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anti p atf2  (Santa Cruz Biotechnology)


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    Santa Cruz Biotechnology anti p atf2
    Anti P Atf2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 578 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p+atf2/ATF-2/pmc13039192-446-84-85
    Average 94 stars, based on 578 article reviews
    anti p atf2 - by Bioz Stars, 2026-10
    94/100 stars

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    Related Articles

    Binding Assay:

    Article Title: GLUT3 Promotes Epithelial-Mesenchymal Transition via TGF-β/JNK/ATF2 Signaling Pathway in Colorectal Cancer Cells.
    Article Snippet: The TGF-β receptor kinase inhibitor, SB431542, was purchased from Tocris Cookson, Inc. (Ellisville, MO, USA). .. The antibodies specific to GLUT3, E-cadherin, N-cadherin, α-smooth muscle actin (α-SMA), connective tissue growth factor (CTGF), fibronectin, vimentin, zinc finger E-box binding homeobox 1 (ZEB1), β-actin, TGF-β RI, p-ATF2, ATF2, p-JNK and JNK were purchased from Santa Cruz Biotechnology (Dallas, TX, USA). .. The antibodies specific to plasminogen activator inhibitor-1 (PAI-1) were purchased from BD Bioscience (Franklin Lakes, NJ, USA).

    Article Title: GLUT3 Promotes Epithelial–Mesenchymal Transition via TGF-β/JNK/ATF2 Signaling Pathway in Colorectal Cancer Cells
    Article Snippet: The TGF-β receptor kinase inhibitor, SB431542, was purchased from Tocris Cookson, Inc. (Ellisville, MO, USA). .. The antibodies specific to GLUT3, E-cadherin, N-cadherin, α-smooth muscle actin (α-SMA), connective tissue growth factor (CTGF), fibronectin, vimentin, zinc finger E-box binding homeobox 1 (ZEB1), β-actin, TGF-β RI, p-ATF2, ATF2, p-JNK and JNK were purchased from Santa Cruz Biotechnology (Dallas, TX, USA). .. The antibodies specific to plasminogen activator inhibitor-1 (PAI-1) were purchased from BD Bioscience (Franklin Lakes, NJ, USA).

    Blocking Assay:

    Article Title: MicroRNA Let-7a, -7e and -133a Attenuate Hypoxia-Induced Atrial Fibrosis via Targeting Collagen Expression and the JNK Pathway in HL1 Cardiomyocytes
    Article Snippet: Protein concentrations were determined using a DC Protein Assay (BioRad Laboratories, Inc., Hercules, CA, USA) and 25 μg of soluble protein per sample was electrophoresed on 8% or 12% SDS poly-acrylamide gels (SDS-PAGE) and then transferred to polyvinylidene difluoride (PVDF) membranes (Millipore). .. After blocking with 3% bovine serum albumin (BSA) for 1 h at room temperature, membranes were incubated with an indicated antibody against HIF-1α (Santa Cruz Biotechnology, Novus Biologicals, Centennial, CO, USA), proCOL1A, proCOL3A (Santa Cruz Biotechnology), p-ATF2, p-MKK4, JNK/SAPK, pJNK/SAPK (pT183/pY185) (Cell Signaling Technology, Danvers, MA, USA), p38 or ERK (BD Biosciences, Bedford, MA, USA) at 4 °C overnight while a duplicate membrane was probed with anti-β-Actin (Geneway) as control. .. The membranes were then incubated with a species-specific horseradish-peroxidase-labeled secondary antibody (BD Biosciences: 1:5000) for 1 h at 37 °C.

    Article Title: Increased ATF2 expression predicts poor prognosis and inhibits sorafenib-induced ferroptosis in gastric cancer
    Article Snippet: Equal amounts of protein samples were separated by SDS-polyacrylamide gel electrophoresis and then transferred onto PVDF membranes (Millipore, MA, USA). .. After blocking in 5% skim milk in TBST for 1 h at room temperature, the membranes were incubated with primary antibodies against ATF2 (1:1000, ab32160, Abcam, Cambridge, UK), p-ATF2 (1:1,000, sc-8398, Santa Cruz Biotechnology, TX, USA), SLC7A11 (1:1000, ab175186, Abcam, Cambridge, UK), HSPH1 (1:1000, ab109624, Abcam, Cambridge, UK), and GAPDH (1:2500, #5174, Cell Signaling Technology, MA, USA) overnight at 4 °C. .. Following incubation with the secondary antibody for 1 h at room temperature, the protein bands were visualized using enhanced chemiluminescence (Bridgen, Beijing, China) and imaged using a Tanon-5200 chemiluminescence detection system (Tanon Science, Shanghai, China).

