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rabbit anti pi3kc3 d9a5 antibodies (Cell Signaling Technology Inc)

Name: rabbit anti pi3kc3 d9a5 antibodies
Brand: Cell Signaling Technology Inc
Rating: 94 (50 reviews)

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Cell Signaling Technology Inc rabbit anti pi3kc3 d9a5 antibodies

( A ) Co-IP analysis is used to study the interactions between RGS19 and RIP3, GNAI3 and RIP3, RGS19 and GNAI3. Myc-GNAI3 with Flag-RIP3 or Flag-RGS19, Flag-RIP3 with Myc-RGS19 were respectively co-expressed in 293T cells, Flag-RIP3 or Flag-RGS19 was then immunoprecipitated with anti-Flag M2-beads, and Myc-GNAI3 or Myc-RGS19 was detected in the immunoprecipitates with anti-myc antibody by Western blotting. ( B ) Knockdown of RGS19 or GNAI3 effectively blocked zVAD-induced cell death, but had no effect on TNF-induced cell death. Control and RGS19- or GNAI3-knockdown L929 cells were treated for 24 h with mock, TNF (10 ng/ml) or zVAD (20 µM). RIP1-, RIP3- or <t>PI3KC3-knockdown</t> L929 cells were also included. Then cell viabilities were measured (upper panel). The knockdown efficiencies were determined by relative mRNA levels calculated from real-time PCR results (lower panel). **, p<0.01.

Rabbit Anti Pi3kc3 D9a5 Antibodies, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 50 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/rabbit anti pi3kc3 d9a5 antibodies/product/Cell Signaling Technology Inc
Average 94 stars, based on 50 article reviews

rabbit anti pi3kc3 d9a5 antibodies - by Bioz Stars, 2026-02

94/100 stars

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1) Product Images from "Regulator of G-Protein Signaling 19 (RGS19) and Its Partner Gα-Inhibiting Activity Polypeptide 3 (GNAI3) Are Required for zVAD-Induced Autophagy and Cell Death in L929 Cells"

Article Title: Regulator of G-Protein Signaling 19 (RGS19) and Its Partner Gα-Inhibiting Activity Polypeptide 3 (GNAI3) Are Required for zVAD-Induced Autophagy and Cell Death in L929 Cells

Journal: PLoS ONE

doi: 10.1371/journal.pone.0094634

Figure Legend Snippet: ( A ) Co-IP analysis is used to study the interactions between RGS19 and RIP3, GNAI3 and RIP3, RGS19 and GNAI3. Myc-GNAI3 with Flag-RIP3 or Flag-RGS19, Flag-RIP3 with Myc-RGS19 were respectively co-expressed in 293T cells, Flag-RIP3 or Flag-RGS19 was then immunoprecipitated with anti-Flag M2-beads, and Myc-GNAI3 or Myc-RGS19 was detected in the immunoprecipitates with anti-myc antibody by Western blotting. ( B ) Knockdown of RGS19 or GNAI3 effectively blocked zVAD-induced cell death, but had no effect on TNF-induced cell death. Control and RGS19- or GNAI3-knockdown L929 cells were treated for 24 h with mock, TNF (10 ng/ml) or zVAD (20 µM). RIP1-, RIP3- or PI3KC3-knockdown L929 cells were also included. Then cell viabilities were measured (upper panel). The knockdown efficiencies were determined by relative mRNA levels calculated from real-time PCR results (lower panel). **, p<0.01.

Techniques Used: Co-Immunoprecipitation Assay, Immunoprecipitation, Western Blot, Knockdown, Control, Real-time Polymerase Chain Reaction

( A–B ) Knockdown of RGS19 or GNAI3 inhibited zVAD-induced modification of LC3. Control and RGS19-knockdown ( A ) or GNAI3 knockdown ( B ) L929 cells were treated with mock or zVAD (20 µM) for 12 h. Cell lysates were subjected to western blot analysis with antibodies against LC3 and β-actin. Results from RIP1- or PI3KC3-knockdown cells were included as controls. ( C–D ) Knockdown of RGS19 or GNAI3 inhibited TNF-induced modification of LC3. Control and RGS19-knockdown ( C ) or GNAI3 knockdown ( D ) L929 cells were treated with mock or TNF (1 ng/ml) for 12 h. Cell lysates were subjected to western blot analysis with the indicated antibodies. ( E ) Knockdown of RGS19 or GNAI3 impaired zVAD-induced LC3 flux. Control and RGS19-knockdown or GNAI3-konckdown L929 cells were cultured with or without chloroquine (25 µM) and treated with or without zVAD (20 µM) for 12 h. LC3 levels were measured by Western blot.

