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Addgene inc myc ciap1
Myc Ciap1, supplied by Addgene inc, used in various techniques. Bioz Stars score: 88/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ciap1+plasmid/pcdna3%2E1+hciap1+(Plasmid+%238311)/pmc11268115-293-9-13
Average 88 stars, based on 7 article reviews
myc ciap1 - by Bioz Stars, 2026-11
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Related Articles

Expressing:

Article Title: USP36 inhibits apoptosis by deubiquitinating cIAP1 and survivin in colorectal cancer cells.
Article Snippet: Chemotherapeutic agents for treating colorectal cancer (CRC) primarily induce apoptosis in tumor cells.. The ubiquitin-proteasome system is critical for apoptosis regulation.. Deubiquitinating enzymes (DUBs) remove ubiquitin from substrates to reverse ubiquitination.

Article Title: Induction of necroptotic cell death by viral activation of the RIG-I or STING pathway
Article Snippet: .. The following expression plasmids were purchased from Addgene (Cambridge, MA, USA): pDEST-HA-CYLD (#15506) and pCDNA3.1-Myc-cIAP1 (#8311). .. Murine RIP1 was purchased from Open Biosystems and subcloned into pCI using NotI and EcoRI.

Article Title: Induction of necroptotic cell death by viral activation of the RIG-I or STING pathway
Article Snippet: 16–18 hours post-infection, cell survival was measured by CellTiter-Glo ATP Assay (Promega). .. Constructs The following expression plasmids were purchased from Addgene (Cambridge, MA, USA): pDEST-HA-CYLD (#15506) and pCDNA3.1-Myc-cIAP1 (#8311). .. Murine RIP1 was purchased from Open Biosystems and subcloned into pCI using NotI and EcoRI.

Article Title: USP36 inhibits apoptosis by deubiquitinating cIAP1 and survivin in colorectal cancer cells
Article Snippet: .. Plasmids expressing Flag-HA-USP36 (WT, Cat# 22579, RRID: Addgene_22579) and Myc-cIAP1 (Cat# 8311, RRID: Addgene_8311) were purchased from Addgene. .. Plasmids expressing Flag-RIPK1 (Cat# F122510) were purchased from Fenghui Biotechnology.

Construct:

Article Title: Induction of necroptotic cell death by viral activation of the RIG-I or STING pathway
Article Snippet: 16–18 hours post-infection, cell survival was measured by CellTiter-Glo ATP Assay (Promega). .. Constructs The following expression plasmids were purchased from Addgene (Cambridge, MA, USA): pDEST-HA-CYLD (#15506) and pCDNA3.1-Myc-cIAP1 (#8311). .. Murine RIP1 was purchased from Open Biosystems and subcloned into pCI using NotI and EcoRI.

Article Title: Caspase-10: a molecular switch from cell-autonomous apoptosis to communal cell death in response to chemotherapeutic drug treatment
Article Snippet: Human cervix carcinoma HeLa cells (ATCC) and human breast carcinoma MDA-MB-231 cells (ATCC) were grown in Dulbecco’s modified eagle medium supplemented with 10% FBS, 100 U/ml penicillin and 100 μg/ml streptomycin. .. Overexpression constructs Flag-cIAP2/pRK5 was a gift from Xiaolu Yang (Addgene, Cambridge, MA, USA, plasmid # 27973), 36 pcdna3.1 hciap1 was a gift from Jon Ashwell (Addgene plasmid # 8311). .. 37 HA-Ubiquitin was a gift from Edward Yeh (Addgene plasmid # 18712).

Over Expression:

Article Title: Caspase-10: a molecular switch from cell-autonomous apoptosis to communal cell death in response to chemotherapeutic drug treatment
Article Snippet: Human cervix carcinoma HeLa cells (ATCC) and human breast carcinoma MDA-MB-231 cells (ATCC) were grown in Dulbecco’s modified eagle medium supplemented with 10% FBS, 100 U/ml penicillin and 100 μg/ml streptomycin. .. Overexpression constructs Flag-cIAP2/pRK5 was a gift from Xiaolu Yang (Addgene, Cambridge, MA, USA, plasmid # 27973), 36 pcdna3.1 hciap1 was a gift from Jon Ashwell (Addgene plasmid # 8311). .. 37 HA-Ubiquitin was a gift from Edward Yeh (Addgene plasmid # 18712).

