutation of the cysteine residue at position 62 within the BH3 domain. |
|
37. |
the anti-apoptotic protein Bcl-xL is phosphorylated by benzylisothiocyanate treatment |
|
38. |
Bcl-Xl deamidation and methylation has a role in protein isoaspartate methyltransferase prevention of apoptosis induced by oxidative stress in endothelial cells |
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39. |
Bcl-xL and UVRAG cause a monomer-dimer switch in Beclin1 |
|
40. |
the present study is the first report of a negative prognostic value for Bcl-XL in bilharzial squamous cell carcinoma of the urinary bladder |
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41. |
SRp30c stimulates splicing to the downstream 5' splice site of Bcl-x(L), thereby attenuating the repressive effect of upstream U1 snRNP binding sit |
|
42. |
BCL-xL is itself responsible for the pre-senescence decline in the ability of a genotoxic stress to induce apoptosis |
|
43. |
Bcl-xL protein levels were significantly higher in tissue samples from nonemphysematous smokers than in those from nonemphysematous nonsmokers |
|
44. |
Bcl-xL plays an important role in carcinogenesis of human colorectal carcinoma and is associated with malignant biological behaviors of human colorectal carcinoma. |
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45. |
insulin-like growth factor 2 differentially regulated the intracellular translocation of Bcl-X(L) |
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46. |
Show that Bcl-XL was down-regulated and Bcl-XS was up-regulated in topotecan-induced apoptosis in HepG2 cells. |
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47. |
IGF1 promotes resistance to apoptosis in melanoma cells through an increased expression of BCL2, BCL-X(L), and survivin |
|
48. |
BI-1 and Bcl-X(L) operate downstream of or parallel to Bax/Bak |
|
49. |
while bcl-2 proteins are not required for ceramide to form protein-permeable channels in mitochondrial outer membranes, both recombinant human Bcl-x(L) and CED-9 disassemble ceramide channels in the mitochondrial outer membranes from rat liver and yeast |
|
50. |
overexpression of Bcl-xL led to decreased cellular proliferation |
|
51. |
Bcl-x was associated with increased survival in thymic neoplasms. Bcl-x:Bax ratio was also associated with survival. |
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52. |
androgen stimulates Bcl-xL expression via the androgen receptor and that increased Bcl-xL expression plays a versatile role in castration-resistant progression of prostate cancer |
|
53. |
The Bcl-X(L) chimeras that are targeted to the mitochondria and the wild type Bcl-X(L) provided same protection against cell death under several death inducing conditions. |
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54. |
Observational study of gene-disease association. (HuGE Navigator) |
|
55. |
Shp2E76K induces cytokine-independent survival of TF-1 cells by a novel mechanism involving up-regulation of Bcl-XL through the Erk1/2 pathway. |
|
56. |
results indicate an action of Bcl-X(L) modulating human neural stem cell differentiation |
|
57. |
activation of HSF1 and stabilization of Bcl-X(L) mediate a protective response that may contribute significantly to the cellular biology of lipid peroxidation |
|
58. |
a caspase-9 signaling cascade induces feedback disruption of the mitochondrion through cleavage of anti-apoptotic Bcl-2, Bcl-xL, and Mcl-1 |
|
59. |
The protein kinase C (PKC) inhibitor and apoptotic inducer staurosporine switches the production of Bcl-x towards the x(S) mRNA isoform in 293 cells. |
|
60. |
low dose doxorubicin-induced cell death through mitotic catastrophe may provide an alternative therapeutic strategy for Bcl-xL-overexpressing hepatoma cells |
|
61. |
