p stat2 Search Results


p-stat2 (tp56499)  (Abmart Inc)
90
Abmart Inc p-stat2 (tp56499)
PEDV-N Interrupts the IFN-I-mediated JAK1/STAT1 Pathway. A. Changes of IFN-α protein. B. Changes of JAK1 protein. C. Changes of TYK2 protein. D. Changes of STAT1 protein. E. Changes of <t>STAT2</t> protein. F. Changes of P-STAT1 protein at 24 h. G. Changes of P-STAT1 protein at 48 h. H. Changes of <t>P-STAT2</t> protein. I. Changes of IRF9 protein. J. Changes of ISG15 mRNA levels. K. Changes of ISG54 mRNA levels. L. Changes of ISG56 mRNA levels. The data are presented as the mean ± SEM, ( n = 3). Significant differences between the control and objective groups are indicated as ⁎⁎ p < 0.01 and * p < 0.05.
P Stat2 (Tp56499), supplied by Abmart Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/p-stat2 (tp56499)/product/Abmart Inc
Average 90 stars, based on 1 article reviews
p-stat2 (tp56499) - by Bioz Stars, 2026-03
90/100 stars
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stat2-defective mutant daudi cells  (Absolute Biotech Inc)
90
Absolute Biotech Inc stat2-defective mutant daudi cells
Figure 2. IFNA2c induced autophagy in Daudi cells, but not in <t>STAT2-deficient</t> Daudi. ( A ) Direct effect of IFNA2c on induction of autophagy. Daudi cells were cultured for 24 h in supernatants from either mock-treated Daudi cells or cells treated with 0.36 ng/mL of IFNA2c for 24 h in the presence or absence of anti-IFNAR2-mAb A10. Lanes: (1) molecular weight marker; (2) negative control, cells plus supernatant from mock-treated cells; (3) negative control, cells plus supernatant from mock-treated cells and anti-IFNAR2 – mAb A10; (4) cells plus supernatant from IFNA2c-treated cells; (5) cells plus supernatant from IFNA2c-treated cells and anti-IFNAR2 – mAb. Data are representative of two individual experiments. Ratios of MAP1LC3 were calculated as the division of the ratio of induced MAP1LC3-I to induced MAP1LC3-II by the ratio of basal MAP1LC3-I to basal MAP1LC3-II, and the numbers are shown below MAP1LC3 lanes. ( B ) Detection of MAP1LC3-I and MAP1LC3-II, SQSTM1, p-STAT1, p-STAT2, p-RPS6 after 48 h treatment of STAT2-defective mutant Daudi cells with IFNA2c. STAT2-defective mutant Daudi cells were incubated with or without IFNA2c for 48 h. Lanes: (1) molecular weight marker; (2) negative control, untreated cells; (3) IFNA2c (3.6 ng/mL). Data are representative of two individual experiments. Ratios of MAP1LC3 were calculated as the division of the ratio of induced MAP1LC3-I to induced MAP1LC3-II by the ratio of basal MAP1LC3-I to basal MAP1LC3-II, and the numbers are shown below the MAP1LC3 lanes.
Stat2 Defective Mutant Daudi Cells, supplied by Absolute Biotech Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/stat2-defective mutant daudi cells/product/Absolute Biotech Inc
Average 90 stars, based on 1 article reviews
stat2-defective mutant daudi cells - by Bioz Stars, 2026-03
90/100 stars
  Buy from Supplier
stat2 d261445-0025 antibody  (Sangon Biotech)
90
Sangon Biotech stat2 d261445-0025 antibody
Figure 2. IFNA2c induced autophagy in Daudi cells, but not in <t>STAT2-deficient</t> Daudi. ( A ) Direct effect of IFNA2c on induction of autophagy. Daudi cells were cultured for 24 h in supernatants from either mock-treated Daudi cells or cells treated with 0.36 ng/mL of IFNA2c for 24 h in the presence or absence of anti-IFNAR2-mAb A10. Lanes: (1) molecular weight marker; (2) negative control, cells plus supernatant from mock-treated cells; (3) negative control, cells plus supernatant from mock-treated cells and anti-IFNAR2 – mAb A10; (4) cells plus supernatant from IFNA2c-treated cells; (5) cells plus supernatant from IFNA2c-treated cells and anti-IFNAR2 – mAb. Data are representative of two individual experiments. Ratios of MAP1LC3 were calculated as the division of the ratio of induced MAP1LC3-I to induced MAP1LC3-II by the ratio of basal MAP1LC3-I to basal MAP1LC3-II, and the numbers are shown below MAP1LC3 lanes. ( B ) Detection of MAP1LC3-I and MAP1LC3-II, SQSTM1, p-STAT1, p-STAT2, p-RPS6 after 48 h treatment of STAT2-defective mutant Daudi cells with IFNA2c. STAT2-defective mutant Daudi cells were incubated with or without IFNA2c for 48 h. Lanes: (1) molecular weight marker; (2) negative control, untreated cells; (3) IFNA2c (3.6 ng/mL). Data are representative of two individual experiments. Ratios of MAP1LC3 were calculated as the division of the ratio of induced MAP1LC3-I to induced MAP1LC3-II by the ratio of basal MAP1LC3-I to basal MAP1LC3-II, and the numbers are shown below the MAP1LC3 lanes.