    Article Title: MicroRNA Let-7a, -7e and -133a Attenuate Hypoxia-Induced Atrial Fibrosis via Targeting Collagen Expression and the JNK Pathway in HL1 Cardiomyocytes.
    Article Snippet: Protein concentrations were determined using a DC Protein Assay (BioRad Laboratories, Inc., Hercules, CA, USA) and 25 μg of soluble protein per sample was electrophoresed on 8% or 12% SDS poly-acrylamide gels (SDS-PAGE) and then transferred to polyvinylidene difluoride (PVDF) membranes (Millipore). .. After blocking with 3% bovine serum albumin (BSA) for 1 h at room temperature, membranes were incubated with an indicated antibody against HIF-1α (Santa Cruz Biotechnology, Novus Biologicals, Centennial, CO, USA), proCOL1A, proCOL3A (Santa Cruz Biotechnology), p-ATF2, p-MKK4, JNK/SAPK, pJNK/SAPK (pT183/pY185) (Cell Signaling Technology, Danvers, MA, USA), p38 or ERK (BD Biosciences, Bedford, MA, USA) at 4 ◦C overnight while a duplicate membrane was probed with anti-β-Actin (Geneway) as control. .. The membranes were then incubated with a species-specific horseradish-peroxidase-labeled secondary antibody (BD Biosciences: 1:5000) for 1 h at 37 ◦C.

    Article Title: Loss of Sirt6 in adipocytes impairs the ability of adipose tissue to adapt to intermittent fasting.
    Article Snippet: .. After blocking with 5% skim milk, the blots were probed with primary antibodies against Sirt6, Akt, p-Akt (Ser473), p38 MAPK, p-p38 MAPK, p-ATGL (Ser406), HSL, p-HSL (Ser563, Ser565, Ser660), CREB, p-CREB (Cell Signaling, Beverly, MA, USA), UCP1, ATGL (Abcam), HSP90 (Enzo Life Sciences, Plymouth Meeting, PA, USA), ATF2, and p-ATF2 (Santa Cruz Biochemicals, Dallas, TX, USA). .. Immunoreactive bands were detected with a Las-4000 imager (GE Healthcare Life Science, Pittsburgh, PA, USA).

    Article Title: Increased ATF2 expression predicts poor prognosis and inhibits sorafenib-induced ferroptosis in gastric cancer.
    Article Snippet: Sorafenib, a tyrosine kinase inhibitor, has an important antitumor effect as a ferroptosis inducer in multiple cancers, including gastric cancer (GC).. However, the status of sorafenib as a ferroptosis inducer has recently been questioned.. There is very limited information about the relationship between ferroptosis and ATF2, and the role of ATF2 in sorafenib-induced ferroptosis has not been studied.

    Incubation:

    Article Title: MicroRNA Let-7a, -7e and -133a Attenuate Hypoxia-Induced Atrial Fibrosis via Targeting Collagen Expression and the JNK Pathway in HL1 Cardiomyocytes
    Article Snippet: Protein concentrations were determined using a DC Protein Assay (BioRad Laboratories, Inc., Hercules, CA, USA) and 25 μg of soluble protein per sample was electrophoresed on 8% or 12% SDS poly-acrylamide gels (SDS-PAGE) and then transferred to polyvinylidene difluoride (PVDF) membranes (Millipore). .. After blocking with 3% bovine serum albumin (BSA) for 1 h at room temperature, membranes were incubated with an indicated antibody against HIF-1α (Santa Cruz Biotechnology, Novus Biologicals, Centennial, CO, USA), proCOL1A, proCOL3A (Santa Cruz Biotechnology), p-ATF2, p-MKK4, JNK/SAPK, pJNK/SAPK (pT183/pY185) (Cell Signaling Technology, Danvers, MA, USA), p38 or ERK (BD Biosciences, Bedford, MA, USA) at 4 °C overnight while a duplicate membrane was probed with anti-β-Actin (Geneway) as control. .. The membranes were then incubated with a species-specific horseradish-peroxidase-labeled secondary antibody (BD Biosciences: 1:5000) for 1 h at 37 °C.