We conclude that alteration in the expression of proapoptotic (Bax, Bak) and antiapoptotic (Bcl-2, Bcl-XL) proteins on surface of thyroid follicular cells may play a role in the pathogenesis of thyroid autoimmune disorders. |
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62. |
Bcl-X(L) conferred complete resistance to apoptosis induced by fas ligation in atherosclerotic carotid artery. |
|
63. |
The structure of Bcl-xL in complex with the Beclin-1 BH3 domain was determined at high resolution by NMR spectroscopy. |
|
64. |
our results support the feasibility of using adenovirus-mediated RNA interference therapy targeting Bcl-XL against colon cancers and warrant further studies of its safety and efficacy. |
|
65. |
Bcl-x(L) interacts with the DNA binding site of p53, but Bak does not interact with this site |
|
66. |
xL is coupled to the stabilization of a cell-cycle checkpoint induced by DNA damage, and this effect is genetically distinct from its function on apoptosis |
|
67. |
Data show that stimulation of PAR1 results in increased DNA binding of the NFkappaB p65 subunit, and that activation of PAR1 attenuates docetaxel induced apoptosis through the upregulation of Bcl-xL. |
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68. |
Bcl-x(L) plays an important role in human RPE cell survival under normal conditions and when cells are exposed to oxidative stress |
|
69. |
preformed Bim(EL)/Mcl-1 and Bim(EL)/Bcl-x(L) complexes can be rapidly dissociated following activation of ERK1/2 by survival factors |
|
70. |
Following UV treatment, Mcl-1 protein synthesis is blocked, the existing pool of Mcl-1 protein is rapidly degraded by the proteasome, and cytosolic Bcl-xL translocates to the mitochondria |
|
71. |
CD28-stimulated T cells actively secrete IL-8, and Bcl-xL up-regulation protects T cells from radiation-induced apoptosis |
|
72. |
Bcl-xL may have a role in underexpression of transcriptional regulators in metastatic breast cancer |
|
73. |
overexpression of the Bcl-2 or Bcl-x(L) associated with the loss of apoptosis in breast cancer cells in vivo may account for their metastatic behavior |
|
74. |
bcl-xL gene overexpression is linked to short overall survival times in follicular lymphoma. |
|
75. |
Infection with OmpA+ E. coli induces the expression of Bcl(XL), an antiapoptotic protein, both at the mRNA level as assessed by gene array analysis and at the protein level |
|
76. |
During endothelial cell apoptosis, Bcl-xl level showed no significant in HUVECs stimulated with TNF-alpha alone or in combination with IFN-gamma. |
|
77. |
Data show that Bcl-x(L) expression is increased in the pulmonary artery undergoing chronic pulmonary vascular remodeling. |
|
78. |
Bcl-XL siRNA contributes to an increase of cisplatin-induced cell death in non-small-cell lung cancer and sensitizes cells to cisplatin |
|
79. |
retinoic acid-induced apoptotic signals were transduced via downregulation of Bcl-xL and the decrease in the mitochondrial membrane function leading to caspase-3 activation |
|
80. |
gene expression level of beta-TUB, Bcl-XL, and GSTpi was closely correlated with the IC50 for docetaxel |
|
81. |
role in inhibiting diamide-induced SM hydrolysis and ceramide accumulation but not the decrease in intracellular GSH |
|
82. |
Bcl-x(L)-anti-apoptotic signal pathway seems to prevent mitochondrial multiple conductance channel opening, cytochrome c release and caspase-3 like activity following 6-OHDA treatment in the human neuroblastoma cell line SH-SY5Y |
|
83. |
Jak-Stat and PI 3-kinase activation pathways regulate the TPO-induced survival of megakaryocytic cells via Bcl-xL gene expression. |
|
84. |
Bcl-XL was higher in plaques than in normal white and gray matter in multiple sclerosis |
|
85. |
Pim phosphorylation of Bad was also found to promote the 14-3-3 binding of Bad and block its association with Bcl-XL |
|
86. |
Data suggest that Bcl-xl has a biochemical function that is capable of partially rescuing loss of function mutations in S. cerevisiae. |