Plasmid Preparation:

Article Title: Caspase-10: a molecular switch from cell-autonomous apoptosis to communal cell death in response to chemotherapeutic drug treatment
Article Snippet: Human cervix carcinoma HeLa cells (ATCC) and human breast carcinoma MDA-MB-231 cells (ATCC) were grown in Dulbecco’s modified eagle medium supplemented with 10% FBS, 100 U/ml penicillin and 100 μg/ml streptomycin. .. Overexpression constructs Flag-cIAP2/pRK5 was a gift from Xiaolu Yang (Addgene, Cambridge, MA, USA, plasmid # 27973), 36 pcdna3.1 hciap1 was a gift from Jon Ashwell (Addgene plasmid # 8311). .. 37 HA-Ubiquitin was a gift from Edward Yeh (Addgene plasmid # 18712).

Article Title: Caspase-10: a molecular switch from cell-autonomous apoptosis to communal cell death in response to chemotherapeutic drug treatment
Article Snippet: Human cervix carcinoma HeLa cells (ATCC) and human breast carcinoma MDA-MB-231 cells (ATCC) were grown in Dulbecco’s modified eagle medium supplemented with 10% FBS, 100 U/ml penicillin and 100 μg/ml streptomycin. .. Flag-cIAP2/pRK5 was a gift from Xiaolu Yang (Addgene, Cambridge, MA, USA, plasmid # 27973), 36 pcdna3.1 hciap1 was a gift from Jon Ashwell (Addgene plasmid # 8311). .. 37 HA-Ubiquitin was a gift from Edward Yeh (Addgene plasmid # 18712).

Article Title: Serum starvation induces anti-apoptotic cIAP1 to promote mitophagy through ubiquitination.
Article Snippet: Accepted Manuscript Serum starvation induces anti-apoptotic cIAP1 to promote mitophagy through ubiquitination Subhadip Mukhopadhyay, Prajna Paramita Naik, Prashanta Kumar Panda, Niharika Sinha, Sujit Kumar Bhutia PII: S0006-291X(16)31617-5 DOI: 10.1016/j.bbrc.2016.09.143 Reference: YBBRC 36522 To appear in: Biochemical and Biophysical Research Communications Received Date: 14 August 2016 Revised Date: 18 September 2016 Accepted Date: 27 September 2016 Please cite this article as: S. Mukhopadhyay, P.P.. Naik, P.K.. Panda, N. Sinha, S.K.

Transfection:

Article Title: Serum starvation induces anti-apoptotic cIAP1 to promote mitophagy through ubiquitination.
Article Snippet: Accepted Manuscript Serum starvation induces anti-apoptotic cIAP1 to promote mitophagy through ubiquitination Subhadip Mukhopadhyay, Prajna Paramita Naik, Prashanta Kumar Panda, Niharika Sinha, Sujit Kumar Bhutia PII: S0006-291X(16)31617-5 DOI: 10.1016/j.bbrc.2016.09.143 Reference: YBBRC 36522 To appear in: Biochemical and Biophysical Research Communications Received Date: 14 August 2016 Revised Date: 18 September 2016 Accepted Date: 27 September 2016 Please cite this article as: S. Mukhopadhyay, P.P.. Naik, P.K.. Panda, N. Sinha, S.K.



