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affinity-purified rabbit polyclonal anti-stat1 ser-708 antibody (GenScript corporation)

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GenScript corporation affinity-purified rabbit polyclonal anti-stat1 ser-708 antibody

Virus infection induces delayed <t>STAT1</t> <t>Ser-708</t> phosphorylation. A, WT or IKKϵ−/− MEFs were mock-stimulated or stimulated with 100IU/ml IFN-β. Protein lysate was collected 16 h post-IFN stimulation and immunoblotted using p-STAT1 Ser-708, p-STAT1 Ser-727, p-STAT1 Tyr-701, and total STAT1 antibodies. B and C, Sendai and WNV virus infections induce STAT1 Ser-708 phosphorylation. HEK293 cells were infected with 100 HA units/ml SenV (B) or West Nile virus strain Madagascar (WNV-MAD) (C) at an m.o.i. of 1. At the indicated times following infection, protein lysates were collected and immunoblotted for p-STAT1 Ser-708, p-STAT1 Tyr-701, total STAT1, p-IRF-3, total IRF-3, IFIT1, and SenV or WNV. Tubulin and GAPDH were used as loading controls.

Affinity Purified Rabbit Polyclonal Anti Stat1 Ser 708 Antibody, supplied by GenScript corporation, 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/affinity-purified rabbit polyclonal anti-stat1 ser-708 antibody/product/GenScript corporation
Average 90 stars, based on 1 article reviews

affinity-purified rabbit polyclonal anti-stat1 ser-708 antibody - by Bioz Stars, 2026-05

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1) Product Images from "Inhibitor of ?B Kinase ? (IKK?), STAT1, and IFIT2 Proteins Define Novel Innate Immune Effector Pathway against West Nile Virus Infection * "

Article Title: Inhibitor of ?B Kinase ? (IKK?), STAT1, and IFIT2 Proteins Define Novel Innate Immune Effector Pathway against West Nile Virus Infection *

Journal: The Journal of Biological Chemistry

doi: 10.1074/jbc.M111.285205

Virus infection induces delayed STAT1 Ser-708 phosphorylation. A, WT or IKKϵ−/− MEFs were mock-stimulated or stimulated with 100IU/ml IFN-β. Protein lysate was collected 16 h post-IFN stimulation and immunoblotted using p-STAT1 Ser-708, p-STAT1 Ser-727, p-STAT1 Tyr-701, and total STAT1 antibodies. B and C, Sendai and WNV virus infections induce STAT1 Ser-708 phosphorylation. HEK293 cells were infected with 100 HA units/ml SenV (B) or West Nile virus strain Madagascar (WNV-MAD) (C) at an m.o.i. of 1. At the indicated times following infection, protein lysates were collected and immunoblotted for p-STAT1 Ser-708, p-STAT1 Tyr-701, total STAT1, p-IRF-3, total IRF-3, IFIT1, and SenV or WNV. Tubulin and GAPDH were used as loading controls.

Figure Legend Snippet: Virus infection induces delayed STAT1 Ser-708 phosphorylation. A, WT or IKKϵ−/− MEFs were mock-stimulated or stimulated with 100IU/ml IFN-β. Protein lysate was collected 16 h post-IFN stimulation and immunoblotted using p-STAT1 Ser-708, p-STAT1 Ser-727, p-STAT1 Tyr-701, and total STAT1 antibodies. B and C, Sendai and WNV virus infections induce STAT1 Ser-708 phosphorylation. HEK293 cells were infected with 100 HA units/ml SenV (B) or West Nile virus strain Madagascar (WNV-MAD) (C) at an m.o.i. of 1. At the indicated times following infection, protein lysates were collected and immunoblotted for p-STAT1 Ser-708, p-STAT1 Tyr-701, total STAT1, p-IRF-3, total IRF-3, IFIT1, and SenV or WNV. Tubulin and GAPDH were used as loading controls.

Techniques Used: Infection

Type I, type II, and type III IFNs induce STAT1 Ser-708 phosphorylation. 2fTGH cells were mock-treated or treated with 100 IU/ml IFN-β (A) or 50 ng/ml IFN-γ (B). C, PH5CH8 cells were mock-treated (lane 1), treated with 100 ng/ml IFN-λ1 (lanes 2-6), or 100 IU/ml IFN-β (lanes 7-9). Protein lysate was collected at respective time points following IFN treatment and immunoblotted for p-STAT1 Ser-708, p-STAT1 Tyr-701, p-STAT1 Ser-727, total STAT1, ADAR1, and IFIT1.

