stat1 β β mice  (Millipore)

 
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    Name:
    STAT1 beta
    Description:
    STAT1beta is a member of the signal transducers and activators of transcription STAT family of proteins that carry out a dual function signal transduction and activation of transcription STAT1beta transcription factor is specific for the IFN pathway and plays a central role in mediating many if not all IFN dependent biological responses Presence of STAT1beta leads to an efficient antiviral response when cells were infected with virus suggesting that a STAT dependent pathway is activated following virus infection by endogenously produced IFN Virus induced STAT protein translocation from the cytoplasmic compartment can be detected within 3 h of infection
    Catalog Number:
    SRP5137
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    None
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    Structured Review

    Millipore stat1 β β mice
    STAT1 beta
    STAT1beta is a member of the signal transducers and activators of transcription STAT family of proteins that carry out a dual function signal transduction and activation of transcription STAT1beta transcription factor is specific for the IFN pathway and plays a central role in mediating many if not all IFN dependent biological responses Presence of STAT1beta leads to an efficient antiviral response when cells were infected with virus suggesting that a STAT dependent pathway is activated following virus infection by endogenously produced IFN Virus induced STAT protein translocation from the cytoplasmic compartment can be detected within 3 h of infection
    https://www.bioz.com/result/stat1 β β mice/product/Millipore
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    stat1 β β mice - by Bioz Stars, 2021-07
    86/100 stars

    Images

    1) Product Images from "STAT1β Is Not Dominant Negative and Is Capable of Contributing to Gamma Interferon-Dependent Innate Immunity"

    Article Title: STAT1β Is Not Dominant Negative and Is Capable of Contributing to Gamma Interferon-Dependent Innate Immunity

    Journal: Molecular and Cellular Biology

    doi: 10.1128/MCB.00295-14

    STAT1β shows prolonged tyrosine 701 phosphorylation. (A to D) BMMϕ derived from WT (+/+), Stat1 β/β (β/β), and Stat1 α/α (α/α) mice were stimulated with IFN-β (A) or
    Figure Legend Snippet: STAT1β shows prolonged tyrosine 701 phosphorylation. (A to D) BMMϕ derived from WT (+/+), Stat1 β/β (β/β), and Stat1 α/α (α/α) mice were stimulated with IFN-β (A) or

    Techniques Used: Derivative Assay, Mouse Assay

    STAT1β shows prolonged nuclear localization and prolonged promoter binding after IFN-γ treatment compared to STAT1α. (A) BMMϕ derived from WT (+/+), Stat1 β/β (β/β), and Stat1 α/α
    Figure Legend Snippet: STAT1β shows prolonged nuclear localization and prolonged promoter binding after IFN-γ treatment compared to STAT1α. (A) BMMϕ derived from WT (+/+), Stat1 β/β (β/β), and Stat1 α/α

    Techniques Used: Binding Assay, Derivative Assay

    STAT1α and STAT1β can mediate type I and type III IFN-dependent antiviral immunity in vivo . (A) EMCV (50 PFU/mouse) was administered i.p. to WT ( Stat1 +/+ ), Stat1 β/β , Stat1 α/α , and Stat1 −/−
    Figure Legend Snippet: STAT1α and STAT1β can mediate type I and type III IFN-dependent antiviral immunity in vivo . (A) EMCV (50 PFU/mouse) was administered i.p. to WT ( Stat1 +/+ ), Stat1 β/β , Stat1 α/α , and Stat1 −/−

    Techniques Used: In Vivo

    STAT1β is transcriptionally active in response to IFN-β and IFN-γ. BMMϕ isolated from WT (+/+), Stat1 β/β (β/β), Stat1 α/α (α/α), and Stat1 −/−
    Figure Legend Snippet: STAT1β is transcriptionally active in response to IFN-β and IFN-γ. BMMϕ isolated from WT (+/+), Stat1 β/β (β/β), Stat1 α/α (α/α), and Stat1 −/−

    Techniques Used: Isolation

    STAT1α and STAT1β show differential efficiencies in immune defense against MCMV and L. monocytogenes infections. (A) WT ( Stat1 +/+ ), Stat1 β/β , Stat1 α/α , and Stat1 −/− mice were infected i.p.
    Figure Legend Snippet: STAT1α and STAT1β show differential efficiencies in immune defense against MCMV and L. monocytogenes infections. (A) WT ( Stat1 +/+ ), Stat1 β/β , Stat1 α/α , and Stat1 −/− mice were infected i.p.

