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anti tab2  (Proteintech)


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    Proteintech anti tab2
    Anti Tab2, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 30 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/tab2/TAB2+Polyclonal+antibody/pmc12659515-109-49-51
    Average 93 stars, based on 30 article reviews
    anti tab2 - by Bioz Stars, 2026-10
    93/100 stars

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    Related Articles

    Blocking Assay:

    Article Title: USP25 Inhibits Neuroinflammatory Responses After Cerebral Ischemic Stroke by Deubiquitinating TAB2.
    Article Snippet: .. After blocking with 5% BSA, membranes were probed for USP25 (Abcam, ab187156, 1:1000), PSD95 (Proteintech, 20665-1-AP, 1:1000), NeuN (Abcam, ab177487, 1:1000), TAB2 (Proteintech, 14410-1-AP, 1:1000), TAB3 (Abcam, ab124723, 1:1000), MyD88 (Cell Signaling Technology, 4283S, Adv. ..

    Article Title: USP25 Inhibits Neuroinflammatory Responses After Cerebral Ischemic Stroke by Deubiquitinating TAB2.
    Article Snippet: .. After blocking with 5% BSA for 30 min at 37 °C, brain sections were stained with primary antibodies against USP25 (Santa Cruz Biotechnology, sc-398414, 1:50), NeuN (Abcam, ab177487, 1:200), GFAP (Santa Cruz Biotechnology, sc-33673), Iba-1 (Cell Signaling Technology, 17198S, 1:200), TNF-α (Proteintech, 60291-1-Ig, 1:50), and TAB2 (Proteintech, 14410-1-AP, 1:200) overnight at 4 °C. .. Thereafter, brain sections were incubated with fluorescence-conjugated secondary antibodies (Yeasen Biotechnology) at 37 °C for 1 h. For cell staining, cells were fixed in 4% PFA for 15 min and then incubated in 0.5% Triton X-100 for 20 min. After blocking with 5% BSA at 37 °C for 30 min, cells were stained with primary antibodies against p65 (Cell Signaling Technology, 8242S, 1:200), USP25 (Santa Cruz Biotechnology, sc-398414, 1:50), and TAB2 (Proteintech, 14410-1-AP, 1:200).

    Article Title: USP25 Inhibits Neuroinflammatory Responses After Cerebral Ischemic Stroke by Deubiquitinating TAB2
    Article Snippet: After blocking with 5% BSA for 30 min at 37 °C, brain sections were stained with primary antibodies against USP25 (Santa Cruz Biotechnology, sc‐398414, 1:50), NeuN (Abcam, ab177487, 1:200), GFAP (Santa Cruz Biotechnology, sc‐33673), Iba‐1 (Cell Signaling Technology, 17198S, 1:200), TNF‐α (Proteintech, 60291‐1‐Ig, 1:50), and TAB2 (Proteintech, 14410‐1‐AP, 1:200) overnight at 4 °C. .. Thereafter, brain sections were incubated with fluorescence‐conjugated secondary antibodies (Yeasen Biotechnology) at 37 °C for 1 h. For cell staining, cells were fixed in 4% PFA for 15 min and then incubated in 0.5% Triton X‐100 for 20 min. After blocking with 5% BSA at 37 °C for 30 min, cells were stained with primary antibodies against p65 (Cell Signaling Technology, 8242S, 1:200), USP25 (Santa Cruz Biotechnology, sc‐398414, 1:50), and TAB2 (Proteintech, 14410‐1‐AP, 1:200). .. Then, cells were incubated with fluorescence‐conjugated secondary antibodies (Yeasen Biotechnology) at 37 °C for 1 h. DAPI was used to stain the nucleus.

