p stat 1 cell signalling 9167s Search Results


phosphortyrosine701 stat1  (Cell Signaling Technology Inc)
98
Cell Signaling Technology Inc phosphortyrosine701 stat1
Fig. 2 cGAS inactivation causes unresponsiveness to DNA-triggered innate immunity in mitotic cells. a, b Chromosome-bound cGAS does not activate the IFN response. HT1080 cells were asynchronized (Asyn) or synchronized with nocodazole (M1) or paclitaxel (M2) before qPCR analysis (left) or FASC analysis (right) (a), and immunoblotting analysis (b). The dsDNA HSV120 (a) or HT-DNA (b)-transfected asynchronous cells were used as positive control. c Activation of cGAS by mitotic DNA. Genomic DNAs (gDNA) derived from asynchronized (Asyn), nocodazole (M1) or paclitaxel (M2) synchronized HeLa cells were transfected into MLF cells before qPCR analysis. The dsDNA DNA90 was used as a positive control. Data shown are mean ± SD, n = 3. d, e cGAS-MITA signaling is impaired in mitotic cells. HT1080 cells asynchronized (Asyn) or synchronized with paclitaxel (Mitotic) were mock-transfected or transfected with the dsDNA DNA90 (d) or HSV120 (e) before qPCR (d) and immunoblotting analysis (e). HSV60-Cy5 was used to analysis the transfection efficiency by FACS (d). **P < 0.01; ***P < 0.001 (Student’s t-test, unpaired, two-tailed). f IFN-β-induced <t>STAT1</t> Y701 phosphorylation in mitosis. HT1080 cells asynchronized (Asyn) or synchronized by paclitaxel (Mitotic) were left untreated or treated with IFN-β for the indicated times before immunoblotting analysis. Data shown are representative of three (a–c) or two (d–f) biological repeats. Data shown in (a), (c), and (d) are mean ± S.D. of one representative experiment performed in triplet.
Phosphortyrosine701 Stat1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/phosphortyrosine701 stat1/product/Cell Signaling Technology Inc
Average 98 stars, based on 1 article reviews
phosphortyrosine701 stat1 - by Bioz Stars, 2026-03
98/100 stars
  Buy from Supplier

Image Search Results


Fig. 2 cGAS inactivation causes unresponsiveness to DNA-triggered innate immunity in mitotic cells. a, b Chromosome-bound cGAS does not activate the IFN response. HT1080 cells were asynchronized (Asyn) or synchronized with nocodazole (M1) or paclitaxel (M2) before qPCR analysis (left) or FASC analysis (right) (a), and immunoblotting analysis (b). The dsDNA HSV120 (a) or HT-DNA (b)-transfected asynchronous cells were used as positive control. c Activation of cGAS by mitotic DNA. Genomic DNAs (gDNA) derived from asynchronized (Asyn), nocodazole (M1) or paclitaxel (M2) synchronized HeLa cells were transfected into MLF cells before qPCR analysis. The dsDNA DNA90 was used as a positive control. Data shown are mean ± SD, n = 3. d, e cGAS-MITA signaling is impaired in mitotic cells. HT1080 cells asynchronized (Asyn) or synchronized with paclitaxel (Mitotic) were mock-transfected or transfected with the dsDNA DNA90 (d) or HSV120 (e) before qPCR (d) and immunoblotting analysis (e). HSV60-Cy5 was used to analysis the transfection efficiency by FACS (d). **P < 0.01; ***P < 0.001 (Student’s t-test, unpaired, two-tailed). f IFN-β-induced STAT1 Y701 phosphorylation in mitosis. HT1080 cells asynchronized (Asyn) or synchronized by paclitaxel (Mitotic) were left untreated or treated with IFN-β for the indicated times before immunoblotting analysis. Data shown are representative of three (a–c) or two (d–f) biological repeats. Data shown in (a), (c), and (d) are mean ± S.D. of one representative experiment performed in triplet.

Journal: Cell discovery

Article Title: Phosphorylation of cGAS by CDK1 impairs self-DNA sensing in mitosis.

doi: 10.1038/s41421-020-0162-2

Figure Lengend Snippet: Fig. 2 cGAS inactivation causes unresponsiveness to DNA-triggered innate immunity in mitotic cells. a, b Chromosome-bound cGAS does not activate the IFN response. HT1080 cells were asynchronized (Asyn) or synchronized with nocodazole (M1) or paclitaxel (M2) before qPCR analysis (left) or FASC analysis (right) (a), and immunoblotting analysis (b). The dsDNA HSV120 (a) or HT-DNA (b)-transfected asynchronous cells were used as positive control. c Activation of cGAS by mitotic DNA. Genomic DNAs (gDNA) derived from asynchronized (Asyn), nocodazole (M1) or paclitaxel (M2) synchronized HeLa cells were transfected into MLF cells before qPCR analysis. The dsDNA DNA90 was used as a positive control. Data shown are mean ± SD, n = 3. d, e cGAS-MITA signaling is impaired in mitotic cells. HT1080 cells asynchronized (Asyn) or synchronized with paclitaxel (Mitotic) were mock-transfected or transfected with the dsDNA DNA90 (d) or HSV120 (e) before qPCR (d) and immunoblotting analysis (e). HSV60-Cy5 was used to analysis the transfection efficiency by FACS (d). **P < 0.01; ***P < 0.001 (Student’s t-test, unpaired, two-tailed). f IFN-β-induced STAT1 Y701 phosphorylation in mitosis. HT1080 cells asynchronized (Asyn) or synchronized by paclitaxel (Mitotic) were left untreated or treated with IFN-β for the indicated times before immunoblotting analysis. Data shown are representative of three (a–c) or two (d–f) biological repeats. Data shown in (a), (c), and (d) are mean ± S.D. of one representative experiment performed in triplet.

Article Snippet: Mouse monoclonal antibodies against HA (Origene, Cat# TA180128); FLAG (Sigma, F3165) and β-actin (Sigma, A2228); rabbit antibodies against cGAS (Cell Signaling Technology, 66546S/31659S), phosphorTyrosine701-STAT1 (Cell Signaling Technology, 9167S), phosphor-Serine727-STAT1(Cell Signaling Technology, Fig. 6 Inactivation of cGAS in mitosis.

Techniques: Western Blot, Transfection, Positive Control, Activation Assay, Derivative Assay, Two Tailed Test, Phospho-proteomics