    Article Title: Increased ATF2 expression predicts poor prognosis and inhibits sorafenib-induced ferroptosis in gastric cancer
    Article Snippet: Equal amounts of protein samples were separated by SDS-polyacrylamide gel electrophoresis and then transferred onto PVDF membranes (Millipore, MA, USA). .. After blocking in 5% skim milk in TBST for 1 h at room temperature, the membranes were incubated with primary antibodies against ATF2 (1:1000, ab32160, Abcam, Cambridge, UK), p-ATF2 (1:1,000, sc-8398, Santa Cruz Biotechnology, TX, USA), SLC7A11 (1:1000, ab175186, Abcam, Cambridge, UK), HSPH1 (1:1000, ab109624, Abcam, Cambridge, UK), and GAPDH (1:2500, #5174, Cell Signaling Technology, MA, USA) overnight at 4 °C. .. Following incubation with the secondary antibody for 1 h at room temperature, the protein bands were visualized using enhanced chemiluminescence (Bridgen, Beijing, China) and imaged using a Tanon-5200 chemiluminescence detection system (Tanon Science, Shanghai, China).

    Article Title: MicroRNA Let-7a, -7e and -133a Attenuate Hypoxia-Induced Atrial Fibrosis via Targeting Collagen Expression and the JNK Pathway in HL1 Cardiomyocytes.
    Article Snippet: Protein concentrations were determined using a DC Protein Assay (BioRad Laboratories, Inc., Hercules, CA, USA) and 25 μg of soluble protein per sample was electrophoresed on 8% or 12% SDS poly-acrylamide gels (SDS-PAGE) and then transferred to polyvinylidene difluoride (PVDF) membranes (Millipore). .. After blocking with 3% bovine serum albumin (BSA) for 1 h at room temperature, membranes were incubated with an indicated antibody against HIF-1α (Santa Cruz Biotechnology, Novus Biologicals, Centennial, CO, USA), proCOL1A, proCOL3A (Santa Cruz Biotechnology), p-ATF2, p-MKK4, JNK/SAPK, pJNK/SAPK (pT183/pY185) (Cell Signaling Technology, Danvers, MA, USA), p38 or ERK (BD Biosciences, Bedford, MA, USA) at 4 ◦C overnight while a duplicate membrane was probed with anti-β-Actin (Geneway) as control. .. The membranes were then incubated with a species-specific horseradish-peroxidase-labeled secondary antibody (BD Biosciences: 1:5000) for 1 h at 37 ◦C.

    Article Title: Increased ATF2 expression predicts poor prognosis and inhibits sorafenib-induced ferroptosis in gastric cancer.
    Article Snippet: Sorafenib, a tyrosine kinase inhibitor, has an important antitumor effect as a ferroptosis inducer in multiple cancers, including gastric cancer (GC).. However, the status of sorafenib as a ferroptosis inducer has recently been questioned.. There is very limited information about the relationship between ferroptosis and ATF2, and the role of ATF2 in sorafenib-induced ferroptosis has not been studied.

    Membrane:

    Article Title: MicroRNA Let-7a, -7e and -133a Attenuate Hypoxia-Induced Atrial Fibrosis via Targeting Collagen Expression and the JNK Pathway in HL1 Cardiomyocytes
    Article Snippet: Protein concentrations were determined using a DC Protein Assay (BioRad Laboratories, Inc., Hercules, CA, USA) and 25 μg of soluble protein per sample was electrophoresed on 8% or 12% SDS poly-acrylamide gels (SDS-PAGE) and then transferred to polyvinylidene difluoride (PVDF) membranes (Millipore). .. After blocking with 3% bovine serum albumin (BSA) for 1 h at room temperature, membranes were incubated with an indicated antibody against HIF-1α (Santa Cruz Biotechnology, Novus Biologicals, Centennial, CO, USA), proCOL1A, proCOL3A (Santa Cruz Biotechnology), p-ATF2, p-MKK4, JNK/SAPK, pJNK/SAPK (pT183/pY185) (Cell Signaling Technology, Danvers, MA, USA), p38 or ERK (BD Biosciences, Bedford, MA, USA) at 4 °C overnight while a duplicate membrane was probed with anti-β-Actin (Geneway) as control. .. The membranes were then incubated with a species-specific horseradish-peroxidase-labeled secondary antibody (BD Biosciences: 1:5000) for 1 h at 37 °C.