    Article Title: USP25 Inhibits Neuroinflammatory Responses After Cerebral Ischemic Stroke by Deubiquitinating TAB2.
    Article Snippet: After blocking with 5% BSA for 30 min at 37 °C, brain sections were stained with primary antibodies against USP25 (Santa Cruz Biotechnology, sc-398414, 1:50), NeuN (Abcam, ab177487, 1:200), GFAP (Santa Cruz Biotechnology, sc-33673), Iba-1 (Cell Signaling Technology, 17198S, 1:200), TNF-α (Proteintech, 60291-1-Ig, 1:50), and TAB2 (Proteintech, 14410-1-AP, 1:200) overnight at 4 °C. .. Thereafter, brain sections were incubated with fluorescence-conjugated secondary antibodies (Yeasen Biotechnology) at 37 °C for 1 h. For cell staining, cells were fixed in 4% PFA for 15 min and then incubated in 0.5% Triton X-100 for 20 min. After blocking with 5% BSA at 37 °C for 30 min, cells were stained with primary antibodies against p65 (Cell Signaling Technology, 8242S, 1:200), USP25 (Santa Cruz Biotechnology, sc-398414, 1:50), and TAB2 (Proteintech, 14410-1-AP, 1:200). .. Then, cells were incubated with fluorescenceconjugated secondary antibodies (Yeasen Biotechnology) at 37 °C for 1 h. DAPI was used to stain the nucleus.

    Staining:

    Article Title: USP25 Inhibits Neuroinflammatory Responses After Cerebral Ischemic Stroke by Deubiquitinating TAB2.
    Article Snippet: .. After blocking with 5% BSA for 30 min at 37 °C, brain sections were stained with primary antibodies against USP25 (Santa Cruz Biotechnology, sc-398414, 1:50), NeuN (Abcam, ab177487, 1:200), GFAP (Santa Cruz Biotechnology, sc-33673), Iba-1 (Cell Signaling Technology, 17198S, 1:200), TNF-α (Proteintech, 60291-1-Ig, 1:50), and TAB2 (Proteintech, 14410-1-AP, 1:200) overnight at 4 °C. .. Thereafter, brain sections were incubated with fluorescence-conjugated secondary antibodies (Yeasen Biotechnology) at 37 °C for 1 h. For cell staining, cells were fixed in 4% PFA for 15 min and then incubated in 0.5% Triton X-100 for 20 min. After blocking with 5% BSA at 37 °C for 30 min, cells were stained with primary antibodies against p65 (Cell Signaling Technology, 8242S, 1:200), USP25 (Santa Cruz Biotechnology, sc-398414, 1:50), and TAB2 (Proteintech, 14410-1-AP, 1:200).

    Article Title: USP25 Inhibits Neuroinflammatory Responses After Cerebral Ischemic Stroke by Deubiquitinating TAB2
    Article Snippet: After blocking with 5% BSA for 30 min at 37 °C, brain sections were stained with primary antibodies against USP25 (Santa Cruz Biotechnology, sc‐398414, 1:50), NeuN (Abcam, ab177487, 1:200), GFAP (Santa Cruz Biotechnology, sc‐33673), Iba‐1 (Cell Signaling Technology, 17198S, 1:200), TNF‐α (Proteintech, 60291‐1‐Ig, 1:50), and TAB2 (Proteintech, 14410‐1‐AP, 1:200) overnight at 4 °C. .. Thereafter, brain sections were incubated with fluorescence‐conjugated secondary antibodies (Yeasen Biotechnology) at 37 °C for 1 h. For cell staining, cells were fixed in 4% PFA for 15 min and then incubated in 0.5% Triton X‐100 for 20 min. After blocking with 5% BSA at 37 °C for 30 min, cells were stained with primary antibodies against p65 (Cell Signaling Technology, 8242S, 1:200), USP25 (Santa Cruz Biotechnology, sc‐398414, 1:50), and TAB2 (Proteintech, 14410‐1‐AP, 1:200). .. Then, cells were incubated with fluorescence‐conjugated secondary antibodies (Yeasen Biotechnology) at 37 °C for 1 h. DAPI was used to stain the nucleus.

    Article Title: USP25 Inhibits Neuroinflammatory Responses After Cerebral Ischemic Stroke by Deubiquitinating TAB2.
    Article Snippet: After blocking with 5% BSA for 30 min at 37 °C, brain sections were stained with primary antibodies against USP25 (Santa Cruz Biotechnology, sc-398414, 1:50), NeuN (Abcam, ab177487, 1:200), GFAP (Santa Cruz Biotechnology, sc-33673), Iba-1 (Cell Signaling Technology, 17198S, 1:200), TNF-α (Proteintech, 60291-1-Ig, 1:50), and TAB2 (Proteintech, 14410-1-AP, 1:200) overnight at 4 °C. .. Thereafter, brain sections were incubated with fluorescence-conjugated secondary antibodies (Yeasen Biotechnology) at 37 °C for 1 h. For cell staining, cells were fixed in 4% PFA for 15 min and then incubated in 0.5% Triton X-100 for 20 min. After blocking with 5% BSA at 37 °C for 30 min, cells were stained with primary antibodies against p65 (Cell Signaling Technology, 8242S, 1:200), USP25 (Santa Cruz Biotechnology, sc-398414, 1:50), and TAB2 (Proteintech, 14410-1-AP, 1:200). .. Then, cells were incubated with fluorescenceconjugated secondary antibodies (Yeasen Biotechnology) at 37 °C for 1 h. DAPI was used to stain the nucleus.

