Procaspase 8 overexpression in non-small-cell lung cancer promotes apoptosis induced by FLIP silencing. - Wikidata - wikimedia - TriplyDB

Procaspase 8 overexpression in non-small-cell lung cancer promotes apoptosis induced by FLIP silencing.

Procaspase 8 overexpression in non-small-cell lung cancer promotes apoptosis induced by FLIP silencing.

http://www.wikidata.org/entity/Q39835258

about

Regulation of tumour necrosis factor signalling: live or let die Voltage dependent anion channel-1 regulates death receptor mediated apoptosis by enabling cleavage of caspase-8.Understanding the Role of the Death Receptor 5/FADD/caspase-8 Death Signaling in Cancer Metastasis Apoptotic cell signaling in cancer progression and therapy Association between CASP8 and CASP10 polymorphisms and toxicity outcomes with platinum-based chemotherapy in Chinese patients with non-small cell lung cancer Inhibition of c-FLIPL expression by miRNA-708 increases the sensitivity of renal cancer cells to anti-cancer drugs.Functional classification of scaffold proteins and related molecules.Apoptosis and molecular targeting therapy in cancer.Prognostic and therapeutic relevance of FLIP and procaspase-8 overexpression in non-small cell lung cancer.Upregulation of c-FLIP-short in response to TRAIL promotes survival of NSCLC cells, which could be suppressed by inhibition of Ca2+/calmodulin signaling Acquired differential regulation of caspase-8 in cisplatin-resistant non-small-cell lung cancer.Type I interferons induce apoptosis by balancing cFLIP and caspase-8 independent of death ligands.Prognostic and therapeutic relevance of c-FLIP in acute myeloid leukaemia.A systems biology approach identifies SART1 as a novel determinant of both 5-fluorouracil and SN38 drug resistance in colorectal cancer.Doxorubicin and etoposide sensitize small cell lung carcinoma cells expressing caspase-8 to TRAIL.IHC-based subcellular quantification provides new insights into prognostic relevance of FLIP and procaspase-8 in non-small-cell lung cancer.Suppressed translation as a mechanism of initiation of CASP8 (caspase 8)-dependent apoptosis in autophagy-deficient NSCLC cells under nutrient limitation.Ophiopogonin B sensitizes TRAIL-induced apoptosis through activation of autophagy flux and downregulates cellular FLICE-like inhibitory protein.Glycogen synthase kinase-3β inhibition promotes lysosome-dependent degradation of c-FLIPL in hepatocellular carcinoma.

P2860

Q28262381-4AD43C6A-D9F3-44C1-B179-F6B363B3908A Q33636849-873AC40E-02FF-4701-B7A2-EC31B2BE8E1E Q34731599-AE752094-A463-4A3E-ACA6-52F7DE6B8CC6 Q35088734-90DB48CD-DB72-45F2-896C-C523BBB8C54D Q36483179-E4CC0684-2CA3-4F47-9572-D787798256E7 Q37362534-0CDAAF17-2E58-41CD-8238-CECF441AF81E Q37795113-35F62041-9B66-4CB5-BFCA-C3DF6DCC9610 Q38228349-1275C6B6-3618-4A70-9CE1-2B8E5FDA61EA Q39047967-F0DEB7D9-07E2-4C5E-ABA3-CFDD8715D523 Q39183627-B46FE77C-E204-45B0-AB9B-2321782738F3 Q39223532-1588635B-B3C3-4A8D-A68E-5BCBB7E7DD33 Q39228077-C27D5049-9723-41AB-94AA-D9B7A85FC677 Q39241897-2F323504-2DDE-45F1-850F-4A206F1A72F2 Q39452744-587D6B53-8193-4637-A8D1-6305E8C430C2 Q39711397-0058D56A-B9E4-48F2-9DC8-3A7753371EBE Q41285625-B71D95D1-B8B1-41AA-A0BD-C16DFF9E3EF3 Q47374563-067B1618-201E-4E45-A36B-4D0161E0EAD8 Q48505113-556E5932-652F-4BF4-BB71-CE2251ADD3BE Q52694975-A7055F64-E413-4FED-8108-86BF6365C957

P2860

Procaspase 8 overexpression in non-small-cell lung cancer promotes apoptosis induced by FLIP silencing.

http://www.wikidata.org/entity/Q39835258

description

2009 nî lūn-bûn

@nan

2009年の論文

@ja

2009年学术文章

@wuu

2009年学术文章

@zh-cn

2009年学术文章

@zh-hans

2009年学术文章

@zh-my

2009年学术文章

@zh-sg

2009年學術文章

@yue

2009年學術文章

@zh

2009年學術文章

@zh-hant

name

Procaspase 8 overexpression in ...... sis induced by FLIP silencing.

@en

Procaspase 8 overexpression in ...... sis induced by FLIP silencing.

@nl

type

label

Procaspase 8 overexpression in ...... sis induced by FLIP silencing.

@en

Procaspase 8 overexpression in ...... sis induced by FLIP silencing.

@nl

prefLabel

Procaspase 8 overexpression in ...... sis induced by FLIP silencing.

@en

Procaspase 8 overexpression in ...... sis induced by FLIP silencing.

