stat3 expression  (Cell Signaling Technology Inc)

 
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 99
    Name:
    Stat3 Antibody
    Description:
    The Stat3 transcription factor is an important signaling molecule for many cytokines and growth factor receptors 1 and is required for murine fetal development 2 Research studies have shown that Stat3 is constitutively activated in a number of human tumors 3 4 and possesses oncogenic potential 5 and anti apoptotic activities 3 Stat3 is activated by phosphorylation at Tyr705 which induces dimerization nuclear translocation and DNA binding 6 7 Transcriptional activation seems to be regulated by phosphorylation at Ser727 through the MAPK or mTOR pathways 8 9 Stat3 isoform expression appears to reflect biological function as the relative expression levels of Stat3α 86 kDa and Stat3β 79 kDa depend on cell type ligand exposure or cell maturation stage 10 It is notable that Stat3β lacks the serine phosphorylation site within the carboxy terminal transcriptional activation domain 8
    Catalog Number:
    9132
    Price:
    None
    Category:
    Primary Antibodies
    Source:
    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to the sequence of mouse Stat3. Antibodies are purified by protein A and peptide affinity chromatography.
    Buy from Supplier


    Structured Review

    Cell Signaling Technology Inc stat3 expression
    Rho-kinase (ROCK) inhibition potentiates <t>Stat3-ca-induced</t> axonal regeneration in the optic nerve and changes the pattern of fiber growth. The ROCK blocker Y27632 was administered intravitreally in adult mice treated with AAV2.Stat3-ca or in mice that were not injected with viruses. ( a–d ) On top- and side-view projections of whole optic nerves, the combination of AAV2.Stat3-ca and Y27632 activated the growth of strikingly long and straight axons ( a and b ) while Y27632 by itself had no effects ( c and d ). ( e ) Quantitatively, the number of axonal fibers was significantly higher with AAV2.Stat3-ca and Y27632 at 500, 800, 1000 and 1500 μ m past the injury site than in control animals or only Y27632-injected mice. Statistical test could not be applied at longer distances as control groups showed no fibers contrary to the combined stimulation. ( f ) With AAV2.Stat3-ca and Y27632, the 20 longest axons reached a distance that was 1.6 times as long as that reached by axons treated with AAV2.Stat3-ca alone. ( g ) The percentage of U-turns was strongly reduced by combining Y27632 and AAV2.Stat3-ca treatment. ( h ) The proportion of branching axons was increased threefold in optic nerves treated with AAV2.Stat3-ca and Y27632 together, compared with AAV2.Stat3-ca alone ( t -test, ** P
    The Stat3 transcription factor is an important signaling molecule for many cytokines and growth factor receptors 1 and is required for murine fetal development 2 Research studies have shown that Stat3 is constitutively activated in a number of human tumors 3 4 and possesses oncogenic potential 5 and anti apoptotic activities 3 Stat3 is activated by phosphorylation at Tyr705 which induces dimerization nuclear translocation and DNA binding 6 7 Transcriptional activation seems to be regulated by phosphorylation at Ser727 through the MAPK or mTOR pathways 8 9 Stat3 isoform expression appears to reflect biological function as the relative expression levels of Stat3α 86 kDa and Stat3β 79 kDa depend on cell type ligand exposure or cell maturation stage 10 It is notable that Stat3β lacks the serine phosphorylation site within the carboxy terminal transcriptional activation domain 8
    https://www.bioz.com/result/stat3 expression/product/Cell Signaling Technology Inc
    Average 99 stars, based on 5 article reviews
    Price from $9.99 to $1999.99
    stat3 expression - by Bioz Stars, 2020-09
    99/100 stars

    Images

    1) Product Images from "Misguidance and modulation of axonal regeneration by Stat3 and Rho/ROCK signaling in the transparent optic nerve"

    Article Title: Misguidance and modulation of axonal regeneration by Stat3 and Rho/ROCK signaling in the transparent optic nerve

    Journal: Cell Death & Disease

    doi: 10.1038/cddis.2013.266

    Rho-kinase (ROCK) inhibition potentiates Stat3-ca-induced axonal regeneration in the optic nerve and changes the pattern of fiber growth. The ROCK blocker Y27632 was administered intravitreally in adult mice treated with AAV2.Stat3-ca or in mice that were not injected with viruses. ( a–d ) On top- and side-view projections of whole optic nerves, the combination of AAV2.Stat3-ca and Y27632 activated the growth of strikingly long and straight axons ( a and b ) while Y27632 by itself had no effects ( c and d ). ( e ) Quantitatively, the number of axonal fibers was significantly higher with AAV2.Stat3-ca and Y27632 at 500, 800, 1000 and 1500 μ m past the injury site than in control animals or only Y27632-injected mice. Statistical test could not be applied at longer distances as control groups showed no fibers contrary to the combined stimulation. ( f ) With AAV2.Stat3-ca and Y27632, the 20 longest axons reached a distance that was 1.6 times as long as that reached by axons treated with AAV2.Stat3-ca alone. ( g ) The percentage of U-turns was strongly reduced by combining Y27632 and AAV2.Stat3-ca treatment. ( h ) The proportion of branching axons was increased threefold in optic nerves treated with AAV2.Stat3-ca and Y27632 together, compared with AAV2.Stat3-ca alone ( t -test, ** P
    Figure Legend Snippet: Rho-kinase (ROCK) inhibition potentiates Stat3-ca-induced axonal regeneration in the optic nerve and changes the pattern of fiber growth. The ROCK blocker Y27632 was administered intravitreally in adult mice treated with AAV2.Stat3-ca or in mice that were not injected with viruses. ( a–d ) On top- and side-view projections of whole optic nerves, the combination of AAV2.Stat3-ca and Y27632 activated the growth of strikingly long and straight axons ( a and b ) while Y27632 by itself had no effects ( c and d ). ( e ) Quantitatively, the number of axonal fibers was significantly higher with AAV2.Stat3-ca and Y27632 at 500, 800, 1000 and 1500 μ m past the injury site than in control animals or only Y27632-injected mice. Statistical test could not be applied at longer distances as control groups showed no fibers contrary to the combined stimulation. ( f ) With AAV2.Stat3-ca and Y27632, the 20 longest axons reached a distance that was 1.6 times as long as that reached by axons treated with AAV2.Stat3-ca alone. ( g ) The percentage of U-turns was strongly reduced by combining Y27632 and AAV2.Stat3-ca treatment. ( h ) The proportion of branching axons was increased threefold in optic nerves treated with AAV2.Stat3-ca and Y27632 together, compared with AAV2.Stat3-ca alone ( t -test, ** P