    Article Title: MicroRNA Let-7a, -7e and -133a Attenuate Hypoxia-Induced Atrial Fibrosis via Targeting Collagen Expression and the JNK Pathway in HL1 Cardiomyocytes.
    Article Snippet: Protein concentrations were determined using a DC Protein Assay (BioRad Laboratories, Inc., Hercules, CA, USA) and 25 μg of soluble protein per sample was electrophoresed on 8% or 12% SDS poly-acrylamide gels (SDS-PAGE) and then transferred to polyvinylidene difluoride (PVDF) membranes (Millipore). .. After blocking with 3% bovine serum albumin (BSA) for 1 h at room temperature, membranes were incubated with an indicated antibody against HIF-1α (Santa Cruz Biotechnology, Novus Biologicals, Centennial, CO, USA), proCOL1A, proCOL3A (Santa Cruz Biotechnology), p-ATF2, p-MKK4, JNK/SAPK, pJNK/SAPK (pT183/pY185) (Cell Signaling Technology, Danvers, MA, USA), p38 or ERK (BD Biosciences, Bedford, MA, USA) at 4 ◦C overnight while a duplicate membrane was probed with anti-β-Actin (Geneway) as control. .. The membranes were then incubated with a species-specific horseradish-peroxidase-labeled secondary antibody (BD Biosciences: 1:5000) for 1 h at 37 ◦C.

    Control:

    Article Title: MicroRNA Let-7a, -7e and -133a Attenuate Hypoxia-Induced Atrial Fibrosis via Targeting Collagen Expression and the JNK Pathway in HL1 Cardiomyocytes
    Article Snippet: Protein concentrations were determined using a DC Protein Assay (BioRad Laboratories, Inc., Hercules, CA, USA) and 25 μg of soluble protein per sample was electrophoresed on 8% or 12% SDS poly-acrylamide gels (SDS-PAGE) and then transferred to polyvinylidene difluoride (PVDF) membranes (Millipore). .. After blocking with 3% bovine serum albumin (BSA) for 1 h at room temperature, membranes were incubated with an indicated antibody against HIF-1α (Santa Cruz Biotechnology, Novus Biologicals, Centennial, CO, USA), proCOL1A, proCOL3A (Santa Cruz Biotechnology), p-ATF2, p-MKK4, JNK/SAPK, pJNK/SAPK (pT183/pY185) (Cell Signaling Technology, Danvers, MA, USA), p38 or ERK (BD Biosciences, Bedford, MA, USA) at 4 °C overnight while a duplicate membrane was probed with anti-β-Actin (Geneway) as control. .. The membranes were then incubated with a species-specific horseradish-peroxidase-labeled secondary antibody (BD Biosciences: 1:5000) for 1 h at 37 °C.

    Article Title: MicroRNA Let-7a, -7e and -133a Attenuate Hypoxia-Induced Atrial Fibrosis via Targeting Collagen Expression and the JNK Pathway in HL1 Cardiomyocytes.
    Article Snippet: Protein concentrations were determined using a DC Protein Assay (BioRad Laboratories, Inc., Hercules, CA, USA) and 25 μg of soluble protein per sample was electrophoresed on 8% or 12% SDS poly-acrylamide gels (SDS-PAGE) and then transferred to polyvinylidene difluoride (PVDF) membranes (Millipore). .. After blocking with 3% bovine serum albumin (BSA) for 1 h at room temperature, membranes were incubated with an indicated antibody against HIF-1α (Santa Cruz Biotechnology, Novus Biologicals, Centennial, CO, USA), proCOL1A, proCOL3A (Santa Cruz Biotechnology), p-ATF2, p-MKK4, JNK/SAPK, pJNK/SAPK (pT183/pY185) (Cell Signaling Technology, Danvers, MA, USA), p38 or ERK (BD Biosciences, Bedford, MA, USA) at 4 ◦C overnight while a duplicate membrane was probed with anti-β-Actin (Geneway) as control. .. The membranes were then incubated with a species-specific horseradish-peroxidase-labeled secondary antibody (BD Biosciences: 1:5000) for 1 h at 37 ◦C.