Figure Legend Snippet: Type I, type II, and type III IFNs induce STAT1 Ser-708 phosphorylation. 2fTGH cells were mock-treated or treated with 100 IU/ml IFN-β (A) or 50 ng/ml IFN-γ (B). C, PH5CH8 cells were mock-treated (lane 1), treated with 100 ng/ml IFN-λ1 (lanes 2-6), or 100 IU/ml IFN-β (lanes 7-9). Protein lysate was collected at respective time points following IFN treatment and immunoblotted for p-STAT1 Ser-708, p-STAT1 Tyr-701, p-STAT1 Ser-727, total STAT1, ADAR1, and IFIT1.

Techniques Used:

Signaling through IFNAR is required for STAT1 Ser-708 phosphorylation following type I IFN treatment or virus infection. WT, IRF-3−/−, or IFNAR−/− (A) and parental 2fTGH cells or their derivative U5A cells (which lack IFNAR) (B) were infected with WNV-MAD at an m.o.i. of 1. Protein lysates were collected at the indicated time points and immunoblotted for p-STAT1 Ser-708, p-STAT1 Tyr-701, p-STAT1 Ser-727, total STAT1, p-IRF-3, total IRF-3, and WNV. C and D, the same cells were also mock-stimulated or stimulated with 100 IU/ml IFN-β for 6 or 16 h. Protein lysates were collected at the indicated time points and immunoblotted for p-STAT1 Ser-708, p-STAT1 Tyr-701, p-STAT1 Ser-727, total STAT1, p-IRF-3, total IRF-3, IFIT2, IFIT3, and IFIT1. Asterisk, nonspecific band.

Figure Legend Snippet: Signaling through IFNAR is required for STAT1 Ser-708 phosphorylation following type I IFN treatment or virus infection. WT, IRF-3−/−, or IFNAR−/− (A) and parental 2fTGH cells or their derivative U5A cells (which lack IFNAR) (B) were infected with WNV-MAD at an m.o.i. of 1. Protein lysates were collected at the indicated time points and immunoblotted for p-STAT1 Ser-708, p-STAT1 Tyr-701, p-STAT1 Ser-727, total STAT1, p-IRF-3, total IRF-3, and WNV. C and D, the same cells were also mock-stimulated or stimulated with 100 IU/ml IFN-β for 6 or 16 h. Protein lysates were collected at the indicated time points and immunoblotted for p-STAT1 Ser-708, p-STAT1 Tyr-701, p-STAT1 Ser-727, total STAT1, p-IRF-3, total IRF-3, IFIT2, IFIT3, and IFIT1. Asterisk, nonspecific band.

Techniques Used: Infection

STAT1 Ser-708 phosphorylation requires de novo protein synthesis, STAT1 tyrosine dephosphorylation, and nuclear export. A, 2fTGH cells were mock-treated (-CHX, lanes 1-5) or treated with CHX (+CHX, lanes 6-11) to block protein synthesis. At 30 min (lanes 6-10) or 16 h (lane 11) following CHX treatment, cells were mock-stimulated (M) or stimulated with IFN-β. Cells were harvested at 10 min as well as 1, 6, and 16 h post-IFN stimulation and immunoblotted to detect p-STAT1 Ser-708, p-STAT1 Tyr-701, total STAT1, ISG15, and IFIT1. B, 2fTGH cells were not treated (NT, lanes 1-3), pretreated with 100 nm LMB (lanes 4-6), or 50 mm pervanadate (Van, lanes 7-9) 1 h before mock stimulation or stimulation with 100 IU/ml IFN-β. Cells were harvested at 1 and 16 h post-stimulation. Immunoblot analysis was performed using p-STAT1 Ser-708, p-STAT1 Tyr-701, p-STAT1 Ser-727, total STAT1, ADAR1, and IFIT1 antibodies.

Figure Legend Snippet: STAT1 Ser-708 phosphorylation requires de novo protein synthesis, STAT1 tyrosine dephosphorylation, and nuclear export. A, 2fTGH cells were mock-treated (-CHX, lanes 1-5) or treated with CHX (+CHX, lanes 6-11) to block protein synthesis. At 30 min (lanes 6-10) or 16 h (lane 11) following CHX treatment, cells were mock-stimulated (M) or stimulated with IFN-β. Cells were harvested at 10 min as well as 1, 6, and 16 h post-IFN stimulation and immunoblotted to detect p-STAT1 Ser-708, p-STAT1 Tyr-701, total STAT1, ISG15, and IFIT1. B, 2fTGH cells were not treated (NT, lanes 1-3), pretreated with 100 nm LMB (lanes 4-6), or 50 mm pervanadate (Van, lanes 7-9) 1 h before mock stimulation or stimulation with 100 IU/ml IFN-β. Cells were harvested at 1 and 16 h post-stimulation. Immunoblot analysis was performed using p-STAT1 Ser-708, p-STAT1 Tyr-701, p-STAT1 Ser-727, total STAT1, ADAR1, and IFIT1 antibodies.