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Fig. 2. TRAF1 stabilizes cIAP2 and protects it from degradation (a) HEK 293T cells overexpressing cIAP2 with or without WT TRAF1 were treated with 5 μg/ml cycloheximide (CHX) to inhibit denovo protein synthesis for the indicated times and lysates were blotted for cIAP2, TRAF1 or as a loading control, β-actin (left panel). Densitometry of band intensity from 3 independent exper iments were quantified by ImageLab software (right panel). (b) shCtrl or shTRAF1 RAJI cells were treated with 5 μg/ml cycloheximide (CHX) for the indicated times, and lysates were blotted for cIAP2, TRAF1 or as a loading control, β-actin (left panel). Densitometry of band intensity from 3 independent experiments were quantified by ImageLab software (right panel). (c) HEK 293T cells overexpressing cIAP2 with or without WT, TRAF1 V203A were treated with cycloheximide (CHX) and blotted, as in panel a (left panel). Densitometry of band intensity from 3 independent experiments were quantified by ImageLab software (right panel). (d) HEK 293T cells overexpressing cIAP2 with or without WT were treated with or without 0.01 mM of the proteasome inhibitor, MG132 or 0.025 mM of the lysosomal inhibitor, chloroquine (CQ). (e) HEK 293T were transfected with various combinations of plasmids to overexpress cIAP2, WT TRAF1, <t>cIAP1,</t> cIAP2 H574A, or cIAP1 H588A as indicated and lysates were blotted for cIAP2, TRAF1 or as a loading control, β-actin. All blots are representative of three independent experiments. * non- specific band.
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Fig. 2. TRAF1 stabilizes cIAP2 and protects it from degradation (a) HEK 293T cells overexpressing cIAP2 with or without WT TRAF1 were treated with 5 μg/ml cycloheximide (CHX) to inhibit denovo protein synthesis for the indicated times and lysates were blotted for cIAP2, TRAF1 or as a loading control, β-actin (left panel). Densitometry of band intensity from 3 independent exper iments were quantified by ImageLab software (right panel). (b) shCtrl or shTRAF1 RAJI cells were treated with 5 μg/ml cycloheximide (CHX) for the indicated times, and lysates were blotted for cIAP2, TRAF1 or as a loading control, β-actin (left panel). Densitometry of band intensity from 3 independent experiments were quantified by ImageLab software (right panel). (c) HEK 293T cells overexpressing cIAP2 with or without WT, TRAF1 V203A were treated with cycloheximide (CHX) and blotted, as in panel a (left panel). Densitometry of band intensity from 3 independent experiments were quantified by ImageLab software (right panel). (d) HEK 293T cells overexpressing cIAP2 with or without WT were treated with or without 0.01 mM of the proteasome inhibitor, MG132 or 0.025 mM of the lysosomal inhibitor, chloroquine (CQ). (e) HEK 293T were transfected with various combinations of plasmids to overexpress cIAP2, WT TRAF1, <t>cIAP1,</t> cIAP2 H574A, or cIAP1 H588A as indicated and lysates were blotted for cIAP2, TRAF1 or as a loading control, β-actin. All blots are representative of three independent experiments. * non- specific band.
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Fig. 2. TRAF1 stabilizes cIAP2 and protects it from degradation (a) HEK 293T cells overexpressing cIAP2 with or without WT TRAF1 were treated with 5 μg/ml cycloheximide (CHX) to inhibit denovo protein synthesis for the indicated times and lysates were blotted for cIAP2, TRAF1 or as a loading control, β-actin (left panel). Densitometry of band intensity from 3 independent exper iments were quantified by ImageLab software (right panel). (b) shCtrl or shTRAF1 RAJI cells were treated with 5 μg/ml cycloheximide (CHX) for the indicated times, and lysates were blotted for cIAP2, TRAF1 or as a loading control, β-actin (left panel). Densitometry of band intensity from 3 independent experiments were quantified by ImageLab software (right panel). (c) HEK 293T cells overexpressing cIAP2 with or without WT, TRAF1 V203A were treated with cycloheximide (CHX) and blotted, as in panel a (left panel). Densitometry of band intensity from 3 independent experiments were quantified by ImageLab software (right panel). (d) HEK 293T cells overexpressing cIAP2 with or without WT were treated with or without 0.01 mM of the proteasome inhibitor, MG132 or 0.025 mM of the lysosomal inhibitor, chloroquine (CQ). (e) HEK 293T were transfected with various combinations of plasmids to overexpress cIAP2, WT TRAF1, <t>cIAP1,</t> cIAP2 H574A, or cIAP1 H588A as indicated and lysates were blotted for cIAP2, TRAF1 or as a loading control, β-actin. All blots are representative of three independent experiments. * non- specific band.
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Fig. 2. TRAF1 stabilizes cIAP2 and protects it from degradation (a) HEK 293T cells overexpressing cIAP2 with or without WT TRAF1 were treated with 5 μg/ml cycloheximide (CHX) to inhibit denovo protein synthesis for the indicated times and lysates were blotted for cIAP2, TRAF1 or as a loading control, β-actin (left panel). Densitometry of band intensity from 3 independent exper iments were quantified by ImageLab software (right panel). (b) shCtrl or shTRAF1 RAJI cells were treated with 5 μg/ml cycloheximide (CHX) for the indicated times, and lysates were blotted for cIAP2, TRAF1 or as a loading control, β-actin (left panel). Densitometry of band intensity from 3 independent experiments were quantified by ImageLab software (right panel). (c) HEK 293T cells overexpressing cIAP2 with or without WT, TRAF1 V203A were treated with cycloheximide (CHX) and blotted, as in panel a (left panel). Densitometry of band intensity from 3 independent experiments were quantified by ImageLab software (right panel). (d) HEK 293T cells overexpressing cIAP2 with or without WT were treated with or without 0.01 mM of the proteasome inhibitor, MG132 or 0.025 mM of the lysosomal inhibitor, chloroquine (CQ). (e) HEK 293T were transfected with various combinations of plasmids to overexpress cIAP2, WT TRAF1, <t>cIAP1,</t> cIAP2 H574A, or cIAP1 H588A as indicated and lysates were blotted for cIAP2, TRAF1 or as a loading control, β-actin. All blots are representative of three independent experiments. * non- specific band.
Myc Ciap1, supplied by Addgene inc, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ciap1+plasmid/pcdna3%2E1+hciap1+(Plasmid+%238311)/pmc11268115-293-9-13
Average 88 stars, based on 1 article reviews
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Image Search Results