Figure Legend Snippet: ( A–B ) Knockdown of RGS19 or GNAI3 inhibited zVAD-induced modification of LC3. Control and RGS19-knockdown ( A ) or GNAI3 knockdown ( B ) L929 cells were treated with mock or zVAD (20 µM) for 12 h. Cell lysates were subjected to western blot analysis with antibodies against LC3 and β-actin. Results from RIP1- or PI3KC3-knockdown cells were included as controls. ( C–D ) Knockdown of RGS19 or GNAI3 inhibited TNF-induced modification of LC3. Control and RGS19-knockdown ( C ) or GNAI3 knockdown ( D ) L929 cells were treated with mock or TNF (1 ng/ml) for 12 h. Cell lysates were subjected to western blot analysis with the indicated antibodies. ( E ) Knockdown of RGS19 or GNAI3 impaired zVAD-induced LC3 flux. Control and RGS19-knockdown or GNAI3-konckdown L929 cells were cultured with or without chloroquine (25 µM) and treated with or without zVAD (20 µM) for 12 h. LC3 levels were measured by Western blot.

Techniques Used: Knockdown, Modification, Control, Western Blot, Cell Culture

( A ) Knockdown of RGS19, GNAI3 or PI3KC3 had no effect on TNF-induced cell death in zVAD insensitive L929 subline. Control and RGS19- or GNAI3-knockdown L929 cells (left panel) and zVAD insensitive L929 cells (right panel) were treated for 24 h with mock, TNF (10 ng/ml) or zVAD (20 µM). Then cell viabilities were measured. ( B ) zVAD insensitive L929 subline had defect in RGS19-, GNAI3- and RIP3-dependent zVAD- or TNF-induced modification of LC3. Control and RGS19-, GNAI3- or RIP3-knockdown zVAD insensitive L929 cells were treated with mock, TNF (1 ng/ml) or zVAD (20 µM) for 12 h. Cell lysates were subjected to western blot analysis with antibodies against LC3 and β-actin. **, p<0.01.

Figure Legend Snippet: ( A ) Knockdown of RGS19, GNAI3 or PI3KC3 had no effect on TNF-induced cell death in zVAD insensitive L929 subline. Control and RGS19- or GNAI3-knockdown L929 cells (left panel) and zVAD insensitive L929 cells (right panel) were treated for 24 h with mock, TNF (10 ng/ml) or zVAD (20 µM). Then cell viabilities were measured. ( B ) zVAD insensitive L929 subline had defect in RGS19-, GNAI3- and RIP3-dependent zVAD- or TNF-induced modification of LC3. Control and RGS19-, GNAI3- or RIP3-knockdown zVAD insensitive L929 cells were treated with mock, TNF (1 ng/ml) or zVAD (20 µM) for 12 h. Cell lysates were subjected to western blot analysis with antibodies against LC3 and β-actin. **, p<0.01.

Techniques Used: Knockdown, Control, Modification, Western Blot

( A ) Knockdown of TNFR1 inhibited both TNF- and zVAD-induced cell deaths. Control and GFP- or TNFR1-knockdown L929 cells were treated with mock, TNF (10 ng/ml) or zVAD (20 µM) for 24 h. Then cell viabilities were measured. ( B ) Knockdown of TNF inhibited zVAD- but not TNF-induced cell death. Control and GFP- or TNF-knockdown L929 cells were treated with mock, TNF (10 ng/ml) or zVAD (20 µM) for 24 h. Then cell viabilities were measured. ( C ) Knockdown of RGS19, GNAI3, RIP3, or PI3KC3 all inhibited zVAD-induced increase of TNF mRNA. Control and RGS19-, GNAI3-, RIP3- or PI3KC3-knockdown L929 cells were treated with mock or zVAD (20 µM) for 3 h. TNF mRNA levels were measured by real-time PCR. ( D ) Knockdown of RGS19, GNAI3, RIP3, or PI3KC3 all inhibited zVAD-induced TNF secretion. Control and RGS19-, GNAI3-, RIP3- or PI3KC3-knockdown L929 cells were treated with mock or zVAD (20 µM) for 24 h. Then the cell culture medium was collected and concentrated 10 folds, and the TNF secretion was determined by ELISA. ( E ) Beclin-1, but not TNF or TNFR1, is required for zVAD-induced LC3 modification. Control and TNF-knockdown or TNFR-knockdown or Bclin 1-knockdown L929 cells were treated with mock or zVAD (20 µM) for 12 h. Cell lysates were subjected to Western blot analysis with antibodies against LC3 and β-actin. ( F ) Control and Bclin 1-knockdown L929 cells were treated with mock or zVAD (20 µM) for 12 h. Then TNF secretion was determined (left) and cell viabilities were measured (right). **, p<0.01.