Techniques Used: De-Phosphorylation Assay, Blocking Assay, Western Blot

IKKϵ mediates IFIT2 expression and protection against WNV pathogenesis in vivo. WT Bl6 and IKKϵ−/− mice were mock-infected (PBS only) or infected with 103 pfu of WNV-MAD subcutaneously through footpad injection. A, mice were monitored and scored daily for clinical symptoms over 17 days. Clinical scores from four representative mice per group were graphed. B, spleens from WT or IKKϵ−/− mice, mock-infected or infected with WNV-MAD, were collected at days 4, 6, and 12 post-infection. Protein lysates were extracted by homogenizing spleens with radioimmune precipitation assay buffer and immunoblotted using p-STAT1 Ser-708, p-STAT1 Tyr-701, p-STAT1 Ser-727, total STAT1, IFIT2, IFIT1, WNV, and IKKϵ antibodies. The immunoblot analysis panel is a representative from four mice per infection group.

Figure Legend Snippet: IKKϵ mediates IFIT2 expression and protection against WNV pathogenesis in vivo. WT Bl6 and IKKϵ−/− mice were mock-infected (PBS only) or infected with 103 pfu of WNV-MAD subcutaneously through footpad injection. A, mice were monitored and scored daily for clinical symptoms over 17 days. Clinical scores from four representative mice per group were graphed. B, spleens from WT or IKKϵ−/− mice, mock-infected or infected with WNV-MAD, were collected at days 4, 6, and 12 post-infection. Protein lysates were extracted by homogenizing spleens with radioimmune precipitation assay buffer and immunoblotted using p-STAT1 Ser-708, p-STAT1 Tyr-701, p-STAT1 Ser-727, total STAT1, IFIT2, IFIT1, WNV, and IKKϵ antibodies. The immunoblot analysis panel is a representative from four mice per infection group.

Techniques Used: Expressing, In Vivo, Infection, Injection, Western Blot

A model illustrating that early and late ISGs induction is regulated by multiple STAT1 posttranslational modifications. 1, the canonical JAK-STAT signaling is activated following type I IFN binding to its receptor, which results in STAT1 Tyr-701 phosphorylation, ISGF3 formation, and its nuclear translocation. ISGF3 binding to the ISRE element induces transcription of ISGs. 2, chromatin-bound STAT1 can be phosphorylated by MAPK at residue Ser-727, which induces its sumoylation. 3 and 4, nuclear STAT1 is also acetylated by histone acetyltransferase (HAT) CREB-binding protein (CBP), resulting in recruitment of TCP1, which catalyzes STAT1 tyrosine dephosphorylation. Sumoylated-acetylated STAT1 cycles back to the cytoplasm, and both modifications render STAT1 unable to be further tyrosine-phosphorylated. 5 and 6, type I IFN signaling and unknown IFN-stimulated factor(s) activate IKKϵ phosphorylation of STAT1 Ser-708. 7, STAT1 molecules phosphorylated at Ser-708 can enter the nucleus and induce expression of a specific ISG subset. pY, tyrosine phosphorylation; pS, serine phosphorylation; Ac, acetylation; Su, sumoylation.

Figure Legend Snippet: A model illustrating that early and late ISGs induction is regulated by multiple STAT1 posttranslational modifications. 1, the canonical JAK-STAT signaling is activated following type I IFN binding to its receptor, which results in STAT1 Tyr-701 phosphorylation, ISGF3 formation, and its nuclear translocation. ISGF3 binding to the ISRE element induces transcription of ISGs. 2, chromatin-bound STAT1 can be phosphorylated by MAPK at residue Ser-727, which induces its sumoylation. 3 and 4, nuclear STAT1 is also acetylated by histone acetyltransferase (HAT) CREB-binding protein (CBP), resulting in recruitment of TCP1, which catalyzes STAT1 tyrosine dephosphorylation. Sumoylated-acetylated STAT1 cycles back to the cytoplasm, and both modifications render STAT1 unable to be further tyrosine-phosphorylated. 5 and 6, type I IFN signaling and unknown IFN-stimulated factor(s) activate IKKϵ phosphorylation of STAT1 Ser-708. 7, STAT1 molecules phosphorylated at Ser-708 can enter the nucleus and induce expression of a specific ISG subset. pY, tyrosine phosphorylation; pS, serine phosphorylation; Ac, acetylation; Su, sumoylation.