    Techniques Used: Mouse Assay, Infection

    Transcriptional activities of STAT1α and STAT1β overlap but are nonredundant. BMMϕ isolated from WT (+/+), Stat1 β/β (β/β), Stat1 α/α (α/α), and Stat1 −/−
    Figure Legend Snippet: Transcriptional activities of STAT1α and STAT1β overlap but are nonredundant. BMMϕ isolated from WT (+/+), Stat1 β/β (β/β), Stat1 α/α (α/α), and Stat1 −/−

    Techniques Used: Isolation

    Related Articles

    Mouse Assay:

    Article Title: STAT1β Is Not Dominant Negative and Is Capable of Contributing to Gamma Interferon-Dependent Innate Immunity
    Article Snippet: Isolated DNAs from ES cell clones were used as templates. .. Genetic screening of WT, Stat1 α/α , and Stat1 β/β mice was performed by a duplex PCR with primers (purchased from Sigma-Aldrich) using DNA from mouse tail biopsy specimens. ..

    Polymerase Chain Reaction:

    Article Title: STAT1β Is Not Dominant Negative and Is Capable of Contributing to Gamma Interferon-Dependent Innate Immunity
    Article Snippet: Isolated DNAs from ES cell clones were used as templates. .. Genetic screening of WT, Stat1 α/α , and Stat1 β/β mice was performed by a duplex PCR with primers (purchased from Sigma-Aldrich) using DNA from mouse tail biopsy specimens. ..

    Binding Assay:

    Article Title: Nuclear export signal located within theDNA-binding domain of the STAT1transcription factor
    Article Snippet: STAT1 antibody was incubated with extract prior to addition of probe ( ). .. A 15 µg aliquot of bacterially expressed GST, GST–STAT1, GST–NESPKI or the corresponding GST–STAT1 fragment protein was bound to glutathione–agarose beads (Sigma) pre-blocked with 1% bovine serum albumin and then washed in binding buffer (50 mM HEPES pH 7.9, 200 mM KCl, 5 mM MgCl2 , 2 mM β-mercaptoethanol, 0.4% Tween-20, 0.4% milk, 2 mM GTP). .. Protein–beads were incubated with CRM1 translated in vitro in the presence of [35 S]methionine (TNT T7 Quick Coupled Transcription/Translation System, Promega) and 5 µg of purified Ran Q69L in 50 µl of binding buffer for 2 h at 4°C.

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    Millipore purified mouse anti total stat1
    Proposed mechanism of signaling pathways initiated by C 4 .T 4 in macrophages. (A) C 4 .T 4 signaling activated RELA/NFKB through MYD88 pathway and enhanced cytokine secretion, which received positive feedback through phosphorylated PtdIns3K, <t>STAT1</t> and activated BCL2L1. Consequently, these macrophages induced autophagy, activated cells, and increased cell survival. This mechanism played a key role in controlling the growth of Mtb . (B) Schematic representation of C 4 .T 4 -mediated clearance of Mtb through modulation of autophagy and lysosomal biogenesis.
    Purified Mouse Anti Total Stat1, supplied by Millipore, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/purified mouse anti total stat1/product/Millipore
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    purified mouse anti total stat1 - by Bioz Stars, 2021-07
    97/100 stars
      Buy from Supplier

    86
    Millipore stat1 β β mice
    STAT1β shows prolonged tyrosine 701 phosphorylation. (A to D) BMMϕ derived from WT (+/+), <t>Stat1</t> <t>β/β</t> (β/β), and Stat1 α/α (α/α) mice were stimulated with IFN-β (A) or
    Stat1 β β Mice, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/stat1 β β mice/product/Millipore
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    stat1 β β mice - by Bioz Stars, 2021-07
    86/100 stars
      Buy from Supplier

    Image Search Results


    Proposed mechanism of signaling pathways initiated by C 4 .T 4 in macrophages. (A) C 4 .T 4 signaling activated RELA/NFKB through MYD88 pathway and enhanced cytokine secretion, which received positive feedback through phosphorylated PtdIns3K, STAT1 and activated BCL2L1. Consequently, these macrophages induced autophagy, activated cells, and increased cell survival. This mechanism played a key role in controlling the growth of Mtb . (B) Schematic representation of C 4 .T 4 -mediated clearance of Mtb through modulation of autophagy and lysosomal biogenesis.