|
87. |
findings indicate that the levels of XIAP and Bcl-X(L) are regulated by distinct pathways during monocytic differentiation, and that upregulation of these proteins contributes to the increased longevity of cells in the monocytic lineage |
|
88. |
the role of Bcl-x(L) in apoptosis in cardiomyocytes and discuss the potential use of Bcl-x(L) as a cardioprotective therapy for cardiac diseases. |
|
89. |
role in sequestering proapoptotic Bak |
|
90. |
A novel molecular mechanism of T-cell apoptosis that contributes to the SARS-CoV-induced lymphopenia observed in most SARS patients is reported. |
|
91. |
p21-mediated cytoprotection against hyperoxia involves regulation of Bcl-XL and is uncoupled from its ability to inhibit proliferation |
|
92. |
Bcl-XL is approximately ten times more active than Bcl-2 in repressing apoptosis induced by doxorubicin. |
|
93. |
the conformation of the BAX alpha9-helix plays a significant role in BAX/BCL-xL interaction |
|
94. |
Bcl-XL expression is induced by HIV-1 Nef in macrophages in an extracellular signal-regulated kinase-dependent manner |
|
95. |
bcl-xl-mediated changes in metabolic pathways of breast cancer cells were studied from survival in the blood stream to organ-specific metastasis. |
|
96. |
Bcl-xL is deamidated in the cellular response to DNA damage and leads to apoptosis resistance |
|
97. |
Bcl-x(L) is a key target mediating the anti-apoptotic effects of glucocorticoids during fibrosarcoma development |
|
98. |
selective expression of Bcl-xL may be involved in the difference in the susceptibility to cell death between immature dendritic cells and mature dendritic cells . |
|
99. |
Rapamycin induces apoptosis of tumor cells by increasing the ratio of Bax to Bcl-xL through mechanisms dependent and independent of its mTOR inhibitory activity |
|
100. |
these data suggest the solution to membrane conformational change is controlled by an electrostatic mechanism |
|
101. |
data demonstrate that OX40 and Bcl-x(L) can control survival of primed CD8 T cells and provide new insights into both regulation of CD8 immunity and control of tumors |
|
102. |
catalase has a critical role in CSF-independent survival of human macrophages via regulation of the expression of BCL-2 and BCL-XL |
|
103. |
Significant coexpression of GLUT-1, Bcl-xL, and Bax points to cooperation of all three regulatory proteins in elimination due to irreversible injury, adaptation to hypoxia, reduction of further damage, and survival of colorectal cancer cells. |
|
104. |
Bcl-XL protects BimEL-induced Bax conformational change and cytochrome C release. |
|
105. |
Natural cytotoxic T cell-defined reactivity is detected against Bcl-xL in peripheral blood leukocytes from patients with breat cancer and melanoma. |
|
106. |
Bcl-2 may not play a physiological role in antagonizing apoptosis signals pertinent to BAD activation in prostate cancer cells |
|
107. |
Overexpression of bcl-2 and bcl-xL leading to prolonged survival of mast cells may contribute to the pathogenesis of mastocytosis. |
|
108. |
Bcl-xL in hepatocellular carcinoma specimens. Bcl-xL may be significant prognostic factor for disease progression in human hepatocellular carcinoma. |
|
109. |
T cell blasts surviving activation-induced cell deathare memory CD44 high cells with increased Bcl-xL expression. |
|
110. |
hnRNP F/H proteins have a positive role in the production of the proapoptotic regulator Bcl-x(S) |
|
111. |
In addition, B cell lymphoma leukemia (Bcl)-x(L), an antiapoptotic regulator, was also highly expressed in macrophages from smokers compared with nonsmokers and subjects with asthma. |
|
112. |
Overexpressed Bcl-xL reduced time-dependent increase of apoptosis induced by ionizing radiation.ROS generation and Bax expression were also lower.These results provide insights into a new strategy for gene therapy of radiation-induced immune injury. |