Techniques Used: Binding Assay, Translocation Assay, De-Phosphorylation Assay, Expressing

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Journal: The Journal of Biological Chemistry

Article Title: Inhibitor of ?B Kinase ? (IKK?), STAT1, and IFIT2 Proteins Define Novel Innate Immune Effector Pathway against West Nile Virus Infection *

doi: 10.1074/jbc.M111.285205

Figure Lengend Snippet: Virus infection induces delayed STAT1 Ser-708 phosphorylation. A, WT or IKKϵ−/− MEFs were mock-stimulated or stimulated with 100IU/ml IFN-β. Protein lysate was collected 16 h post-IFN stimulation and immunoblotted using p-STAT1 Ser-708, p-STAT1 Ser-727, p-STAT1 Tyr-701, and total STAT1 antibodies. B and C, Sendai and WNV virus infections induce STAT1 Ser-708 phosphorylation. HEK293 cells were infected with 100 HA units/ml SenV (B) or West Nile virus strain Madagascar (WNV-MAD) (C) at an m.o.i. of 1. At the indicated times following infection, protein lysates were collected and immunoblotted for p-STAT1 Ser-708, p-STAT1 Tyr-701, total STAT1, p-IRF-3, total IRF-3, IFIT1, and SenV or WNV. Tubulin and GAPDH were used as loading controls.

Article Snippet: Affinity-purified rabbit polyclonal anti-STAT1 Ser-708 antibody was generated by repeat-immunization with the STAT1 Ser-708 phospho-specific peptide (YIKTELI{pS}VSEVHP, amino acids 701–714) (GenScript).

Techniques: Infection

Journal: The Journal of Biological Chemistry

Article Title: Inhibitor of ?B Kinase ? (IKK?), STAT1, and IFIT2 Proteins Define Novel Innate Immune Effector Pathway against West Nile Virus Infection *

doi: 10.1074/jbc.M111.285205

Figure Lengend Snippet: Type I, type II, and type III IFNs induce STAT1 Ser-708 phosphorylation. 2fTGH cells were mock-treated or treated with 100 IU/ml IFN-β (A) or 50 ng/ml IFN-γ (B). C, PH5CH8 cells were mock-treated (lane 1), treated with 100 ng/ml IFN-λ1 (lanes 2-6), or 100 IU/ml IFN-β (lanes 7-9). Protein lysate was collected at respective time points following IFN treatment and immunoblotted for p-STAT1 Ser-708, p-STAT1 Tyr-701, p-STAT1 Ser-727, total STAT1, ADAR1, and IFIT1.

Techniques:

Journal: The Journal of Biological Chemistry

Article Title: Inhibitor of ?B Kinase ? (IKK?), STAT1, and IFIT2 Proteins Define Novel Innate Immune Effector Pathway against West Nile Virus Infection *

doi: 10.1074/jbc.M111.285205

Figure Lengend Snippet: Signaling through IFNAR is required for STAT1 Ser-708 phosphorylation following type I IFN treatment or virus infection. WT, IRF-3−/−, or IFNAR−/− (A) and parental 2fTGH cells or their derivative U5A cells (which lack IFNAR) (B) were infected with WNV-MAD at an m.o.i. of 1. Protein lysates were collected at the indicated time points and immunoblotted for p-STAT1 Ser-708, p-STAT1 Tyr-701, p-STAT1 Ser-727, total STAT1, p-IRF-3, total IRF-3, and WNV. C and D, the same cells were also mock-stimulated or stimulated with 100 IU/ml IFN-β for 6 or 16 h. Protein lysates were collected at the indicated time points and immunoblotted for p-STAT1 Ser-708, p-STAT1 Tyr-701, p-STAT1 Ser-727, total STAT1, p-IRF-3, total IRF-3, IFIT2, IFIT3, and IFIT1. Asterisk, nonspecific band.