    other:

    Article Title: Exploring dual effects of dinutuximab beta on cell death and proliferation of insulinoma.
    Article Snippet: The glycosphingolipid disialoganglioside (GD2) is found in many tumor tissues and is a tumorassociated antigen (Ladenstein et al., 2018, 2020).. Dinutuximab beta is a monoclonal antibody that binds to GD2.. DB binds to GD2 and ensures that tumor cells are destroyed by their own immune system.



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    Effect of transient SUMOylation inhibition in pre-adipocytes on cAMP-PKA-p38 signaling and adaptive thermogenesis in mature adipocytes. ( A ) Heatmap showing the stable upregulation of most genes involved in adaptive thermogenesis and cAMP-PKA-p38 signaling 22 days after adipogenic induction. Z -scores were calculated and plotted in GraphPad Prism. Treatments of pre-adipocytes were performed as shown in Fig. . ( B ) Western blot analysis of PKA substrates phosphorylation, assessed using a pan-PKA-target antibody, 22 days after adipogenic induction. TBP was used as a loading control. The asterisk (*) indicates substrates significantly affected by TAK-981 and/or rosiglitazone treatment. ( C ) Quantification of PKA substrate signals from panel (B). The signal for PKA substrates and TBP was quantified using Fiji software, with PKA substrate signals normalized to TBP. Error bars represent the standard deviation of four independent experiments. Student’s t -test was used to calculate P -values. ( D ) Western blot analysis of p-CREB, p-ATF1, p38, p-p38, and <t>p-ATF2,</t> 22 days after adipogenic induction. TBP was used as a loading control. ( E ) Quantification of p-CREB/ATF-1 signals from panel (D). Signals were normalized to TBP. Error bars represent the standard deviation of three independent experiments. Student’s t -test was used to calculate P -values. ( F ) Western blot analysis of p-CREB in the absence or presence of the PKA inhibitor RP-8-CPT-cAMPS. TBP was used as a loading control. Quantification of p-CREB, normalized to TBP, is showed in the lower panel. Error bars represent the standard deviation of two independent experiments. Quantification of p-p38 ( G ) and <t>p-ATF2</t> ( H ) from experiment in panel (D). Signals were normalized to TBP for p-ATF2 and to p38 for p-p38. Error bars represent the standard deviation of three independent experiments. Student’s t -test was used to calculate P -values.
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    Image Search Results


    Effect of transient SUMOylation inhibition in pre-adipocytes on cAMP-PKA-p38 signaling and adaptive thermogenesis in mature adipocytes. ( A ) Heatmap showing the stable upregulation of most genes involved in adaptive thermogenesis and cAMP-PKA-p38 signaling 22 days after adipogenic induction. Z -scores were calculated and plotted in GraphPad Prism. Treatments of pre-adipocytes were performed as shown in Fig. . ( B ) Western blot analysis of PKA substrates phosphorylation, assessed using a pan-PKA-target antibody, 22 days after adipogenic induction. TBP was used as a loading control. The asterisk (*) indicates substrates significantly affected by TAK-981 and/or rosiglitazone treatment. ( C ) Quantification of PKA substrate signals from panel (B). The signal for PKA substrates and TBP was quantified using Fiji software, with PKA substrate signals normalized to TBP. Error bars represent the standard deviation of four independent experiments. Student’s t -test was used to calculate P -values. ( D ) Western blot analysis of p-CREB, p-ATF1, p38, p-p38, and p-ATF2, 22 days after adipogenic induction. TBP was used as a loading control. ( E ) Quantification of p-CREB/ATF-1 signals from panel (D). Signals were normalized to TBP. Error bars represent the standard deviation of three independent experiments. Student’s t -test was used to calculate P -values. ( F ) Western blot analysis of p-CREB in the absence or presence of the PKA inhibitor RP-8-CPT-cAMPS. TBP was used as a loading control. Quantification of p-CREB, normalized to TBP, is showed in the lower panel. Error bars represent the standard deviation of two independent experiments. Quantification of p-p38 ( G ) and p-ATF2 ( H ) from experiment in panel (D). Signals were normalized to TBP for p-ATF2 and to p38 for p-p38. Error bars represent the standard deviation of three independent experiments. Student’s t -test was used to calculate P -values.