    Techniques Used: Inhibition, Mouse Assay, Injection

    Combining AAV2.Stat3-ca and Y27632 promotes a similar extent of axonal regeneration as the overexpression of CNTF by Müller glia. ( a and b ) Side-view and top-view projections of CTb-594 stained retinal axons distal to the crush site (arrow heads) in the whole-mounted optic nerve after ShH10.DH-CNTF-mediated infection of Müller glia 2 weeks after optic nerve crush. ( c and d ) High-magnification pictures of distal optic nerve segments showed the improvement of long-range axonal regeneration after adding Y27632 to ShH10.DH-CNTF-injected mice. ( e ) Quantitatively, the number of growing fibers was not different between the groups receiving AAV2.Stat3-ca/Y27632 and CNTF but significantly increased by combining ShH10.DH-CNTF and Y27632. ( f ) The longest distance from the lesion site reached by the 20 longest axons after the injury was comparable between the AAV2.Stat3-ca and ShH10.DH-CNTF groups but was enhanced in mice receiving the double ShH10.DH-CNTF/Y27632 treatment ( t -test, * P
    Figure Legend Snippet: Combining AAV2.Stat3-ca and Y27632 promotes a similar extent of axonal regeneration as the overexpression of CNTF by Müller glia. ( a and b ) Side-view and top-view projections of CTb-594 stained retinal axons distal to the crush site (arrow heads) in the whole-mounted optic nerve after ShH10.DH-CNTF-mediated infection of Müller glia 2 weeks after optic nerve crush. ( c and d ) High-magnification pictures of distal optic nerve segments showed the improvement of long-range axonal regeneration after adding Y27632 to ShH10.DH-CNTF-injected mice. ( e ) Quantitatively, the number of growing fibers was not different between the groups receiving AAV2.Stat3-ca/Y27632 and CNTF but significantly increased by combining ShH10.DH-CNTF and Y27632. ( f ) The longest distance from the lesion site reached by the 20 longest axons after the injury was comparable between the AAV2.Stat3-ca and ShH10.DH-CNTF groups but was enhanced in mice receiving the double ShH10.DH-CNTF/Y27632 treatment ( t -test, * P

    Techniques Used: Over Expression, CtB Assay, Staining, Infection, Injection, Mouse Assay

    Y27632 boosts growth gene transcription by Stat3. ( a and b ) The activation of the Jak/Stat3, Erk1/2 and PI3K/Akt signaling cascades was monitored by western blot analysis, 5 days after the optic nerve crush. Stat3 phosphorylation was dramatically increased on Tyr705 when Y27632 and AAV2.Stat3-ca were applied together, while the two separate treatments had much weaker effects. Note that CNTF also stimulated P-Akt and P-Erk1/2 phosphorylation in addition to P-Stat3. Values in ( b ) were quantified by densitometry and normalized to total, unphosphorylated proteins. ( c ) The expression of Stat3-dependent growth-related genes was monitored by qRT-PCR in the different experimental groups. The combination of Y27632 and AAV2.Stat3-ca resulted in a higher upregulation than AAV2.Stat3-ca alone and was comparable to that obtained with CNTF for 4/6 of the markers. Statistics: one-way ANOVA, * P
    Figure Legend Snippet: Y27632 boosts growth gene transcription by Stat3. ( a and b ) The activation of the Jak/Stat3, Erk1/2 and PI3K/Akt signaling cascades was monitored by western blot analysis, 5 days after the optic nerve crush. Stat3 phosphorylation was dramatically increased on Tyr705 when Y27632 and AAV2.Stat3-ca were applied together, while the two separate treatments had much weaker effects. Note that CNTF also stimulated P-Akt and P-Erk1/2 phosphorylation in addition to P-Stat3. Values in ( b ) were quantified by densitometry and normalized to total, unphosphorylated proteins. ( c ) The expression of Stat3-dependent growth-related genes was monitored by qRT-PCR in the different experimental groups. The combination of Y27632 and AAV2.Stat3-ca resulted in a higher upregulation than AAV2.Stat3-ca alone and was comparable to that obtained with CNTF for 4/6 of the markers. Statistics: one-way ANOVA, * P