    Journal: Autophagy

    Article Title: Induction of autophagy through CLEC4E in combination with TLR4: an innovative strategy to restrict the survival of Mycobacterium tuberculosis

    doi: 10.1080/15548627.2019.1658436

    Figure Lengend Snippet: Proposed mechanism of signaling pathways initiated by C 4 .T 4 in macrophages. (A) C 4 .T 4 signaling activated RELA/NFKB through MYD88 pathway and enhanced cytokine secretion, which received positive feedback through phosphorylated PtdIns3K, STAT1 and activated BCL2L1. Consequently, these macrophages induced autophagy, activated cells, and increased cell survival. This mechanism played a key role in controlling the growth of Mtb . (B) Schematic representation of C 4 .T 4 -mediated clearance of Mtb through modulation of autophagy and lysosomal biogenesis.

    Article Snippet: Other reagents were procured from the specified companies: inhibitors against PtdIns3K (Ly294002; Sigma Aldrich, 440202) and NOS2 [NM] (Calbiochem, 475886), FlexiTube siRNA-specific for mouse Becn1 (Qiagen, GS56208), acridine orange (Sigma Aldrich, A6014), monodansylcadaverine (Sigma Aldrich, D4008), rabbit polyclonal Ab against LC3 (Sigma Aldrich, L8918), anti-ACTB antibody (Sigma Aldrich, A1978), p-STAT1 (BD Pharmingen, 612232), STAT1 (BD Pharmingen, 610115), LysoTracker Red (Life Technologies, L-7528), anti-fade reagent (Life Technologies, ), dihydrorhodamine 123 (Sigma Aldrich, D1054), 4′,6-diamidino-2-phenylindole dihydrochloride (DAPI; Sigma Aldrich, D8417), 3-methyladenine (3MA; Sigma Aldrich, M9281), rapamycin (Sigma Aldrich, B1793), 5(6)-carboxyfluorescein diacetate N-succinimidyl ester (CFSE; Sigma Aldrich, 21888F), phorbol 12-myristate 13-acetate (PMA; Calbiochem, 524400), DMSO (Sigma Aldrich, D8418), RELA/NFKB consensus oligonucleotide (Promega, E3292), paraformaldehyde (Sigma Aldrich, P6148), Griess reagent (Sigma Aldrich, G4410), poly-L-lysine solution (Sigma Aldrich, P8920), HBSS (GIBCO, 14185052), isoniazid (Sigma Aldrich, 13377), rifampicin (Sigma Aldrich, R3501), bovine serum albumin (BSA) (Sigma Aldrich, A0281), Triton™ X-100 solution (Sigma Aldrich, 93443), glycerol (Sigma Aldrich, G5516), TWEEN 20 (Sigma Aldrich, P9416), TWEEN 80 (Sigma Aldrich, P4780), avidin–peroxidase (Sigma Aldrich, A7419), o-Phenylenediamine (Sigma Aldrich, P9029), Middlebrook 7H9 broth (Difco-Becton Dickinson, 271310), Middlebrook 7H11 agar (Difco-Becton Dickinson, 283810), Middlebrook OADC growth supplement (Sigma Aldrich, M0678), saponin (Sigma Aldrich, 84510), PVDF western blotting membranes (Sigma Aldrich, 3010040001), amikacin hydrate (Sigma Aldrich, A3650), sodium nitrite (Sigma Aldrich, 237213), phenylmethanesulfonyl fluoride (PMSF; Sigma Aldrich, 78830), protease and phosphatase inhibitor cocktail (Sigma Aldrich, PPC1010).