    Journal: Nucleic Acids Research

    Article Title: Transient SUMOylation inhibition in human pre-adipocytes stably imprints a transcriptional beiging fate

    doi: 10.1093/nar/gkag232

    Figure Lengend Snippet: Effect of transient SUMOylation inhibition in pre-adipocytes on cAMP-PKA-p38 signaling and adaptive thermogenesis in mature adipocytes. ( A ) Heatmap showing the stable upregulation of most genes involved in adaptive thermogenesis and cAMP-PKA-p38 signaling 22 days after adipogenic induction. Z -scores were calculated and plotted in GraphPad Prism. Treatments of pre-adipocytes were performed as shown in Fig. . ( B ) Western blot analysis of PKA substrates phosphorylation, assessed using a pan-PKA-target antibody, 22 days after adipogenic induction. TBP was used as a loading control. The asterisk (*) indicates substrates significantly affected by TAK-981 and/or rosiglitazone treatment. ( C ) Quantification of PKA substrate signals from panel (B). The signal for PKA substrates and TBP was quantified using Fiji software, with PKA substrate signals normalized to TBP. Error bars represent the standard deviation of four independent experiments. Student’s t -test was used to calculate P -values. ( D ) Western blot analysis of p-CREB, p-ATF1, p38, p-p38, and p-ATF2, 22 days after adipogenic induction. TBP was used as a loading control. ( E ) Quantification of p-CREB/ATF-1 signals from panel (D). Signals were normalized to TBP. Error bars represent the standard deviation of three independent experiments. Student’s t -test was used to calculate P -values. ( F ) Western blot analysis of p-CREB in the absence or presence of the PKA inhibitor RP-8-CPT-cAMPS. TBP was used as a loading control. Quantification of p-CREB, normalized to TBP, is showed in the lower panel. Error bars represent the standard deviation of two independent experiments. Quantification of p-p38 ( G ) and p-ATF2 ( H ) from experiment in panel (D). Signals were normalized to TBP for p-ATF2 and to p38 for p-p38. Error bars represent the standard deviation of three independent experiments. Student’s t -test was used to calculate P -values.

    Article Snippet: The following antibodies were used: UCP1, abcam, ab209483; PKA phospho-substrates, Cell Signaling, 9624; p-CREB/p-ATF1, Cell Signaling, 9198; p38 MAPK, Cell Signaling, 9212; p-p38 MAPK, Cell Signaling, 9211; p-ATF2, Cell Signaling, 24329; SUMO2/3, abcam, ab81371; PPARG, Cell signaling, 2443; and TBP, Protein Tech, 22006-1-AP or abcam, 282715; γ-tubulin, Sigma, T5326: CEBPB, Santa Cruz, sc-7962 quantifications were performed using FiJi [ ].

    Techniques: Inhibition, Western Blot, Phospho-proteomics, Control, Software, Standard Deviation

    The p38 MAPK activator LX-3 rescues the malignant behavior of HPSCC cells repressed by the silencing of THBS1 (A) Western blot analysis of the extent of p38, ATF2, and MK2 phosphorylation, as well as total p38 expression in KD-THBS1-treated HPSCC cells. (B) Western blot analysis of the extent of p38, ATF2, and MK2 phosphorylation, as well as total p38 expression in HPSCC cells treated with 2 μM LX-3 after knockdown of THBS1. (C–E) HPSCC cell proliferative capacity was examined using EdU staining. Transwell assay detects changes in the migratory (D) and invasive (E) abilities of HPSCC cells. (F) Expression of E-cadherin and N-cadherin in HPSCC cells was examined using dual-labeling immunofluorescence. The results are expressed as the mean ± SD (A–F). These values are derived from three independent experiments. Statistical analysis was performed using an unpaired t test.