    Techniques Used: Activation Assay, Western Blot, Expressing, Quantitative RT-PCR

    Retinal ganglion cell transduction with wild-type (WT) or constitutively active (ca) Stat3 is sufficient to promote axonal regeneration in the injured optic nerve. ( a ) Four weeks after AAV2.Stat3-ca injection into adult mouse eyes, a high density of Stat3-labeled cells was visualized using immunohistochemistry on retinal flat mounts, whereas endogenous Stat3 was undetectable in untreated contralateral retina. White circle indicated optic nerve head. ( b ) Double immunofluorescent staining shows that β 3Tubulin-positive RGCs expressed Stat3 after AAV2.Stat3-ca infection while no endogenous Stat3 signal could be detected in untreated RGCs. ( c ) Using semi-qRT-PCR, Stat3 mRNA was significantly elevated by AAV2.Stat3-wt and AAV2.Stat3-ca relative to AAV2.GFP. The transcript levels of the growth-associated protein Sprr1a and GAP-43 were markedly increased by Stat3 5 days after optic nerve crush, compared with the control groups, but not in the intact retina. ( d–h ) Axonal regeneration was observed on optic nerve longitudinal sections at 2 weeks post lesion and after anterograde tracing with cholera toxin β subunit coupled to alexa-594 (CTb-594). AAV2.Stat3-wt and AAV2.Stat3-ca caused more axons to grow across the injury site (white asterisks) than control AAV2.GFP virus. ( e and g ) Magnified pictures from ( d and f ) reveal CTb-594-labeled fibers distal to the lesion. ( h ) The quantification of axons at distances from 100 to 1000 μ m shows that AAV2.Stat3-wt and AAV2.Stat3-ca promoted more growth—respectively, up to 500 and 700 μ m past the lesion site than in uninjected or AAV2.GFP-injected mice. ( i and j ) Surviving RGCs 2 weeks after the optic nerve crush were visualized using immunohistochemistry on retinal flat-mounts. AAV2.Stat3-ca had no significant (NS) neuroprotective effect on axotomized RGCs compared with other groups. Statistics: one-way ANOVA, * P
    Figure Legend Snippet: Retinal ganglion cell transduction with wild-type (WT) or constitutively active (ca) Stat3 is sufficient to promote axonal regeneration in the injured optic nerve. ( a ) Four weeks after AAV2.Stat3-ca injection into adult mouse eyes, a high density of Stat3-labeled cells was visualized using immunohistochemistry on retinal flat mounts, whereas endogenous Stat3 was undetectable in untreated contralateral retina. White circle indicated optic nerve head. ( b ) Double immunofluorescent staining shows that β 3Tubulin-positive RGCs expressed Stat3 after AAV2.Stat3-ca infection while no endogenous Stat3 signal could be detected in untreated RGCs. ( c ) Using semi-qRT-PCR, Stat3 mRNA was significantly elevated by AAV2.Stat3-wt and AAV2.Stat3-ca relative to AAV2.GFP. The transcript levels of the growth-associated protein Sprr1a and GAP-43 were markedly increased by Stat3 5 days after optic nerve crush, compared with the control groups, but not in the intact retina. ( d–h ) Axonal regeneration was observed on optic nerve longitudinal sections at 2 weeks post lesion and after anterograde tracing with cholera toxin β subunit coupled to alexa-594 (CTb-594). AAV2.Stat3-wt and AAV2.Stat3-ca caused more axons to grow across the injury site (white asterisks) than control AAV2.GFP virus. ( e and g ) Magnified pictures from ( d and f ) reveal CTb-594-labeled fibers distal to the lesion. ( h ) The quantification of axons at distances from 100 to 1000 μ m shows that AAV2.Stat3-wt and AAV2.Stat3-ca promoted more growth—respectively, up to 500 and 700 μ m past the lesion site than in uninjected or AAV2.GFP-injected mice. ( i and j ) Surviving RGCs 2 weeks after the optic nerve crush were visualized using immunohistochemistry on retinal flat-mounts. AAV2.Stat3-ca had no significant (NS) neuroprotective effect on axotomized RGCs compared with other groups. Statistics: one-way ANOVA, * P

    Techniques Used: Transduction, Injection, Labeling, Immunohistochemistry, Staining, Infection, Quantitative RT-PCR, Anterograde Tracing, CtB Assay, Mouse Assay

    Three-dimensional analysis of axonal regeneration in the cleared optic nerve reveals guidance and directionality errors. Whole, unsectioned optic nerves were submitted to clearing (see methods) after CTb-594 tracing and reconstructed from serial confocal optical sections in 3D. ( a–f ) Top- or side-view projections of CTb-594-filled fibers illustrate the in-depth trajectories of single axons in the whole optic nerves. Two weeks after the optic nerve crush and without stimulation, the few spontaneously growing axons could be followed over ∼0.5 mm, and individual axons were traced ( e and f ). Colored arrowheads indicate the enlarged ends of single axons ( c and d ). Note the oblique, irregular course of the axons; some fibers show U-turns. ( g–l ) Stat3-ca-induced axonal regeneration was characterized by a high density of intermingled axons extending up to > 1 mm. Fiber growth is highly irregular, and many fibers present U-turns at the regeneration front. ( m ) Quantitatively, AAV2.Stat3-ca stimulated significantly more axonal growth at 500, 800, and 1000 μ m past the lesion site than what is found in the untreated optic nerves (one-way ANOVA, ** P
    Figure Legend Snippet: Three-dimensional analysis of axonal regeneration in the cleared optic nerve reveals guidance and directionality errors. Whole, unsectioned optic nerves were submitted to clearing (see methods) after CTb-594 tracing and reconstructed from serial confocal optical sections in 3D. ( a–f ) Top- or side-view projections of CTb-594-filled fibers illustrate the in-depth trajectories of single axons in the whole optic nerves. Two weeks after the optic nerve crush and without stimulation, the few spontaneously growing axons could be followed over ∼0.5 mm, and individual axons were traced ( e and f ). Colored arrowheads indicate the enlarged ends of single axons ( c and d ). Note the oblique, irregular course of the axons; some fibers show U-turns. ( g–l ) Stat3-ca-induced axonal regeneration was characterized by a high density of intermingled axons extending up to > 1 mm. Fiber growth is highly irregular, and many fibers present U-turns at the regeneration front. ( m ) Quantitatively, AAV2.Stat3-ca stimulated significantly more axonal growth at 500, 800, and 1000 μ m past the lesion site than what is found in the untreated optic nerves (one-way ANOVA, ** P