    Techniques:

    C 4 .T 4 induced phosphorylation of STAT1, PtdIns3K and enhanced nuclear translocation of RELA/NFKB. Macrophages were infected with H37Rv for 4 h and cultured with C 4 .T 4 for 15–30 min and 24 h. The cell lysate was prepared, and western blot was performed to monitor the expression of (A) p-STAT1; (B) p-PtdIns3K; (C) BCL2L1. The densitometry data represent fold change. The ratio for untreated cells was considered to be 1. LPS was used as a positive control. UI, uninfected; UT, untreated and Mtb- infected; C 4 , CLEC4E agonist (TDB); T 4 , TLR4 agonist (ultra-pure LPS). The data are representative of 2–3 independent experiments. (D–G) BMDMs were stimulated with C 4 (24 µg/ml) and T 4 (10 ng/ml) individually or in combination (C 4 .T 4 ) for 30 min. (D) Nuclear translocation of RELA/NFKB was monitored by EMSA. The data were graphed as fold change in the form of a bar diagram. Unstimulated cells were considered as 1. FP, free probe; US, unstimulated. The data are shown as the mean ± SEM and are from 2 independent experiments. Data were analyzed by one-way ANOVA repeated measure. ***p ≤ 0.001, ****p ≤ 0.0001. (E) Translocation of RELA/NFKB p65 into the nucleus was further monitored by confocal microscopy and (F,G) the generation of ROS was observed by flow cytometry after labeling with dihydrorhodamine 123 dye. (F) The histogram depicted ROS generation (percentage). (G) The bar diagram represented integrated MFI of ROS generation. The data represented in each histogram or contour plot depicted the percentage of cells from the ADGRE1/F4/80 gated population. US, unstimulated; UT, untreated and Mtb- infected; C 4 , CLEC4E agonist (TDB); T 4 , TLR4 agonist (ultra-pure LPS). The integrated MFI (iMFI) is calculated by multiplying the relative frequency (% positive population) of cells generating ROS with the mean fluorescence intensity (MFI) of that population. Data are shown as the mean ± SD and are representative of 2–3 independent experiments. Data were analyzed by one-way ANOVA repeated measure. *p ≤ 0.05.

    Journal: Autophagy

    Article Title: Induction of autophagy through CLEC4E in combination with TLR4: an innovative strategy to restrict the survival of Mycobacterium tuberculosis

    doi: 10.1080/15548627.2019.1658436

    Figure Lengend Snippet: C 4 .T 4 induced phosphorylation of STAT1, PtdIns3K and enhanced nuclear translocation of RELA/NFKB. Macrophages were infected with H37Rv for 4 h and cultured with C 4 .T 4 for 15–30 min and 24 h. The cell lysate was prepared, and western blot was performed to monitor the expression of (A) p-STAT1; (B) p-PtdIns3K; (C) BCL2L1. The densitometry data represent fold change. The ratio for untreated cells was considered to be 1. LPS was used as a positive control. UI, uninfected; UT, untreated and Mtb- infected; C 4 , CLEC4E agonist (TDB); T 4 , TLR4 agonist (ultra-pure LPS). The data are representative of 2–3 independent experiments. (D–G) BMDMs were stimulated with C 4 (24 µg/ml) and T 4 (10 ng/ml) individually or in combination (C 4 .T 4 ) for 30 min. (D) Nuclear translocation of RELA/NFKB was monitored by EMSA. The data were graphed as fold change in the form of a bar diagram. Unstimulated cells were considered as 1. FP, free probe; US, unstimulated. The data are shown as the mean ± SEM and are from 2 independent experiments. Data were analyzed by one-way ANOVA repeated measure. ***p ≤ 0.001, ****p ≤ 0.0001. (E) Translocation of RELA/NFKB p65 into the nucleus was further monitored by confocal microscopy and (F,G) the generation of ROS was observed by flow cytometry after labeling with dihydrorhodamine 123 dye. (F) The histogram depicted ROS generation (percentage). (G) The bar diagram represented integrated MFI of ROS generation. The data represented in each histogram or contour plot depicted the percentage of cells from the ADGRE1/F4/80 gated population. US, unstimulated; UT, untreated and Mtb- infected; C 4 , CLEC4E agonist (TDB); T 4 , TLR4 agonist (ultra-pure LPS). The integrated MFI (iMFI) is calculated by multiplying the relative frequency (% positive population) of cells generating ROS with the mean fluorescence intensity (MFI) of that population. Data are shown as the mean ± SD and are representative of 2–3 independent experiments. Data were analyzed by one-way ANOVA repeated measure. *p ≤ 0.05.