    Journal: iScience

    Article Title: THBS1 upregulation by KLF7 in hypopharyngeal squamous cell carcinoma contributes to lung metastasis through the p38 MAPK signaling

    doi: 10.1016/j.isci.2026.114816

    Figure Lengend Snippet: The p38 MAPK activator LX-3 rescues the malignant behavior of HPSCC cells repressed by the silencing of THBS1 (A) Western blot analysis of the extent of p38, ATF2, and MK2 phosphorylation, as well as total p38 expression in KD-THBS1-treated HPSCC cells. (B) Western blot analysis of the extent of p38, ATF2, and MK2 phosphorylation, as well as total p38 expression in HPSCC cells treated with 2 μM LX-3 after knockdown of THBS1. (C–E) HPSCC cell proliferative capacity was examined using EdU staining. Transwell assay detects changes in the migratory (D) and invasive (E) abilities of HPSCC cells. (F) Expression of E-cadherin and N-cadherin in HPSCC cells was examined using dual-labeling immunofluorescence. The results are expressed as the mean ± SD (A–F). These values are derived from three independent experiments. Statistical analysis was performed using an unpaired t test.

    Article Snippet: The primary antibodies used were as follows: anti-THBS1 (1:250, A2125, BioAb), anti-E-cadherin (1:1000, 3195, Cell Signaling Technologies), anti-N-cadherin (1:100, PA5-19486m Invitrogen), anti-Phospho-p38 MAPK (Thr180/Tyr182) (1:1000, 4511, Cell Signaling Technologies), anti-total p38 (1:1000, 9212, Cell Signaling Technologies), anti- p -ATF2 (Thr71) (1:1000, 44-295G, Invitrogen), anti-p-MK2 (Thr334) (1:1000, 3007, Cell Signaling Technologies), anti-KLF7 (1:1000, CSB- PA126129 , Cusabio), anti-Slug (1:1000, 12129-1-AP, ProteinTech Group), anti-Vimentin (1:20000, 10366-1-AP, ProteinTech Group), anti-HDAC6 (1:1000, 12834-1-AP, ProteinTech Group), and anti-GAPDH (1:20000, AC001, BioAb).

    Techniques: Western Blot, Phospho-proteomics, Expressing, Knockdown, Staining, Transwell Assay, Labeling, Immunofluorescence, Derivative Assay

    Reactivation of THBS1 rescues the HPSCC cell malignant biological behavior curtailed by knockdown of KLF7 (A) Western blot analysis of protein expression of KLF7 and THBS1 in HPSCC cells treated with knockdown of KLF7 combined with the overexpression of THBS1. (B–D) HPSCC cell proliferative capacity was examined using EdU staining. Transwell assay detects changes in the migratory (C) and invasive (D) abilities of HPSCC cells. (E) Expression of E-cadherin and N-cadherin in HPSCC cells was examined using dual-labeling immunofluorescence. (F) Western blot analysis of the extent of p38, ATF2, and MK2 phosphorylation, as well as total p38 expression in HPSCC cells. The results are expressed as the mean ± SD (A–F). These values are derived from three independent experiments. Statistical analysis was performed using a one-way ANOVA followed by Tukey’s multiple comparison test.

    Journal: iScience

    Article Title: THBS1 upregulation by KLF7 in hypopharyngeal squamous cell carcinoma contributes to lung metastasis through the p38 MAPK signaling

    doi: 10.1016/j.isci.2026.114816

    Figure Lengend Snippet: Reactivation of THBS1 rescues the HPSCC cell malignant biological behavior curtailed by knockdown of KLF7 (A) Western blot analysis of protein expression of KLF7 and THBS1 in HPSCC cells treated with knockdown of KLF7 combined with the overexpression of THBS1. (B–D) HPSCC cell proliferative capacity was examined using EdU staining. Transwell assay detects changes in the migratory (C) and invasive (D) abilities of HPSCC cells. (E) Expression of E-cadherin and N-cadherin in HPSCC cells was examined using dual-labeling immunofluorescence. (F) Western blot analysis of the extent of p38, ATF2, and MK2 phosphorylation, as well as total p38 expression in HPSCC cells. The results are expressed as the mean ± SD (A–F). These values are derived from three independent experiments. Statistical analysis was performed using a one-way ANOVA followed by Tukey’s multiple comparison test.