@nl

P1433

Q39835258-FC323BDF-F1AA-42EA-AFD0-36B8C64B3FA5

P1476

Q39835258-ABFDDEBC-3276-48B9-BF83-74E4087FF645

P2093

Q39835258-0F074A58-5CDF-44E4-8FA3-2841AAEEE807

Q39835258-10AB218D-AD50-4329-AA7D-F4486D2119D6

Q39835258-11E7724C-D6CD-44AB-8A34-BE4DA6F7CB43

Q39835258-57A23610-B60C-4F7F-8FF7-2A0FC761A389

Q39835258-581D15FC-B4F3-4B75-B691-18E2423E58D2

Q39835258-59CEB428-15A6-4E2E-AB8C-030436DD23D0

Q39835258-73FFA4CD-EE2D-487B-B701-A33B2CBE7803

Q39835258-84177B6B-AB60-41C2-8243-E82E2CF784A8

Q39835258-93D87639-3EC8-4767-9859-6844CB92BC20

Q39835258-993848CB-6CD6-431F-B203-2AF8E13AFA7F

P2860

Q39835258-0013BDF5-7B76-46D6-8348-887E36016DAB

Q39835258-0A3FB1F6-9A4D-4C9F-8578-8266FFF6CF03

Q39835258-0F5B105C-3F2B-47F5-B425-C32EBFFE28AD

Q39835258-10FFC351-F7E1-4FB0-95A7-D66468105431

Q39835258-12AE359C-EFE2-4868-A235-EFA937965F89

Q39835258-1BC3DCAE-7D61-42F4-9984-4729BDA02329

Q39835258-2B1EFF67-02D0-4366-AE86-D32412F3D215

Q39835258-36300D0D-B181-435D-BE60-F9A3E02AF934

Q39835258-3B256D04-94C2-48B6-A5F8-0CA03A70ED0A

Q39835258-3F7D884E-9DC1-4568-8F1D-EED1ECC6C399

P2888

Q39835258-1C7DA792-A657-4CDC-9F8E-D7E24E69DAA1

P304

Q39835258-4001D52D-F2DC-4D29-8791-E0F9C2320485

P31

Q39835258-CAA54DEA-30BE-42A3-8579-5FA6D73E2C70

P356

Q39835258-BB026744-82FC-45F6-A833-DB18A42C4FA7

P433

Q39835258-E48836B4-9476-48D1-8A93-1CB7928ECD4C

P478

Q39835258-76B611A0-211B-4122-807D-E6D642D1E716

P577

Q39835258-394926BD-ED5A-44BB-A2BD-34380C14C842

P5875

Q39835258-1349ED9E-8CBC-43F0-825D-36E0716F56A9

P6179

Q39835258-302236CA-4C9E-473F-A78B-0289F4878DDC

P698

Q39835258-CC4DBD38-F9C5-4D7A-A9BA-D41381F70F5E

P921

Q39835258-395E81A7-4586-48E3-9D2E-78090AA1AD02

Q39835258-52A1E3FD-D29F-473D-BD0C-3296955DF15B

P356

P1433

Cell Death & Differentiation

P1476

Procaspase 8 overexpression in ...... sis induced by FLIP silencing.

@en

P2093

C Holohan

http://www.w3.org/2001/XMLSchema#string

C Le-Clorrenec

http://www.w3.org/2001/XMLSchema#string

D A Fennell

http://www.w3.org/2001/XMLSchema#string

D B Longley

http://www.w3.org/2001/XMLSchema#string

K Gately

http://www.w3.org/2001/XMLSchema#string

K M McLaughlin

http://www.w3.org/2001/XMLSchema#string

K M Redmond

http://www.w3.org/2001/XMLSchema#string

K O'Byrne

http://www.w3.org/2001/XMLSchema#string

N Crawford

http://www.w3.org/2001/XMLSchema#string

P G Johnston

http://www.w3.org/2001/XMLSchema#string

P2860

FADD, a novel death domain-containing protein, interacts with the death domain of Fas and initiates apoptosis

Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis

Inhibition of death receptor signals by cellular FLIP

TRAIL receptor-2 signals apoptosis through FADD and caspase-8

The caspase-8 inhibitor FLIP promotes activation of NF-kappaB and Erk signaling pathways

The long form of FLIP is an activator of caspase-8 at the Fas death-inducing signaling complex

A novel receptor for Apo2L/TRAIL contains a truncated death domain

Death receptors: signaling and modulation

Two CD95 (APO-1/Fas) signaling pathways

Identification of small molecules that sensitize resistant tumor cells to tumor necrosis factor-family death receptors.

P2888

P304

1352-1361

http://www.w3.org/2001/XMLSchema#string

P31

scholarly article

P356

10.1038/CDD.2009.76

http://www.w3.org/2001/XMLSchema#string

P433

10

http://www.w3.org/2001/XMLSchema#string

P478

16

http://www.w3.org/2001/XMLSchema#string

P577

2009-06-19T00:00:00Z

http://www.w3.org/2001/XMLSchema#dateTime

P5875

26307929

http://www.w3.org/2001/XMLSchema#string

P6179

1019063180

http://www.w3.org/2001/XMLSchema#string

P698

19543235

http://www.w3.org/2001/XMLSchema#string

P921

apoptotic process