    Article Snippet: Other reagents were procured from the specified companies: inhibitors against PtdIns3K (Ly294002; Sigma Aldrich, 440202) and NOS2 [NM] (Calbiochem, 475886), FlexiTube siRNA-specific for mouse Becn1 (Qiagen, GS56208), acridine orange (Sigma Aldrich, A6014), monodansylcadaverine (Sigma Aldrich, D4008), rabbit polyclonal Ab against LC3 (Sigma Aldrich, L8918), anti-ACTB antibody (Sigma Aldrich, A1978), p-STAT1 (BD Pharmingen, 612232), STAT1 (BD Pharmingen, 610115), LysoTracker Red (Life Technologies, L-7528), anti-fade reagent (Life Technologies, ), dihydrorhodamine 123 (Sigma Aldrich, D1054), 4′,6-diamidino-2-phenylindole dihydrochloride (DAPI; Sigma Aldrich, D8417), 3-methyladenine (3MA; Sigma Aldrich, M9281), rapamycin (Sigma Aldrich, B1793), 5(6)-carboxyfluorescein diacetate N-succinimidyl ester (CFSE; Sigma Aldrich, 21888F), phorbol 12-myristate 13-acetate (PMA; Calbiochem, 524400), DMSO (Sigma Aldrich, D8418), RELA/NFKB consensus oligonucleotide (Promega, E3292), paraformaldehyde (Sigma Aldrich, P6148), Griess reagent (Sigma Aldrich, G4410), poly-L-lysine solution (Sigma Aldrich, P8920), HBSS (GIBCO, 14185052), isoniazid (Sigma Aldrich, 13377), rifampicin (Sigma Aldrich, R3501), bovine serum albumin (BSA) (Sigma Aldrich, A0281), Triton™ X-100 solution (Sigma Aldrich, 93443), glycerol (Sigma Aldrich, G5516), TWEEN 20 (Sigma Aldrich, P9416), TWEEN 80 (Sigma Aldrich, P4780), avidin–peroxidase (Sigma Aldrich, A7419), o-Phenylenediamine (Sigma Aldrich, P9029), Middlebrook 7H9 broth (Difco-Becton Dickinson, 271310), Middlebrook 7H11 agar (Difco-Becton Dickinson, 283810), Middlebrook OADC growth supplement (Sigma Aldrich, M0678), saponin (Sigma Aldrich, 84510), PVDF western blotting membranes (Sigma Aldrich, 3010040001), amikacin hydrate (Sigma Aldrich, A3650), sodium nitrite (Sigma Aldrich, 237213), phenylmethanesulfonyl fluoride (PMSF; Sigma Aldrich, 78830), protease and phosphatase inhibitor cocktail (Sigma Aldrich, PPC1010).

    Techniques: Translocation Assay, Infection, Cell Culture, Western Blot, Expressing, Positive Control, Confocal Microscopy, Flow Cytometry, Labeling, Fluorescence

    STAT1β shows prolonged tyrosine 701 phosphorylation. (A to D) BMMϕ derived from WT (+/+), Stat1 β/β (β/β), and Stat1 α/α (α/α) mice were stimulated with IFN-β (A) or

    Journal: Molecular and Cellular Biology

    Article Title: STAT1β Is Not Dominant Negative and Is Capable of Contributing to Gamma Interferon-Dependent Innate Immunity

    doi: 10.1128/MCB.00295-14

    Figure Lengend Snippet: STAT1β shows prolonged tyrosine 701 phosphorylation. (A to D) BMMϕ derived from WT (+/+), Stat1 β/β (β/β), and Stat1 α/α (α/α) mice were stimulated with IFN-β (A) or

    Article Snippet: Genetic screening of WT, Stat1 α/α , and Stat1 β/β mice was performed by a duplex PCR with primers (purchased from Sigma-Aldrich) using DNA from mouse tail biopsy specimens.

    Techniques: Derivative Assay, Mouse Assay

    STAT1β shows prolonged nuclear localization and prolonged promoter binding after IFN-γ treatment compared to STAT1α. (A) BMMϕ derived from WT (+/+), Stat1 β/β (β/β), and Stat1 α/α

    Journal: Molecular and Cellular Biology

    Article Title: STAT1β Is Not Dominant Negative and Is Capable of Contributing to Gamma Interferon-Dependent Innate Immunity

    doi: 10.1128/MCB.00295-14

    Figure Lengend Snippet: STAT1β shows prolonged nuclear localization and prolonged promoter binding after IFN-γ treatment compared to STAT1α. (A) BMMϕ derived from WT (+/+), Stat1 β/β (β/β), and Stat1 α/α

    Article Snippet: Genetic screening of WT, Stat1 α/α , and Stat1 β/β mice was performed by a duplex PCR with primers (purchased from Sigma-Aldrich) using DNA from mouse tail biopsy specimens.