Stat2 D261445 0025 Antibody, supplied by Sangon Biotech, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/stat2 d261445-0025 antibody/product/Sangon Biotech
Average 90 stars, based on 1 article reviews
stat2 d261445-0025 antibody - by Bioz Stars, 2026-03
90/100 stars
  Buy from Supplier
p- stat2 (py689) antibody  (Abbexa Ltd)
90
Abbexa Ltd p- stat2 (py689) antibody
Figure 2. IFNA2c induced autophagy in Daudi cells, but not in <t>STAT2-deficient</t> Daudi. ( A ) Direct effect of IFNA2c on induction of autophagy. Daudi cells were cultured for 24 h in supernatants from either mock-treated Daudi cells or cells treated with 0.36 ng/mL of IFNA2c for 24 h in the presence or absence of anti-IFNAR2-mAb A10. Lanes: (1) molecular weight marker; (2) negative control, cells plus supernatant from mock-treated cells; (3) negative control, cells plus supernatant from mock-treated cells and anti-IFNAR2 – mAb A10; (4) cells plus supernatant from IFNA2c-treated cells; (5) cells plus supernatant from IFNA2c-treated cells and anti-IFNAR2 – mAb. Data are representative of two individual experiments. Ratios of MAP1LC3 were calculated as the division of the ratio of induced MAP1LC3-I to induced MAP1LC3-II by the ratio of basal MAP1LC3-I to basal MAP1LC3-II, and the numbers are shown below MAP1LC3 lanes. ( B ) Detection of MAP1LC3-I and MAP1LC3-II, SQSTM1, p-STAT1, p-STAT2, p-RPS6 after 48 h treatment of STAT2-defective mutant Daudi cells with IFNA2c. STAT2-defective mutant Daudi cells were incubated with or without IFNA2c for 48 h. Lanes: (1) molecular weight marker; (2) negative control, untreated cells; (3) IFNA2c (3.6 ng/mL). Data are representative of two individual experiments. Ratios of MAP1LC3 were calculated as the division of the ratio of induced MAP1LC3-I to induced MAP1LC3-II by the ratio of basal MAP1LC3-I to basal MAP1LC3-II, and the numbers are shown below the MAP1LC3 lanes.
P Stat2 (Py689) Antibody, supplied by Abbexa Ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/p- stat2 (py689) antibody/product/Abbexa Ltd
Average 90 stars, based on 1 article reviews
p- stat2 (py689) antibody - by Bioz Stars, 2026-03
90/100 stars
  Buy from Supplier
p-stat2 pab11305 antibody  (Abnova)
90
Abnova p-stat2 pab11305 antibody
Figure 2. IFNA2c induced autophagy in Daudi cells, but not in <t>STAT2-deficient</t> Daudi. ( A ) Direct effect of IFNA2c on induction of autophagy. Daudi cells were cultured for 24 h in supernatants from either mock-treated Daudi cells or cells treated with 0.36 ng/mL of IFNA2c for 24 h in the presence or absence of anti-IFNAR2-mAb A10. Lanes: (1) molecular weight marker; (2) negative control, cells plus supernatant from mock-treated cells; (3) negative control, cells plus supernatant from mock-treated cells and anti-IFNAR2 – mAb A10; (4) cells plus supernatant from IFNA2c-treated cells; (5) cells plus supernatant from IFNA2c-treated cells and anti-IFNAR2 – mAb. Data are representative of two individual experiments. Ratios of MAP1LC3 were calculated as the division of the ratio of induced MAP1LC3-I to induced MAP1LC3-II by the ratio of basal MAP1LC3-I to basal MAP1LC3-II, and the numbers are shown below MAP1LC3 lanes. ( B ) Detection of MAP1LC3-I and MAP1LC3-II, SQSTM1, p-STAT1, p-STAT2, p-RPS6 after 48 h treatment of STAT2-defective mutant Daudi cells with IFNA2c. STAT2-defective mutant Daudi cells were incubated with or without IFNA2c for 48 h. Lanes: (1) molecular weight marker; (2) negative control, untreated cells; (3) IFNA2c (3.6 ng/mL). Data are representative of two individual experiments. Ratios of MAP1LC3 were calculated as the division of the ratio of induced MAP1LC3-I to induced MAP1LC3-II by the ratio of basal MAP1LC3-I to basal MAP1LC3-II, and the numbers are shown below the MAP1LC3 lanes.
P Stat2 Pab11305 Antibody, supplied by Abnova, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/p-stat2 pab11305 antibody/product/Abnova
Average 90 stars, based on 1 article reviews
p-stat2 pab11305 antibody - by Bioz Stars, 2026-03
90/100 stars
  Buy from Supplier