Fig. 2. TRAF1 stabilizes cIAP2 and protects it from degradation (a) HEK 293T cells overexpressing cIAP2 with or without WT TRAF1 were treated with 5 μg/ml cycloheximide (CHX) to inhibit denovo protein synthesis for the indicated times and lysates were blotted for cIAP2, TRAF1 or as a loading control, β-actin (left panel). Densitometry of band intensity from 3 independent exper iments were quantified by ImageLab software (right panel). (b) shCtrl or shTRAF1 RAJI cells were treated with 5 μg/ml cycloheximide (CHX) for the indicated times, and lysates were blotted for cIAP2, TRAF1 or as a loading control, β-actin (left panel). Densitometry of band intensity from 3 independent experiments were quantified by ImageLab software (right panel). (c) HEK 293T cells overexpressing cIAP2 with or without WT, TRAF1 V203A were treated with cycloheximide (CHX) and blotted, as in panel a (left panel). Densitometry of band intensity from 3 independent experiments were quantified by ImageLab software (right panel). (d) HEK 293T cells overexpressing cIAP2 with or without WT were treated with or without 0.01 mM of the proteasome inhibitor, MG132 or 0.025 mM of the lysosomal inhibitor, chloroquine (CQ). (e) HEK 293T were transfected with various combinations of plasmids to overexpress cIAP2, WT TRAF1, cIAP1, cIAP2 H574A, or cIAP1 H588A as indicated and lysates were blotted for cIAP2, TRAF1 or as a loading control, β-actin. All blots are representative of three independent experiments. * non- specific band.

Journal: Journal of autoimmunity

Article Title: Selective disruption of Traf1/cIAP2 interaction attenuates inflammatory responses and rheumatoid arthritis.

doi: 10.1016/j.jaut.2025.103377

Figure Lengend Snippet: Fig. 2. TRAF1 stabilizes cIAP2 and protects it from degradation (a) HEK 293T cells overexpressing cIAP2 with or without WT TRAF1 were treated with 5 μg/ml cycloheximide (CHX) to inhibit denovo protein synthesis for the indicated times and lysates were blotted for cIAP2, TRAF1 or as a loading control, β-actin (left panel). Densitometry of band intensity from 3 independent exper iments were quantified by ImageLab software (right panel). (b) shCtrl or shTRAF1 RAJI cells were treated with 5 μg/ml cycloheximide (CHX) for the indicated times, and lysates were blotted for cIAP2, TRAF1 or as a loading control, β-actin (left panel). Densitometry of band intensity from 3 independent experiments were quantified by ImageLab software (right panel). (c) HEK 293T cells overexpressing cIAP2 with or without WT, TRAF1 V203A were treated with cycloheximide (CHX) and blotted, as in panel a (left panel). Densitometry of band intensity from 3 independent experiments were quantified by ImageLab software (right panel). (d) HEK 293T cells overexpressing cIAP2 with or without WT were treated with or without 0.01 mM of the proteasome inhibitor, MG132 or 0.025 mM of the lysosomal inhibitor, chloroquine (CQ). (e) HEK 293T were transfected with various combinations of plasmids to overexpress cIAP2, WT TRAF1, cIAP1, cIAP2 H574A, or cIAP1 H588A as indicated and lysates were blotted for cIAP2, TRAF1 or as a loading control, β-actin. All blots are representative of three independent experiments. * non- specific band.

Article Snippet: The TRAF1 mutated plasmids were sub-cloned into c-Flag pcDNA3. c-Flag pcDNA3 was a gift from Stephen Smale (Addgene plasmid # 20011) [37]; Flag-cIAP2/pRK5 was a gift from Xiaolu Yang (Addgene plasmid # 27973) [38]; pEBB HA cIAP1 was a gift from Colin Duckett (Addgene plasmid # 38232) [39].

Techniques: Control, Software, Transfection