    Techniques: Binding Assay, Derivative Assay

    STAT1α and STAT1β can mediate type I and type III IFN-dependent antiviral immunity in vivo . (A) EMCV (50 PFU/mouse) was administered i.p. to WT ( Stat1 +/+ ), Stat1 β/β , Stat1 α/α , and Stat1 −/−

    Journal: Molecular and Cellular Biology

    Article Title: STAT1β Is Not Dominant Negative and Is Capable of Contributing to Gamma Interferon-Dependent Innate Immunity

    doi: 10.1128/MCB.00295-14

    Figure Lengend Snippet: STAT1α and STAT1β can mediate type I and type III IFN-dependent antiviral immunity in vivo . (A) EMCV (50 PFU/mouse) was administered i.p. to WT ( Stat1 +/+ ), Stat1 β/β , Stat1 α/α , and Stat1 −/−

    Article Snippet: Genetic screening of WT, Stat1 α/α , and Stat1 β/β mice was performed by a duplex PCR with primers (purchased from Sigma-Aldrich) using DNA from mouse tail biopsy specimens.

    Techniques: In Vivo

    STAT1β is transcriptionally active in response to IFN-β and IFN-γ. BMMϕ isolated from WT (+/+), Stat1 β/β (β/β), Stat1 α/α (α/α), and Stat1 −/−

    Journal: Molecular and Cellular Biology

    Article Title: STAT1β Is Not Dominant Negative and Is Capable of Contributing to Gamma Interferon-Dependent Innate Immunity

    doi: 10.1128/MCB.00295-14

    Figure Lengend Snippet: STAT1β is transcriptionally active in response to IFN-β and IFN-γ. BMMϕ isolated from WT (+/+), Stat1 β/β (β/β), Stat1 α/α (α/α), and Stat1 −/−

    Article Snippet: Genetic screening of WT, Stat1 α/α , and Stat1 β/β mice was performed by a duplex PCR with primers (purchased from Sigma-Aldrich) using DNA from mouse tail biopsy specimens.

    Techniques: Isolation

    STAT1α and STAT1β show differential efficiencies in immune defense against MCMV and L. monocytogenes infections. (A) WT ( Stat1 +/+ ), Stat1 β/β , Stat1 α/α , and Stat1 −/− mice were infected i.p.

    Journal: Molecular and Cellular Biology

    Article Title: STAT1β Is Not Dominant Negative and Is Capable of Contributing to Gamma Interferon-Dependent Innate Immunity

    doi: 10.1128/MCB.00295-14

    Figure Lengend Snippet: STAT1α and STAT1β show differential efficiencies in immune defense against MCMV and L. monocytogenes infections. (A) WT ( Stat1 +/+ ), Stat1 β/β , Stat1 α/α , and Stat1 −/− mice were infected i.p.

    Article Snippet: Genetic screening of WT, Stat1 α/α , and Stat1 β/β mice was performed by a duplex PCR with primers (purchased from Sigma-Aldrich) using DNA from mouse tail biopsy specimens.

    Techniques: Mouse Assay, Infection

    Transcriptional activities of STAT1α and STAT1β overlap but are nonredundant. BMMϕ isolated from WT (+/+), Stat1 β/β (β/β), Stat1 α/α (α/α), and Stat1 −/−

    Journal: Molecular and Cellular Biology

    Article Title: STAT1β Is Not Dominant Negative and Is Capable of Contributing to Gamma Interferon-Dependent Innate Immunity

    doi: 10.1128/MCB.00295-14

    Figure Lengend Snippet: Transcriptional activities of STAT1α and STAT1β overlap but are nonredundant. BMMϕ isolated from WT (+/+), Stat1 β/β (β/β), Stat1 α/α (α/α), and Stat1 −/−

    Article Snippet: Genetic screening of WT, Stat1 α/α , and Stat1 β/β mice was performed by a duplex PCR with primers (purchased from Sigma-Aldrich) using DNA from mouse tail biopsy specimens.

    Techniques: Isolation