Techniques: Infection

Journal: The Journal of Biological Chemistry

Article Title: Inhibitor of ?B Kinase ? (IKK?), STAT1, and IFIT2 Proteins Define Novel Innate Immune Effector Pathway against West Nile Virus Infection *

doi: 10.1074/jbc.M111.285205

Figure Lengend Snippet: STAT1 Ser-708 phosphorylation requires de novo protein synthesis, STAT1 tyrosine dephosphorylation, and nuclear export. A, 2fTGH cells were mock-treated (-CHX, lanes 1-5) or treated with CHX (+CHX, lanes 6-11) to block protein synthesis. At 30 min (lanes 6-10) or 16 h (lane 11) following CHX treatment, cells were mock-stimulated (M) or stimulated with IFN-β. Cells were harvested at 10 min as well as 1, 6, and 16 h post-IFN stimulation and immunoblotted to detect p-STAT1 Ser-708, p-STAT1 Tyr-701, total STAT1, ISG15, and IFIT1. B, 2fTGH cells were not treated (NT, lanes 1-3), pretreated with 100 nm LMB (lanes 4-6), or 50 mm pervanadate (Van, lanes 7-9) 1 h before mock stimulation or stimulation with 100 IU/ml IFN-β. Cells were harvested at 1 and 16 h post-stimulation. Immunoblot analysis was performed using p-STAT1 Ser-708, p-STAT1 Tyr-701, p-STAT1 Ser-727, total STAT1, ADAR1, and IFIT1 antibodies.

Techniques: De-Phosphorylation Assay, Blocking Assay, Western Blot

Journal: The Journal of Biological Chemistry

Article Title: Inhibitor of ?B Kinase ? (IKK?), STAT1, and IFIT2 Proteins Define Novel Innate Immune Effector Pathway against West Nile Virus Infection *

doi: 10.1074/jbc.M111.285205

Figure Lengend Snippet: IKKϵ mediates IFIT2 expression and protection against WNV pathogenesis in vivo. WT Bl6 and IKKϵ−/− mice were mock-infected (PBS only) or infected with 103 pfu of WNV-MAD subcutaneously through footpad injection. A, mice were monitored and scored daily for clinical symptoms over 17 days. Clinical scores from four representative mice per group were graphed. B, spleens from WT or IKKϵ−/− mice, mock-infected or infected with WNV-MAD, were collected at days 4, 6, and 12 post-infection. Protein lysates were extracted by homogenizing spleens with radioimmune precipitation assay buffer and immunoblotted using p-STAT1 Ser-708, p-STAT1 Tyr-701, p-STAT1 Ser-727, total STAT1, IFIT2, IFIT1, WNV, and IKKϵ antibodies. The immunoblot analysis panel is a representative from four mice per infection group.

Techniques: Expressing, In Vivo, Infection, Injection, Western Blot

Journal: The Journal of Biological Chemistry

Article Title: Inhibitor of ?B Kinase ? (IKK?), STAT1, and IFIT2 Proteins Define Novel Innate Immune Effector Pathway against West Nile Virus Infection *

doi: 10.1074/jbc.M111.285205

Figure Lengend Snippet: A model illustrating that early and late ISGs induction is regulated by multiple STAT1 posttranslational modifications. 1, the canonical JAK-STAT signaling is activated following type I IFN binding to its receptor, which results in STAT1 Tyr-701 phosphorylation, ISGF3 formation, and its nuclear translocation. ISGF3 binding to the ISRE element induces transcription of ISGs. 2, chromatin-bound STAT1 can be phosphorylated by MAPK at residue Ser-727, which induces its sumoylation. 3 and 4, nuclear STAT1 is also acetylated by histone acetyltransferase (HAT) CREB-binding protein (CBP), resulting in recruitment of TCP1, which catalyzes STAT1 tyrosine dephosphorylation. Sumoylated-acetylated STAT1 cycles back to the cytoplasm, and both modifications render STAT1 unable to be further tyrosine-phosphorylated. 5 and 6, type I IFN signaling and unknown IFN-stimulated factor(s) activate IKKϵ phosphorylation of STAT1 Ser-708. 7, STAT1 molecules phosphorylated at Ser-708 can enter the nucleus and induce expression of a specific ISG subset. pY, tyrosine phosphorylation; pS, serine phosphorylation; Ac, acetylation; Su, sumoylation.

Techniques: Binding Assay, Translocation Assay, De-Phosphorylation Assay, Expressing

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1) Product Images from "Inhibitor of ?B Kinase ? (IKK?), STAT1, and IFIT2 Proteins Define Novel Innate Immune Effector Pathway against West Nile Virus Infection * "

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