    Techniques Used: CtB Assay

    2) Product Images from "Bone marrow endothelium-targeted therapeutics for metastatic breast cancer"

    Article Title: Bone marrow endothelium-targeted therapeutics for metastatic breast cancer

    Journal: Journal of controlled release : official journal of the Controlled Release Society

    doi: 10.1016/j.jconrel.2014.04.057

    Targeted delivery of STAT3 siRNA and efficacy evaluation
    Figure Legend Snippet: Targeted delivery of STAT3 siRNA and efficacy evaluation

    Techniques Used:

    3) Product Images from "Signal transducer and activator of transcription 3 promotes angiogenesis and drives malignant progression in glioma"

    Article Title: Signal transducer and activator of transcription 3 promotes angiogenesis and drives malignant progression in glioma

    Journal: Neuro-Oncology

    doi: 10.1093/neuonc/nos139

    Tumors induced by RCAS- PDGFB and RCAS- STAT3 after treatment with WP1066. (A) WP1066 treatment decreases the percentage of high-grade gliomas compared with untreated RCAS- PDGFB + RCAS- STAT3 injected mice (control). (B) WP1066 decreases microvascular proliferation as determined by staining for CD31 in tumors (horizontal line indicates the mean). (C) The median tumor latency was significantly longer in mice injected with RCAS-PDGFB + RCAS-STAT3 treated with WP1066 compared with the original group of untreated mice.
    Figure Legend Snippet: Tumors induced by RCAS- PDGFB and RCAS- STAT3 after treatment with WP1066. (A) WP1066 treatment decreases the percentage of high-grade gliomas compared with untreated RCAS- PDGFB + RCAS- STAT3 injected mice (control). (B) WP1066 decreases microvascular proliferation as determined by staining for CD31 in tumors (horizontal line indicates the mean). (C) The median tumor latency was significantly longer in mice injected with RCAS-PDGFB + RCAS-STAT3 treated with WP1066 compared with the original group of untreated mice.

    Techniques Used: Injection, Mouse Assay, Staining

    Tumors induced by RCAS- PDGFB + RCAS- STAT3 display increased microvascular proliferation. (A) Photomicrograph (400×) of VEGF staining in high-grade tumors induced by RCAS- PDGFB or by RCAS- PDGFB + RCAS- STAT3 . Tumors induced by RCAS- PDGFB + RCAS- STAT3 demonstrate large foci of VEGF staining throughout the tumor mass, whereas there is minimal staining in high-grade tumors induced by RCAS- PDGFB alone. Whole-mount photomicrograph (50×) of VEGF staining in a high-grade tumor, showing the localization of VEGF to the high-grade areas (areas surrounding necrosis or microvascular proliferation) (scale bar = 2.5 mm). (B) Expression of CD31 in tumors induced by RCAS- PDGFB or by RCAS- PDGFB + RCAS- STAT3 . Horizontal lines indicate the mean.
    Figure Legend Snippet: Tumors induced by RCAS- PDGFB + RCAS- STAT3 display increased microvascular proliferation. (A) Photomicrograph (400×) of VEGF staining in high-grade tumors induced by RCAS- PDGFB or by RCAS- PDGFB + RCAS- STAT3 . Tumors induced by RCAS- PDGFB + RCAS- STAT3 demonstrate large foci of VEGF staining throughout the tumor mass, whereas there is minimal staining in high-grade tumors induced by RCAS- PDGFB alone. Whole-mount photomicrograph (50×) of VEGF staining in a high-grade tumor, showing the localization of VEGF to the high-grade areas (areas surrounding necrosis or microvascular proliferation) (scale bar = 2.5 mm). (B) Expression of CD31 in tumors induced by RCAS- PDGFB or by RCAS- PDGFB + RCAS- STAT3 . Horizontal lines indicate the mean.