Figure Legend Snippet: ( A ) Knockdown of TNFR1 inhibited both TNF- and zVAD-induced cell deaths. Control and GFP- or TNFR1-knockdown L929 cells were treated with mock, TNF (10 ng/ml) or zVAD (20 µM) for 24 h. Then cell viabilities were measured. ( B ) Knockdown of TNF inhibited zVAD- but not TNF-induced cell death. Control and GFP- or TNF-knockdown L929 cells were treated with mock, TNF (10 ng/ml) or zVAD (20 µM) for 24 h. Then cell viabilities were measured. ( C ) Knockdown of RGS19, GNAI3, RIP3, or PI3KC3 all inhibited zVAD-induced increase of TNF mRNA. Control and RGS19-, GNAI3-, RIP3- or PI3KC3-knockdown L929 cells were treated with mock or zVAD (20 µM) for 3 h. TNF mRNA levels were measured by real-time PCR. ( D ) Knockdown of RGS19, GNAI3, RIP3, or PI3KC3 all inhibited zVAD-induced TNF secretion. Control and RGS19-, GNAI3-, RIP3- or PI3KC3-knockdown L929 cells were treated with mock or zVAD (20 µM) for 24 h. Then the cell culture medium was collected and concentrated 10 folds, and the TNF secretion was determined by ELISA. ( E ) Beclin-1, but not TNF or TNFR1, is required for zVAD-induced LC3 modification. Control and TNF-knockdown or TNFR-knockdown or Bclin 1-knockdown L929 cells were treated with mock or zVAD (20 µM) for 12 h. Cell lysates were subjected to Western blot analysis with antibodies against LC3 and β-actin. ( F ) Control and Bclin 1-knockdown L929 cells were treated with mock or zVAD (20 µM) for 12 h. Then TNF secretion was determined (left) and cell viabilities were measured (right). **, p<0.01.

Techniques Used: Knockdown, Control, Real-time Polymerase Chain Reaction, Cell Culture, Enzyme-linked Immunosorbent Assay, Modification, Western Blot

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Journal: PLoS ONE

Article Title: Regulator of G-Protein Signaling 19 (RGS19) and Its Partner Gα-Inhibiting Activity Polypeptide 3 (GNAI3) Are Required for zVAD-Induced Autophagy and Cell Death in L929 Cells

doi: 10.1371/journal.pone.0094634

Figure Lengend Snippet: ( A ) Co-IP analysis is used to study the interactions between RGS19 and RIP3, GNAI3 and RIP3, RGS19 and GNAI3. Myc-GNAI3 with Flag-RIP3 or Flag-RGS19, Flag-RIP3 with Myc-RGS19 were respectively co-expressed in 293T cells, Flag-RIP3 or Flag-RGS19 was then immunoprecipitated with anti-Flag M2-beads, and Myc-GNAI3 or Myc-RGS19 was detected in the immunoprecipitates with anti-myc antibody by Western blotting. ( B ) Knockdown of RGS19 or GNAI3 effectively blocked zVAD-induced cell death, but had no effect on TNF-induced cell death. Control and RGS19- or GNAI3-knockdown L929 cells were treated for 24 h with mock, TNF (10 ng/ml) or zVAD (20 µM). RIP1-, RIP3- or PI3KC3-knockdown L929 cells were also included. Then cell viabilities were measured (upper panel). The knockdown efficiencies were determined by relative mRNA levels calculated from real-time PCR results (lower panel). **, p<0.01.

Article Snippet: Rabbit anti-p-ERK, rabbit anti-ERK, rabbit anti-p38, rabbit anti-p-p38, rabbit anti-p-JNK and rabbit anti-PI3KC3 (D9A5) antibodies were obtained from Cell Signaling (Danvers, MA, USA).

Techniques: Co-Immunoprecipitation Assay, Immunoprecipitation, Western Blot, Knockdown, Control, Real-time Polymerase Chain Reaction