|
113. |
Bcl-xL prevents TRAIL-induced apoptosis by abrogating caspase activation and cleavage of BH3 interacting domain death agonist protein in acute myelogenous leukemia HL-60 cells. |
|
114. |
Overexpression of bcl-xl is associated with colonic neoplasms |
|
115. |
c-erb-B2 and Bcl-xl expression can be useful for the histopatologic diagnosis of Barrett exophagux and correct interpretation of dysplasia. |
|
116. |
There may be a dominance expression of proapoptotic proteins in optic nerve axons in glaucoma. |
|
117. |
Bcl-X(L) may regulate Bax translocation through modulation of protein phosphatase or kinase signaling. |
|
118. |
treatment with an antisense oligonucleotide (5'Bcl-x AS) shifts the splicing pattern of Bcl-x pre-mRNA from the anti-apoptotic variant, Bcl-xL, to the pro-apoptotic variant, Bcl-xS |
|
119. |
a novel role in cell fate decisions /during hematopoietic differentiation/ beyond cell survival |
|
120. |
Bcl-XL has a role in suppressing proliferation of 5-fluorouracil-resistant human colon cancer cells |
|
121. |
Bcl-xl has a role in suppressing a p53 and Bax-dependent apoptotic pathway in colorectal cancer cells |
|
122. |
Human Bcl-xL is deamidated at asparagines 52 and 66 & the rate of deamidation is significantly lower in hepatocellular carcinomas than in normal liver. Tumor cells may gain apoptosis resistance & a survival advantage by suppressing Bcl-xL deamidation. |
|
123. |
Mature dendritic cells are protected from Fas/CD95-mediated apoptosis by upregulation of Bcl-X(L). |
|
124. |
Reduced levels of Bcl-xL may play an important role in the increased sensitivity to apoptosis of HIV-specific CD8+ T cells. |
|
125. |
HER-2 overexpression is highly correlated with the expression of the apoptosis-suppressing gene bck-xL. |
|
126. |
Role of bcl-xl protein on indomethacin-induced cell division inhibition in chronic myelogenous leukemia cells. |
|
127. |
Significant correlation between Bcl-x(L) expression and number of inflammatory cells in subsynovium of rheumatoid arthritis and osteoarthritis patients. May play role in extended survival of synoviocytes and inflammatory cells in rheumatoid synovium. |
|
128. |
the interaction of BAD with membranes is tied to binding of 14-3-3 protein and activation and membrane translocation of Bcl-XL |
|
129. |
Downregulation of Bcl-xL (but not Bcl-2, Bax, or Bid) connects cathepsin D and the mitochondrial pathway during glucosamine sulfate-induced apoptosis. |
|
130. |
Bcl-xL can bind to one or two VDAC1 molecules forming heterodimers and heterotrimers. |
|
131. |
Bcl-xl over-expression does not confer protection against cell death in U937 cells. |
|
132. |
Overexpression of antiapoptotic proteins Bcl-2 and Bcl-X(L) and down-regulation of caspase-3 activity may be associated with cisplatin resistance in human ovarian cancer. |
|
133. |
ligand engagement of uPAR promotes cell survival by activating Bcl-xL transcription through the MEK/ERK- and phosphatidylinositol 3-kinase/Akt-dependent pathways |
|
134. |
dissociation of Bad from Bcl-xL and an increase in the intracellular level of Bcl-xL are responsible for development of acquired TRAIL resistance |
|
135. |
Antiapoptotic proteins Bcl-2 and Bcl-X(L) bind and suppress NALP1, reducing caspase-1 activation and interleukin-1beta (IL-1beta) production. |
|
136. |
We speculate that the TM1 helices of Bax may serve as 'structural antagonists' for BH3-Bcl-xL interactions. |
|
137. |
Bcl-xL inhibits p53- but not apoptin-induced apoptosis in head and neck neoplasms |
|
138. |
androgen receptor silencing has a role in apoptotic cell death by disrupting the Bcl-xL-mediated survival signal in human prostate cancer cell lines |
|
139. |
regulation of alternative splicing in lung adenocarcinoma cells by de novo ceramide |
|
140. |