Image Search Results


PEDV-N Interrupts the IFN-I-mediated JAK1/STAT1 Pathway. A. Changes of IFN-α protein. B. Changes of JAK1 protein. C. Changes of TYK2 protein. D. Changes of STAT1 protein. E. Changes of STAT2 protein. F. Changes of P-STAT1 protein at 24 h. G. Changes of P-STAT1 protein at 48 h. H. Changes of P-STAT2 protein. I. Changes of IRF9 protein. J. Changes of ISG15 mRNA levels. K. Changes of ISG54 mRNA levels. L. Changes of ISG56 mRNA levels. The data are presented as the mean ± SEM, ( n = 3). Significant differences between the control and objective groups are indicated as ⁎⁎ p < 0.01 and * p < 0.05.

Journal: Virus Research

Article Title: Angiotensin converting enzyme 2 does not facilitate porcine epidemic diarrhea virus entry into porcine intestinal epithelial cells and inhibits it-induced inflammatory injury by promoting STAT1 phosphorylation

doi: 10.1016/j.virusres.2023.199300

Figure Lengend Snippet: PEDV-N Interrupts the IFN-I-mediated JAK1/STAT1 Pathway. A. Changes of IFN-α protein. B. Changes of JAK1 protein. C. Changes of TYK2 protein. D. Changes of STAT1 protein. E. Changes of STAT2 protein. F. Changes of P-STAT1 protein at 24 h. G. Changes of P-STAT1 protein at 48 h. H. Changes of P-STAT2 protein. I. Changes of IRF9 protein. J. Changes of ISG15 mRNA levels. K. Changes of ISG54 mRNA levels. L. Changes of ISG56 mRNA levels. The data are presented as the mean ± SEM, ( n = 3). Significant differences between the control and objective groups are indicated as ⁎⁎ p < 0.01 and * p < 0.05.

Article Snippet: P-JAK1 (TP56310), TYK2 (PU511505), P-TYK2 (TA7288), P-STAT2 (TP56499) and IRF9 (PH1824) rabbit polyclonal antibody were purchased from Abmart (China).