    Techniques Used: Staining, Expressing

    Expression of pSTAT3 is increased in tumors induced by RCAS- PDGFB + RCAS- STAT3 and pSTAT3-expressing cells appear to localize to areas of necrosis. (A) Photomicrograph (400× magnification) showing relatively minimal pSTAT3 expression in the nuclei within an HGG induced by RCAS- PDGFB compared with a tumor induced by RCAS- PDGFB + RCAS- STAT3 (scale bar = 50 µm). (B) Photomicrograph (400×) showing pSTAT3-expressing cells preferentially localizing to areas of necrosis (denoted as NE) in HGGs induced by RCAS- PDGFB + RCAS- STAT3 but not in the only HGG induced by RCAS- PDGFB alone that displayed necrosis (scale bar = 50 µm). (C) Percentage of cells expressing pSTAT3 in mice killed due to symptomatic tumor formation before the end of the 90-day observation period (labeled “short-term survival”) compared with those who survived to 90 days (labeled “long-term survival”) in RCAS- PDGFB (left) and RCAS- PDGFB + RCAS- STAT3 (right) injection sets. Error bars indicate SEM.
    Figure Legend Snippet: Expression of pSTAT3 is increased in tumors induced by RCAS- PDGFB + RCAS- STAT3 and pSTAT3-expressing cells appear to localize to areas of necrosis. (A) Photomicrograph (400× magnification) showing relatively minimal pSTAT3 expression in the nuclei within an HGG induced by RCAS- PDGFB compared with a tumor induced by RCAS- PDGFB + RCAS- STAT3 (scale bar = 50 µm). (B) Photomicrograph (400×) showing pSTAT3-expressing cells preferentially localizing to areas of necrosis (denoted as NE) in HGGs induced by RCAS- PDGFB + RCAS- STAT3 but not in the only HGG induced by RCAS- PDGFB alone that displayed necrosis (scale bar = 50 µm). (C) Percentage of cells expressing pSTAT3 in mice killed due to symptomatic tumor formation before the end of the 90-day observation period (labeled “short-term survival”) compared with those who survived to 90 days (labeled “long-term survival”) in RCAS- PDGFB (left) and RCAS- PDGFB + RCAS- STAT3 (right) injection sets. Error bars indicate SEM.

    Techniques Used: Expressing, Mouse Assay, Labeling, Injection

    The incidence of high-grade gliomas was significantly higher in mice injected with RCAS- PDGFB + RCAS- STAT3 than in those injected with RCAS- PDGFB alone. RCAS- STAT3 was insufficient to induce tumor formation.
    Figure Legend Snippet: The incidence of high-grade gliomas was significantly higher in mice injected with RCAS- PDGFB + RCAS- STAT3 than in those injected with RCAS- PDGFB alone. RCAS- STAT3 was insufficient to induce tumor formation.

    Techniques Used: Mouse Assay, Injection

    STAT3 promotes tumor cell proliferation and suppression of apoptosis. Representative hematoxylin and eosin (H E) photomicrographs (400× magnification) of HGGs induced by RCAS- PDGFB or by RCAS- PDGFB + RCAS- STAT3 . These tumors were studied for expression of pHH3 as a marker of tumor cell proliferation and cleaved caspase 3 (CC3) as a marker of apoptosis. HGGs induced by RCAS- PDGFB + RCAS- STAT3 showed higher expression of pHH3 and lower expression of CC3 compared with tumors induced by RCAS- PDGFB alone (scale bar = 50 µm).
    Figure Legend Snippet: STAT3 promotes tumor cell proliferation and suppression of apoptosis. Representative hematoxylin and eosin (H E) photomicrographs (400× magnification) of HGGs induced by RCAS- PDGFB or by RCAS- PDGFB + RCAS- STAT3 . These tumors were studied for expression of pHH3 as a marker of tumor cell proliferation and cleaved caspase 3 (CC3) as a marker of apoptosis. HGGs induced by RCAS- PDGFB + RCAS- STAT3 showed higher expression of pHH3 and lower expression of CC3 compared with tumors induced by RCAS- PDGFB alone (scale bar = 50 µm).

    Techniques Used: Expressing, Marker

    Related Articles

    Western Blot:

    Article Title: IL-22+CD4+ T cells promote colorectal cancer stemness via STAT3 transcription factor activation and induction of the methyltransferase DOT1L
    Article Snippet: .. Western blotting was performed with specific antibodies against human STAT3 (9132, Cell Signaling), phosphorylated STAT3 (9138, Cell Signaling), Oct3/4 (sc-5279, Santa Cruz biotechnology), Nanog (ab21624, Abcam), Sox2 (MAB4343, Millipore), H3K79me2 (ab3594, Abcam), H3K9me2 (ab1220, Abcam), H3K9me3 (ab8898, Abcam), H4K20me3 (07-463, Millipore), H3K27me3 (07-449, Millipore), H3K36me3 (ab9050, Abcam), acetyl-Histone H3 (06-599, Millipore), Histone H3 (9715, Cell Signaling), β-Actin (A5441, Sigma), Dot1L (ab72454, Abcam), and Cleaved Notch1 (NICD, ab52301, Abcam). .. Signals were detected by ECL reagents (GE Healthcare, Buckinghamshire, UK).

    Incubation:

    Article Title: Chemokine CCL2–CCR2 Signaling Induces Neuronal Cell Death via STAT3 Activation and IL-1β Production after Status Epilepticus
    Article Snippet: .. The sections were first blocked with 5% goat or donkey serum for 1 h at room temperature, and then incubated overnight at 4°C with the following primary antibodies: Iba-1 antibody (rabbit, 1:1000; Wako), NeuN antibody (rabbit, 1:500; Abcam), GFAP (rabbit, 1:500; Millipore Bioscience Research Reagents), MCP-1 antibody (mouse, 1:200; Novus Biologicals), RFP (mouse, 1;500; Abcam), Iba-1 antibody (goat, 1:200; Abcam), IL-1β (rabbit, 1:500; Abcam), phosphorylated STAT3 (pSTAT3) or total-STAT3 (1:200, rabbit; Cell Signaling Technology). .. The sections were then incubated for 1 h at room temperature with Cy3-conjugated or FITC-conjugated secondary antibodies (1:500; Jackson ImmunoResearch).