Journal: PLoS ONE

Article Title: Regulator of G-Protein Signaling 19 (RGS19) and Its Partner Gα-Inhibiting Activity Polypeptide 3 (GNAI3) Are Required for zVAD-Induced Autophagy and Cell Death in L929 Cells

doi: 10.1371/journal.pone.0094634

Figure Lengend Snippet: ( A–B ) Knockdown of RGS19 or GNAI3 inhibited zVAD-induced modification of LC3. Control and RGS19-knockdown ( A ) or GNAI3 knockdown ( B ) L929 cells were treated with mock or zVAD (20 µM) for 12 h. Cell lysates were subjected to western blot analysis with antibodies against LC3 and β-actin. Results from RIP1- or PI3KC3-knockdown cells were included as controls. ( C–D ) Knockdown of RGS19 or GNAI3 inhibited TNF-induced modification of LC3. Control and RGS19-knockdown ( C ) or GNAI3 knockdown ( D ) L929 cells were treated with mock or TNF (1 ng/ml) for 12 h. Cell lysates were subjected to western blot analysis with the indicated antibodies. ( E ) Knockdown of RGS19 or GNAI3 impaired zVAD-induced LC3 flux. Control and RGS19-knockdown or GNAI3-konckdown L929 cells were cultured with or without chloroquine (25 µM) and treated with or without zVAD (20 µM) for 12 h. LC3 levels were measured by Western blot.

Techniques: Knockdown, Modification, Control, Western Blot, Cell Culture

Journal: PLoS ONE

Article Title: Regulator of G-Protein Signaling 19 (RGS19) and Its Partner Gα-Inhibiting Activity Polypeptide 3 (GNAI3) Are Required for zVAD-Induced Autophagy and Cell Death in L929 Cells

doi: 10.1371/journal.pone.0094634

Figure Lengend Snippet: ( A ) Knockdown of RGS19, GNAI3 or PI3KC3 had no effect on TNF-induced cell death in zVAD insensitive L929 subline. Control and RGS19- or GNAI3-knockdown L929 cells (left panel) and zVAD insensitive L929 cells (right panel) were treated for 24 h with mock, TNF (10 ng/ml) or zVAD (20 µM). Then cell viabilities were measured. ( B ) zVAD insensitive L929 subline had defect in RGS19-, GNAI3- and RIP3-dependent zVAD- or TNF-induced modification of LC3. Control and RGS19-, GNAI3- or RIP3-knockdown zVAD insensitive L929 cells were treated with mock, TNF (1 ng/ml) or zVAD (20 µM) for 12 h. Cell lysates were subjected to western blot analysis with antibodies against LC3 and β-actin. **, p<0.01.

Techniques: Knockdown, Control, Modification, Western Blot

Journal: PLoS ONE

Article Title: Regulator of G-Protein Signaling 19 (RGS19) and Its Partner Gα-Inhibiting Activity Polypeptide 3 (GNAI3) Are Required for zVAD-Induced Autophagy and Cell Death in L929 Cells

doi: 10.1371/journal.pone.0094634

Figure Lengend Snippet: ( A ) Knockdown of TNFR1 inhibited both TNF- and zVAD-induced cell deaths. Control and GFP- or TNFR1-knockdown L929 cells were treated with mock, TNF (10 ng/ml) or zVAD (20 µM) for 24 h. Then cell viabilities were measured. ( B ) Knockdown of TNF inhibited zVAD- but not TNF-induced cell death. Control and GFP- or TNF-knockdown L929 cells were treated with mock, TNF (10 ng/ml) or zVAD (20 µM) for 24 h. Then cell viabilities were measured. ( C ) Knockdown of RGS19, GNAI3, RIP3, or PI3KC3 all inhibited zVAD-induced increase of TNF mRNA. Control and RGS19-, GNAI3-, RIP3- or PI3KC3-knockdown L929 cells were treated with mock or zVAD (20 µM) for 3 h. TNF mRNA levels were measured by real-time PCR. ( D ) Knockdown of RGS19, GNAI3, RIP3, or PI3KC3 all inhibited zVAD-induced TNF secretion. Control and RGS19-, GNAI3-, RIP3- or PI3KC3-knockdown L929 cells were treated with mock or zVAD (20 µM) for 24 h. Then the cell culture medium was collected and concentrated 10 folds, and the TNF secretion was determined by ELISA. ( E ) Beclin-1, but not TNF or TNFR1, is required for zVAD-induced LC3 modification. Control and TNF-knockdown or TNFR-knockdown or Bclin 1-knockdown L929 cells were treated with mock or zVAD (20 µM) for 12 h. Cell lysates were subjected to Western blot analysis with antibodies against LC3 and β-actin. ( F ) Control and Bclin 1-knockdown L929 cells were treated with mock or zVAD (20 µM) for 12 h. Then TNF secretion was determined (left) and cell viabilities were measured (right). **, p<0.01.

Techniques: Knockdown, Control, Real-time Polymerase Chain Reaction, Cell Culture, Enzyme-linked Immunosorbent Assay, Modification, Western Blot

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1) Product Images from "Regulator of G-Protein Signaling 19 (RGS19) and Its Partner Gα-Inhibiting Activity Polypeptide 3 (GNAI3) Are Required for zVAD-Induced Autophagy and Cell Death in L929 Cells"

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