Techniques:

PEDV Infection Interrupts the IFN-I-mediated JAK1/STAT1 Pathway. A. Changes of IFN-α protein. B. Changes of JAK1 protein. C. Changes of TYK2 protein. D. Changes of STAT1 protein. E. Changes of STAT2 protein. F. Changes of P-STAT1 protein at 24 h. G. Changes of P-STAT1 protein at 48 h. H. Changes of P-STAT2 protein. I. Changes of IRF9 protein. J. Changes of ISG15 mRNA levels. K. Changes of ISG54 mRNA levels. L. Changes of ISG56 mRNA levels. The data are presented as the mean ± SEM, ( n = 3). Significant differences between the control and objective groups are indicated as ⁎⁎ p < 0.01 and * p < 0.05.

Journal: Virus Research

Article Title: Angiotensin converting enzyme 2 does not facilitate porcine epidemic diarrhea virus entry into porcine intestinal epithelial cells and inhibits it-induced inflammatory injury by promoting STAT1 phosphorylation

doi: 10.1016/j.virusres.2023.199300

Figure Lengend Snippet: PEDV Infection Interrupts the IFN-I-mediated JAK1/STAT1 Pathway. A. Changes of IFN-α protein. B. Changes of JAK1 protein. C. Changes of TYK2 protein. D. Changes of STAT1 protein. E. Changes of STAT2 protein. F. Changes of P-STAT1 protein at 24 h. G. Changes of P-STAT1 protein at 48 h. H. Changes of P-STAT2 protein. I. Changes of IRF9 protein. J. Changes of ISG15 mRNA levels. K. Changes of ISG54 mRNA levels. L. Changes of ISG56 mRNA levels. The data are presented as the mean ± SEM, ( n = 3). Significant differences between the control and objective groups are indicated as ⁎⁎ p < 0.01 and * p < 0.05.

Article Snippet: P-JAK1 (TP56310), TYK2 (PU511505), P-TYK2 (TA7288), P-STAT2 (TP56499) and IRF9 (PH1824) rabbit polyclonal antibody were purchased from Abmart (China).

Techniques: Infection

Schematic Diagram of the mechanism of ACE2 inhibits PEDV-induced inflammatory injury by promoting STAT1 phosphorylation. ACE2 can not be used as a functional receptor for PEDV to assist its entry into cells. PEDV (or PEDV-N) induces STAT1 degradation and interrupts STAT1 phosphorylation to inhibit the IFN-I-mediated JAK1/STAT1 signaling pathway. PEDV can activate the Renin-angiotensin system and produce excessive Ang II and pro-inflammatory cytokines. However, ACE2 can promote the phosphorylation of STAT1, further dimerization of P-STAT1 and P-STAT2, and then recruit IRF9 to form ISGF3, which binds to ISRE after entering the nucleus and promotes the expression of ISGs. At the same time, ACE2 can also hydrolyze excessive Ang II to Ang (1–7) into maintain the balance of inflammatory cytokines and alleviate PEDV infection.

Journal: Virus Research

Article Title: Angiotensin converting enzyme 2 does not facilitate porcine epidemic diarrhea virus entry into porcine intestinal epithelial cells and inhibits it-induced inflammatory injury by promoting STAT1 phosphorylation

doi: 10.1016/j.virusres.2023.199300

Figure Lengend Snippet: Schematic Diagram of the mechanism of ACE2 inhibits PEDV-induced inflammatory injury by promoting STAT1 phosphorylation. ACE2 can not be used as a functional receptor for PEDV to assist its entry into cells. PEDV (or PEDV-N) induces STAT1 degradation and interrupts STAT1 phosphorylation to inhibit the IFN-I-mediated JAK1/STAT1 signaling pathway. PEDV can activate the Renin-angiotensin system and produce excessive Ang II and pro-inflammatory cytokines. However, ACE2 can promote the phosphorylation of STAT1, further dimerization of P-STAT1 and P-STAT2, and then recruit IRF9 to form ISGF3, which binds to ISRE after entering the nucleus and promotes the expression of ISGs. At the same time, ACE2 can also hydrolyze excessive Ang II to Ang (1–7) into maintain the balance of inflammatory cytokines and alleviate PEDV infection.