    Article Title: Dysregulated LIF-STAT3 pathway is responsible for impaired embryo implantation in a Streptozotocin-induced diabetic mouse model
    Article Snippet: .. After blocking with 5% non-fat milk containing 0.5% Tween 20 for 1 h, the membrane was incubated with rabbit anti-total STAT3 antibody (1:1000; #9132, Cell Signaling Technology) or rabbit anti-phosphorylated (Tyr 705) STAT3 antibody (1:1000; #9131, Cell Signaling Technology) overnight at 4°C. .. The membrane was then incubated with HRP-conjugated secondary antibody (1:5000) for 1 h. Signals were analyzed by ECL Chemiluminescent kit (Amersham Pharmacia Biotech, IL USA).

    Stripping Membranes:

    Article Title: Novel CD47: SIRP? Dependent Mechanism for the Activation of STAT3 in Antigen-Presenting Cell
    Article Snippet: .. Following stripping, membranes were re-probed with anti STAT3 mAb (Cell Signaling). .. Cytokine Production IL-10 and IL-27 secretion was determined in a 24 hour conditioned media of either monocytes, MCF-7 alone, or co-culture of the two using commercial ELISA (R & D Systems).

    other:

    Article Title: Leptin-Dependent Toll-Like Receptor Expression and Responsiveness in Preadipocytes and Adipocytes
    Article Snippet: Antibodies against Akt, phospho-Akt (Ser473), STAT-3, as well as STAT-3P (Tyr705) were purchased from Cell Signaling (Beverly, MA).

    Blocking Assay:

    Article Title: Dysregulated LIF-STAT3 pathway is responsible for impaired embryo implantation in a Streptozotocin-induced diabetic mouse model
    Article Snippet: .. After blocking with 5% non-fat milk containing 0.5% Tween 20 for 1 h, the membrane was incubated with rabbit anti-total STAT3 antibody (1:1000; #9132, Cell Signaling Technology) or rabbit anti-phosphorylated (Tyr 705) STAT3 antibody (1:1000; #9131, Cell Signaling Technology) overnight at 4°C. .. The membrane was then incubated with HRP-conjugated secondary antibody (1:5000) for 1 h. Signals were analyzed by ECL Chemiluminescent kit (Amersham Pharmacia Biotech, IL USA).

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 92
    Cell Signaling Technology Inc stat3
    ATF3 regulates IL-6-pSTAT3 signaling in intestinal Th17 cells. Flow cytometry analysis of <t>phospho-STAT3</t> in (A) IL-6 or IL-22 stimulated freshly isolated ileum crypts or IL-6-stimulated peripheral blood mononuclear cell (PBMC) from wild-type mice, or in (B) IL-6-stimulated PBMC from wild-type and ATF3-deficient mice. (C) Flow cytometry analysis of intracellular IL-17A and IL-22 expression in naïve lamina propria T cells from the indicated mice. Cells were treated with PMA, ionomycin and IL-23 in the presence of BFA for 4 h before analysis and gated on live CD45 + EpCAM − Lin − CD3 + population as shown. (D) Quantitative real-time PCR analysis of IL-17A and IL-22 mRNA levels in freshly isolated lamina propria (LPL) cells, mesenteric lymph nodes (mLN), or splenocytes. (E) Model of ATF3-mediated mucosal immunity via cross-regulation between IL-22-pSTAT3 signaling in epithelium (associated with AMP production and epithelial fucosylation) and IL-6-pSTAT3 signaling in Th17 cells (associated with signature IL-17A and IL-22 production). “n” refers to the number of mice analyzed. Statistical analysis was done by multiple comparison in Two-way ANOVA test using Prism software. * P
    Stat3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 92/100, based on 1596 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/stat3/product/Cell Signaling Technology Inc
    Average 92 stars, based on 1596 article reviews
    Price from $9.99 to $1999.99
    stat3 - by Bioz Stars, 2020-09
    92/100 stars
      Buy from Supplier

    Image Search Results


    ATF3 regulates IL-6-pSTAT3 signaling in intestinal Th17 cells. Flow cytometry analysis of phospho-STAT3 in (A) IL-6 or IL-22 stimulated freshly isolated ileum crypts or IL-6-stimulated peripheral blood mononuclear cell (PBMC) from wild-type mice, or in (B) IL-6-stimulated PBMC from wild-type and ATF3-deficient mice. (C) Flow cytometry analysis of intracellular IL-17A and IL-22 expression in naïve lamina propria T cells from the indicated mice. Cells were treated with PMA, ionomycin and IL-23 in the presence of BFA for 4 h before analysis and gated on live CD45 + EpCAM − Lin − CD3 + population as shown. (D) Quantitative real-time PCR analysis of IL-17A and IL-22 mRNA levels in freshly isolated lamina propria (LPL) cells, mesenteric lymph nodes (mLN), or splenocytes. (E) Model of ATF3-mediated mucosal immunity via cross-regulation between IL-22-pSTAT3 signaling in epithelium (associated with AMP production and epithelial fucosylation) and IL-6-pSTAT3 signaling in Th17 cells (associated with signature IL-17A and IL-22 production). “n” refers to the number of mice analyzed. Statistical analysis was done by multiple comparison in Two-way ANOVA test using Prism software. * P