Therefore, Bcl-X(L), a promising therapeutic candidate for ischemia and neurodegenerative diseases, is only of partial efficacy in preventing the direct neurotoxicity of pneumolysin. |
|
141. |
Expression of Cx26, Bax and Bcl-xL in colorectal cancers. Association of Cx26, Bax and Bcl-xLwith histological G2 grade of tumors. |
|
142. |
Antisense strategy shows that Mcl-1 rather than Bcl-2 or Bcl-x(L) is an essential survival protein of human myeloma cells. |
|
143. |
Bcl-XL has a role in preventing Bax activation at the mitochondrial membrane |
|
144. |
The amphipathic alpha 6 helix fragment of Bcl-xL inserts in membranes as part of the alpha 5-alpha 6 hairpins in a model chimeric system, showing direct potentiality for this Bcl-xL fragment to acquire a membrane inserted state. |
|
145. |
BCL-XL is induced during rapamycin-resistant proliferation of CD8+ T cells |
|
146. |
The BCLX pre-mRNA is splicing by extracellular factors and their distinct requirements for pre-mRNA elements. |
|
147. |
Stable Bcl-XL siRNA transfectants have an increased spontaneous apoptosis. |
|
148. |
Data show that Bcl-x(L) in the cytosol forms homodimers, and that the C-terminal hydrophobic tails of two Bcl-x(L) molecules are involved in homodimer formation. |
|
149. |
Bcl-xL/Bax ratio can block the apoptotic response in TNFalpha-stimulated cells but allows cell death initiation when it is altered by a crosstalk between IFNgamma presensitization and TNFalpha induced signaling. |
|
150. |
PXR expression is required for Bcl-2 and Bcl-xL up-regulation upon PXR activators treatment in human and rat hepatocytes. |
|
151. |
Results describe the structure of BCL-X(L) homodimers as a 3D-domain swapped dimer. |
|
152. |
PUMA initiates apoptosis in part by dissociating Bax and Bcl-X(L), thereby promoting Bax multimerization and mitochondrial translocation |
|
153. |
Bcl-xL is capable of giving rise to Epo-independent erythroid colony formation. |
|
154. |
Radiation therapy for squamous cell carcinoma of cervix results in increased apoptosis with the up-regulation of Bax, a proapoptotic protein, the down-regulation of Bcl-XL, an antiapoptotic protein, and no significant change in the levels of Bcl-2. |
|
155. |
Expression of Bcl-x was strongly expression in both reactive astrocytes and astrocytomas. Expression of Bcl-x is more focal in oligodendrogliomas, with staining of mainly intervening astrocytic processes. |
|
156. |
distal Bcl-X 1B promoter plays a critical role in driving constitutive expression-mediated via Ets family proteins in malignant B cells |
|
157. |
GX15-070 induced apoptosis in vitro in MCL cell lines and primary cells from patients with MCL by releasing Bak from Mcl-1 and Bcl-X(L). |
|
158. |
In Parkinson's disease patients, Bcl-xL mRNA expression per dopaminergic neuron is almost double that of controls, an effect that may be mediated by a redistribution of Bcl-xL from the cytosol to the outer mitochondrial membrane. |
|
159. |
role in modulating HIV-1/monocyte-derived macrophage-induced neuronal apoptosis |
|
160. |
A very low mRNA level was indicated at bax, bcl-2 and bcl-xL in hepatocellular carcinoma tissues in contrast to normal liver. |
|
161. |
Anti-apoptotic factors, Bcl-2 and Bcl-xL, were significantly decreased in epithelial cells under a hypoxic condition as assessed by Western blotting |
|
162. |
1-Bromopropane inhibits nuclear factor kappa B activation to reduce Bcl-xL expression in astrocytes. |
|
163. |
Thus EPO promotes survival of endothelial cells through PI3K-dependent Bcl-x(L)-induction and BIM regulation, as well as through a separate mechanism involving the ERK pathway. |
|
164. |
increased expression associated with low levels of apoptosis in renal cell carcinoma; may have role in progression of cancer and treatment resistance |
|
165. |
Erythrocyte survival is suppressed by a Bak-derived BH3 peptide that interacts with membrane-associated Bcl-X(L). |