    Article Snippet: The primary antibodies used were as follows: anti-THBS1 (1:250, A2125, BioAb), anti-E-cadherin (1:1000, 3195, Cell Signaling Technologies), anti-N-cadherin (1:100, PA5-19486m Invitrogen), anti-Phospho-p38 MAPK (Thr180/Tyr182) (1:1000, 4511, Cell Signaling Technologies), anti-total p38 (1:1000, 9212, Cell Signaling Technologies), anti- p -ATF2 (Thr71) (1:1000, 44-295G, Invitrogen), anti-p-MK2 (Thr334) (1:1000, 3007, Cell Signaling Technologies), anti-KLF7 (1:1000, CSB- PA126129 , Cusabio), anti-Slug (1:1000, 12129-1-AP, ProteinTech Group), anti-Vimentin (1:20000, 10366-1-AP, ProteinTech Group), anti-HDAC6 (1:1000, 12834-1-AP, ProteinTech Group), and anti-GAPDH (1:20000, AC001, BioAb).

    Techniques: Knockdown, Western Blot, Expressing, Over Expression, Staining, Transwell Assay, Labeling, Immunofluorescence, Phospho-proteomics, Derivative Assay, Comparison

    Activation of the THBS1/p38 MAPK axis by KLF7 promotes the lung metastasis of HPSCC cells (A) Lung metastasis in nude mice injected with FaDu cells in the tail vein was assessed by HE staining. (B–D) Quantitative results of lung metastatic nodules. IHC scores (C) and protein expression (D) of Slug and Vimentin within lung metastases in nude mice. (E) RT-qPCR detection of mRNA expression levels of KLF7 and THBS1 in lung metastases. (F) IHC scores of KLF7 and THBS1 within lung metastases in nude mice. (G) Western blot analysis of the extent of p38, ATF2, and MK2 phosphorylation, as well as total p38 expression in lung metastases. The results are expressed as the mean ± SD (A–G). These values are derived from five mice. Statistical analysis was performed using a one-way ANOVA followed by Tukey’s multiple comparison test.

    Journal: iScience

    Article Title: THBS1 upregulation by KLF7 in hypopharyngeal squamous cell carcinoma contributes to lung metastasis through the p38 MAPK signaling

    doi: 10.1016/j.isci.2026.114816

    Figure Lengend Snippet: Activation of the THBS1/p38 MAPK axis by KLF7 promotes the lung metastasis of HPSCC cells (A) Lung metastasis in nude mice injected with FaDu cells in the tail vein was assessed by HE staining. (B–D) Quantitative results of lung metastatic nodules. IHC scores (C) and protein expression (D) of Slug and Vimentin within lung metastases in nude mice. (E) RT-qPCR detection of mRNA expression levels of KLF7 and THBS1 in lung metastases. (F) IHC scores of KLF7 and THBS1 within lung metastases in nude mice. (G) Western blot analysis of the extent of p38, ATF2, and MK2 phosphorylation, as well as total p38 expression in lung metastases. The results are expressed as the mean ± SD (A–G). These values are derived from five mice. Statistical analysis was performed using a one-way ANOVA followed by Tukey’s multiple comparison test.

    Article Snippet: The primary antibodies used were as follows: anti-THBS1 (1:250, A2125, BioAb), anti-E-cadherin (1:1000, 3195, Cell Signaling Technologies), anti-N-cadherin (1:100, PA5-19486m Invitrogen), anti-Phospho-p38 MAPK (Thr180/Tyr182) (1:1000, 4511, Cell Signaling Technologies), anti-total p38 (1:1000, 9212, Cell Signaling Technologies), anti- p -ATF2 (Thr71) (1:1000, 44-295G, Invitrogen), anti-p-MK2 (Thr334) (1:1000, 3007, Cell Signaling Technologies), anti-KLF7 (1:1000, CSB- PA126129 , Cusabio), anti-Slug (1:1000, 12129-1-AP, ProteinTech Group), anti-Vimentin (1:20000, 10366-1-AP, ProteinTech Group), anti-HDAC6 (1:1000, 12834-1-AP, ProteinTech Group), and anti-GAPDH (1:20000, AC001, BioAb).

    Techniques: Activation Assay, Injection, Staining, Expressing, Quantitative RT-PCR, Western Blot, Phospho-proteomics, Derivative Assay, Comparison