    Journal: Frontiers in Immunology

    Article Title: ATF3 Sustains IL-22-Induced STAT3 Phosphorylation to Maintain Mucosal Immunity Through Inhibiting Phosphatases

    doi: 10.3389/fimmu.2018.02522

    Figure Lengend Snippet: ATF3 regulates IL-6-pSTAT3 signaling in intestinal Th17 cells. Flow cytometry analysis of phospho-STAT3 in (A) IL-6 or IL-22 stimulated freshly isolated ileum crypts or IL-6-stimulated peripheral blood mononuclear cell (PBMC) from wild-type mice, or in (B) IL-6-stimulated PBMC from wild-type and ATF3-deficient mice. (C) Flow cytometry analysis of intracellular IL-17A and IL-22 expression in naïve lamina propria T cells from the indicated mice. Cells were treated with PMA, ionomycin and IL-23 in the presence of BFA for 4 h before analysis and gated on live CD45 + EpCAM − Lin − CD3 + population as shown. (D) Quantitative real-time PCR analysis of IL-17A and IL-22 mRNA levels in freshly isolated lamina propria (LPL) cells, mesenteric lymph nodes (mLN), or splenocytes. (E) Model of ATF3-mediated mucosal immunity via cross-regulation between IL-22-pSTAT3 signaling in epithelium (associated with AMP production and epithelial fucosylation) and IL-6-pSTAT3 signaling in Th17 cells (associated with signature IL-17A and IL-22 production). “n” refers to the number of mice analyzed. Statistical analysis was done by multiple comparison in Two-way ANOVA test using Prism software. * P

    Article Snippet: Consistent to a study showing that loss of IL-6 did not affect epithelial STAT3 phosphorylation , we found IL-6 does not activate STAT3 in gut epithelial cells (Figure ).

    Techniques: Flow Cytometry, Cytometry, Isolation, Mouse Assay, Expressing, Real-time Polymerase Chain Reaction, Software

    ATF3 promotes IL-22-induced STAT3 phosphorylation by suppressing phosphatases. (A) Freshly isolated ileum crypts, or (B) ileum organoids at day 6 of culture, were stimulated with IL-22, followed by fixation and intracellular staining of phospho-STAT3, and analyzed by flow cytometry. Western blot analysis of (C) IL-22-stimulated CMT93 cells, or (D) IL-22-stimuated colon fragments isolated from the indicated mice, for the expression of the indicated proteins. (E) Quantitative real-time PCR analysis of IL-22R1 and IL-10R2 mRNA levels in freshly isolated ileum crypts from mice. (F) Flow cytometry analysis of IL-22R1 in freshly isolated ileum crypt cells gated on the CD45 − EpCAM + population. (G,H) Western blot analysis of unstimulated or IL-22-stimulated CMT93 cells for the indicated proteins. ATF3 −/− CMT93 cells with SHP2 knockdown (ATF3 −/− SHP2 KD ) were indicated. Images were representative of four independent experiments (G–H) . Results were from two independent experiments (A–F) . “n” refers to the number of mice analyzed (A,B,E,F) . Statistical analysis was done by multiple comparison in Two-way ANOVA test using Prism software. * P

    Journal: Frontiers in Immunology

    Article Title: ATF3 Sustains IL-22-Induced STAT3 Phosphorylation to Maintain Mucosal Immunity Through Inhibiting Phosphatases

    doi: 10.3389/fimmu.2018.02522

    Figure Lengend Snippet: ATF3 promotes IL-22-induced STAT3 phosphorylation by suppressing phosphatases. (A) Freshly isolated ileum crypts, or (B) ileum organoids at day 6 of culture, were stimulated with IL-22, followed by fixation and intracellular staining of phospho-STAT3, and analyzed by flow cytometry. Western blot analysis of (C) IL-22-stimulated CMT93 cells, or (D) IL-22-stimuated colon fragments isolated from the indicated mice, for the expression of the indicated proteins. (E) Quantitative real-time PCR analysis of IL-22R1 and IL-10R2 mRNA levels in freshly isolated ileum crypts from mice. (F) Flow cytometry analysis of IL-22R1 in freshly isolated ileum crypt cells gated on the CD45 − EpCAM + population. (G,H) Western blot analysis of unstimulated or IL-22-stimulated CMT93 cells for the indicated proteins. ATF3 −/− CMT93 cells with SHP2 knockdown (ATF3 −/− SHP2 KD ) were indicated. Images were representative of four independent experiments (G–H) . Results were from two independent experiments (A–F) . “n” refers to the number of mice analyzed (A,B,E,F) . Statistical analysis was done by multiple comparison in Two-way ANOVA test using Prism software. * P

    Article Snippet: Consistent to a study showing that loss of IL-6 did not affect epithelial STAT3 phosphorylation , we found IL-6 does not activate STAT3 in gut epithelial cells (Figure ).

    Techniques: Isolation, Staining, Flow Cytometry, Cytometry, Western Blot, Mouse Assay, Expressing, Real-time Polymerase Chain Reaction, Software

    STAT3 contributes to the increased susceptibility of day 3 BSI- Ifnar1 −/− mice post-IAV. (A) WT, Ifnar1 −/− , and Ifnar2 −/− mice were infected with IAV or PBS on day 0 and gene expression from RNA isolated from the whole lung was analyzed. (B) STAT3 protein was analyzed from cytoplasmic and nuclear fractions isolated from WT, Ifnar1 −/− , and Ifnar2 −/− primary alveolar epithelial cells infected with IAV or inoculated PBS for 24 h. STAT3 was normalized to b-actin protein level and fold change over WT-PBS was calculated (Whole western blots: Supplemental Figures 2 – 5 ). (C–E) WT, Ifnar1 −/− , and Ifnar2 −/− mice were infected with IAV on day 0, inoculated with STAT3 inhibitor or PBS 6 h post-IAV, and challenged with S. aureus on day 3. (C) Lung CFUs, (D) differential counts from the cell-free BALF, and (E) indicated cytokines from cell-free BALF were analyzed 24 h post- S.a .-challenge. Data shown are mean ± SD results of ≥4 animals per group from one representative experiment. N.D. is not detectable. *** P > 0.001; ** P > 0.01; * P > 0.05.