|
166. |
bcl-xL directly binds to Apaf-1. |
|
167. |
show that the Bcl-x(L) interaction surface on p53 involves the same region that is used by the protein to contact DNA. The p53-binding site on Bcl-x(L) is also defined. |
|
168. |
p38 MAPK and Bcl-XL expression play critical roles in the survival of UVA-irradiated HaCaT cells |
|
169. |
The role of Bcl-xL in megakaryocyte (MK) differentiation was studied using siRNA to block its expression in essential thrombocythemia, chronic myeloid leukemia, & polycythemia vera cells. It is down-regulated early in MK differentiation of MKs from ET. |
|
170. |
Mitochondrial targeting of Bcl-x(L) requires the COOH-terminal transmembrane (TM) domain flanked at both ends by at least two basic amino acids |
|
171. |
Fibroblast growth factor-2 induces translational regulation of Bcl-XL and Bcl-2 via a MEK-dependent pathway: correlation with resistance to etoposide-induced apoptosis |
|
172. |
results show a pivotal role for Bcl-XL in ALK-mediated oncogenicity |
|
173. |
Transgenic mice crrossed with c-MYC transgenic mice develop multiple myeloma. |
|
174. |
The results of the current study suggest that the potential ability of 15d-PGJ(2) in regulation of cell cycle and inhibition of Bcl-xL expression might be beneficial in the development of novel pharmacological agents for chondrosarcoma. |
|
175. |
ABL-MYC retroviral infection only elicits bone marrow plasma cell tumors in mice that ectopically express Bcl-X(L) in their B- and plasma cells. |
|
176. |
BCL-xL levels decreased when H202 was greater than 250 micro M. |
|
177. |
Gossypol is a potent and novel therapeutic able to overcome apoptosis resistance by specifically targeting the activity of antiapoptotic Bcl-2 and Bcl-xl family members. |
|
178. |
Gossypol induced complete cytochrome c release from mitochondria, increased caspases-3 and -9 activity, and caused apoptotic death without affecting protein levels of Bcl-2 and Bcl-X(L.) |
|
179. |
Bcl-xL expression contributes to androgen resistance and progression of prostate cancer |
|
180. |
These results suggest a relevant role for STAT5 and Bcl-xL as apoptosis-regulatory proteins in the pathogenesis of lung cancer, and overexpression of both Neu and activated STAT3, could be related with the proliferation rate in lung carcinoma cells. |
|
181. |
overexpression of Bcl-x(L) or Bcl-2 in PC12 cells markedly suppressed brefeldin A-induced activation of caspases and resulting cell death. |
|
182. |
recombinant GM-CSF-Bcl-XL binds the GM-CSF receptor on human monocyte/macrophage cells and bone marrow progenitors inducing differentiation and allowing Bcl-XL entry into cells |
|
183. |
severe acute respiratory syndrome coronavirus 7a protein induction of apoptosis is dependent on its interaction with the Bcl-XL protein |
|
184. |
Bcl-xl RNA silencing in transfected HepG2 cells induced apoptosis and increased sensitivity of cells to 5-FU and 10-hydroxycamptothecin. |
|
185. |
Bcl-xL and E1B-19K proteins inhibit p53-induced irreversible growth arrest and senescence by preventing reactive oxygen species-dependent p38 activation |
|
186. |
BCL-XL binds to Siva-1 putative amphipathic helical region which sensitizes cells to UV radiation induced apoptosis |
|
187. |
identified SAP155 as an RNA trans-acting factor that binds to CRCE 1, functions to regulate the alternative 5' splice site selection of Bcl-x pre-mRNA, and is required for ceramide to induce the activation of the Bcl-x(s) 5' splice site |
|
188. |
Results describe the specific modulation of apoptosis and Bcl-xL phosphorylation in yeast by distinct mammalian protein kinase C isoforms. |
|
189. |
This study is the first to show a clear dissociation between changes in Bcl-2 expression (downregulation) and Bcl-XL, Mcl-1 expression (upregulation) during progression of melanoma. |