Article Snippet: P-JAK1 (TP56310), TYK2 (PU511505), P-TYK2 (TA7288), P-STAT2 (TP56499) and IRF9 (PH1824) rabbit polyclonal antibody were purchased from Abmart (China).

Techniques: Functional Assay, Expressing, Infection

Figure 2. IFNA2c induced autophagy in Daudi cells, but not in STAT2-deficient Daudi. ( A ) Direct effect of IFNA2c on induction of autophagy. Daudi cells were cultured for 24 h in supernatants from either mock-treated Daudi cells or cells treated with 0.36 ng/mL of IFNA2c for 24 h in the presence or absence of anti-IFNAR2-mAb A10. Lanes: (1) molecular weight marker; (2) negative control, cells plus supernatant from mock-treated cells; (3) negative control, cells plus supernatant from mock-treated cells and anti-IFNAR2 – mAb A10; (4) cells plus supernatant from IFNA2c-treated cells; (5) cells plus supernatant from IFNA2c-treated cells and anti-IFNAR2 – mAb. Data are representative of two individual experiments. Ratios of MAP1LC3 were calculated as the division of the ratio of induced MAP1LC3-I to induced MAP1LC3-II by the ratio of basal MAP1LC3-I to basal MAP1LC3-II, and the numbers are shown below MAP1LC3 lanes. ( B ) Detection of MAP1LC3-I and MAP1LC3-II, SQSTM1, p-STAT1, p-STAT2, p-RPS6 after 48 h treatment of STAT2-defective mutant Daudi cells with IFNA2c. STAT2-defective mutant Daudi cells were incubated with or without IFNA2c for 48 h. Lanes: (1) molecular weight marker; (2) negative control, untreated cells; (3) IFNA2c (3.6 ng/mL). Data are representative of two individual experiments. Ratios of MAP1LC3 were calculated as the division of the ratio of induced MAP1LC3-I to induced MAP1LC3-II by the ratio of basal MAP1LC3-I to basal MAP1LC3-II, and the numbers are shown below the MAP1LC3 lanes.

Journal: Autophagy

Article Title: Type I interferons induce autophagy in certain human cancer cell lines

doi: 10.4161/auto.23921

Figure Lengend Snippet: Figure 2. IFNA2c induced autophagy in Daudi cells, but not in STAT2-deficient Daudi. ( A ) Direct effect of IFNA2c on induction of autophagy. Daudi cells were cultured for 24 h in supernatants from either mock-treated Daudi cells or cells treated with 0.36 ng/mL of IFNA2c for 24 h in the presence or absence of anti-IFNAR2-mAb A10. Lanes: (1) molecular weight marker; (2) negative control, cells plus supernatant from mock-treated cells; (3) negative control, cells plus supernatant from mock-treated cells and anti-IFNAR2 – mAb A10; (4) cells plus supernatant from IFNA2c-treated cells; (5) cells plus supernatant from IFNA2c-treated cells and anti-IFNAR2 – mAb. Data are representative of two individual experiments. Ratios of MAP1LC3 were calculated as the division of the ratio of induced MAP1LC3-I to induced MAP1LC3-II by the ratio of basal MAP1LC3-I to basal MAP1LC3-II, and the numbers are shown below MAP1LC3 lanes. ( B ) Detection of MAP1LC3-I and MAP1LC3-II, SQSTM1, p-STAT1, p-STAT2, p-RPS6 after 48 h treatment of STAT2-defective mutant Daudi cells with IFNA2c. STAT2-defective mutant Daudi cells were incubated with or without IFNA2c for 48 h. Lanes: (1) molecular weight marker; (2) negative control, untreated cells; (3) IFNA2c (3.6 ng/mL). Data are representative of two individual experiments. Ratios of MAP1LC3 were calculated as the division of the ratio of induced MAP1LC3-I to induced MAP1LC3-II by the ratio of basal MAP1LC3-I to basal MAP1LC3-II, and the numbers are shown below the MAP1LC3 lanes.

Article Snippet: STAT2-defective mutant Daudi cells were purchased from KeraFAST (EH0001).

Techniques: Cell Culture, Molecular Weight, Marker, Negative Control, Mutagenesis, Incubation