    Journal: Frontiers in Immunology

    Article Title: IFNAR2 Is Required for Anti-influenza Immunity and Alters Susceptibility to Post-influenza Bacterial Superinfections

    doi: 10.3389/fimmu.2018.02589

    Figure Lengend Snippet: STAT3 contributes to the increased susceptibility of day 3 BSI- Ifnar1 −/− mice post-IAV. (A) WT, Ifnar1 −/− , and Ifnar2 −/− mice were infected with IAV or PBS on day 0 and gene expression from RNA isolated from the whole lung was analyzed. (B) STAT3 protein was analyzed from cytoplasmic and nuclear fractions isolated from WT, Ifnar1 −/− , and Ifnar2 −/− primary alveolar epithelial cells infected with IAV or inoculated PBS for 24 h. STAT3 was normalized to b-actin protein level and fold change over WT-PBS was calculated (Whole western blots: Supplemental Figures 2 – 5 ). (C–E) WT, Ifnar1 −/− , and Ifnar2 −/− mice were infected with IAV on day 0, inoculated with STAT3 inhibitor or PBS 6 h post-IAV, and challenged with S. aureus on day 3. (C) Lung CFUs, (D) differential counts from the cell-free BALF, and (E) indicated cytokines from cell-free BALF were analyzed 24 h post- S.a .-challenge. Data shown are mean ± SD results of ≥4 animals per group from one representative experiment. N.D. is not detectable. *** P > 0.001; ** P > 0.01; * P > 0.05.

    Article Snippet: We found that this engagement of STAT3 contributed to the increased BSI susceptibility of Ifnar1 −/− mice at day 3 post-IAV.

    Techniques: Mouse Assay, Infection, Expressing, Isolation, Western Blot

    Impaired phosphorylation of STAT3 in endometria from women with adenomyosis. Timed midsecretory endometrial biopsies from normal control women (n=20) and women with adenomyosis (n=20) were analyzed for STAT3 and p-STAT3 expression via western blotting (a), and the expression levels of STAT3 (b) and p-STAT3 (c) were compared between the two groups. The correlation between IL-10 and STAT3 protein levels was analyzed in all of the women (n=40) (d). Representative images of STAT3 and p-STAT3 staining in the endometria of women with adenomyosis and normal controls are shown (e). The integrated optical density (IOD) levels of STAT3 (f) and p-STAT3 (g) were compared between the two groups (n=3). The data are plotted as the mean ± SEM. ∗ P

    Journal: BioMed Research International

    Article Title: Decreased Endometrial IL-10 Impairs Endometrial Receptivity by Downregulating HOXA10 Expression in Women with Adenomyosis

    doi: 10.1155/2018/2549789

    Figure Lengend Snippet: Impaired phosphorylation of STAT3 in endometria from women with adenomyosis. Timed midsecretory endometrial biopsies from normal control women (n=20) and women with adenomyosis (n=20) were analyzed for STAT3 and p-STAT3 expression via western blotting (a), and the expression levels of STAT3 (b) and p-STAT3 (c) were compared between the two groups. The correlation between IL-10 and STAT3 protein levels was analyzed in all of the women (n=40) (d). Representative images of STAT3 and p-STAT3 staining in the endometria of women with adenomyosis and normal controls are shown (e). The integrated optical density (IOD) levels of STAT3 (f) and p-STAT3 (g) were compared between the two groups (n=3). The data are plotted as the mean ± SEM. ∗ P

    Article Snippet: The phosphorylation of STAT3 might be a critical mediator of IL-10-induced HOXA10 expression [ , ].

    Techniques: Expressing, Western Blot, Staining

    IL-10 increases HOXA10 expression via phosphorylation of STAT3. The expression of HOXA10 mRNA and protein was examined by qRT-PCR and western blotting in Ishikawa cells treated with different concentrations of rIL-10 for 12 h ((a) and (c)) or with 100 ng/mL rIL-10 for different times ((b) and (d)). The expression levels of STAT3, p-STAT3, and HOXA10 were examined by western blotting in Ishikawa cells treated with 4.6 μ M cryptotanshinone for 24 h, followed by 100 ng/mL rIL-10 for 12 h, or in controls (e).

    Journal: BioMed Research International

    Article Title: Decreased Endometrial IL-10 Impairs Endometrial Receptivity by Downregulating HOXA10 Expression in Women with Adenomyosis

    doi: 10.1155/2018/2549789

    Figure Lengend Snippet: IL-10 increases HOXA10 expression via phosphorylation of STAT3. The expression of HOXA10 mRNA and protein was examined by qRT-PCR and western blotting in Ishikawa cells treated with different concentrations of rIL-10 for 12 h ((a) and (c)) or with 100 ng/mL rIL-10 for different times ((b) and (d)). The expression levels of STAT3, p-STAT3, and HOXA10 were examined by western blotting in Ishikawa cells treated with 4.6 μ M cryptotanshinone for 24 h, followed by 100 ng/mL rIL-10 for 12 h, or in controls (e).

    Article Snippet: The phosphorylation of STAT3 might be a critical mediator of IL-10-induced HOXA10 expression [ , ].

    Techniques: Expressing, Quantitative RT-PCR, Western Blot