    Incubation:

    Article Title: USP25 Inhibits Neuroinflammatory Responses After Cerebral Ischemic Stroke by Deubiquitinating TAB2
    Article Snippet: After blocking with 5% BSA for 30 min at 37 °C, brain sections were stained with primary antibodies against USP25 (Santa Cruz Biotechnology, sc‐398414, 1:50), NeuN (Abcam, ab177487, 1:200), GFAP (Santa Cruz Biotechnology, sc‐33673), Iba‐1 (Cell Signaling Technology, 17198S, 1:200), TNF‐α (Proteintech, 60291‐1‐Ig, 1:50), and TAB2 (Proteintech, 14410‐1‐AP, 1:200) overnight at 4 °C. .. Thereafter, brain sections were incubated with fluorescence‐conjugated secondary antibodies (Yeasen Biotechnology) at 37 °C for 1 h. For cell staining, cells were fixed in 4% PFA for 15 min and then incubated in 0.5% Triton X‐100 for 20 min. After blocking with 5% BSA at 37 °C for 30 min, cells were stained with primary antibodies against p65 (Cell Signaling Technology, 8242S, 1:200), USP25 (Santa Cruz Biotechnology, sc‐398414, 1:50), and TAB2 (Proteintech, 14410‐1‐AP, 1:200). .. Then, cells were incubated with fluorescence‐conjugated secondary antibodies (Yeasen Biotechnology) at 37 °C for 1 h. DAPI was used to stain the nucleus.

    Article Title: TAB2 deficiency induces dilated cardiomyopathy by promoting mitochondrial calcium overload in human iPSC-derived cardiomyocytes.
    Article Snippet: .. The membrane was then sealed with 5% skim milk before the primary antibody was incubated overnight, including TAB2 (1:1000, 14410-1-AP, Proteintech, China), RIPK (1:1000, 17519-1-AP, Proteintech, China), MCU (1:1000, ab272488, Abcam, USA), SERCA2 (1:1000, #9580, Cell signaling Technology, USA), P-AMPK (1:1000, ab39400, Abcam, USA), P-CaMKII (1:1000, #12716, Cell Signaling Technology, USA) and GAPDH (1:1000, 60004-1-lg, Proteintech, CHINA). .. The second antibody (HRP-conjugated Affinipure goat Anti-Mouse IgG H&L (HRP), SA00001-1, 1:2000; HRP-conjugated Affinipure goat Anti-Rabbit IgG H&L (HRP), SA00001-2, 1:2000, Proteintech, CHINA) was incubated at room temperature for 2 h on the second day.

    Article Title: USP25 Inhibits Neuroinflammatory Responses After Cerebral Ischemic Stroke by Deubiquitinating TAB2.
    Article Snippet: After blocking with 5% BSA for 30 min at 37 °C, brain sections were stained with primary antibodies against USP25 (Santa Cruz Biotechnology, sc-398414, 1:50), NeuN (Abcam, ab177487, 1:200), GFAP (Santa Cruz Biotechnology, sc-33673), Iba-1 (Cell Signaling Technology, 17198S, 1:200), TNF-α (Proteintech, 60291-1-Ig, 1:50), and TAB2 (Proteintech, 14410-1-AP, 1:200) overnight at 4 °C. .. Thereafter, brain sections were incubated with fluorescence-conjugated secondary antibodies (Yeasen Biotechnology) at 37 °C for 1 h. For cell staining, cells were fixed in 4% PFA for 15 min and then incubated in 0.5% Triton X-100 for 20 min. After blocking with 5% BSA at 37 °C for 30 min, cells were stained with primary antibodies against p65 (Cell Signaling Technology, 8242S, 1:200), USP25 (Santa Cruz Biotechnology, sc-398414, 1:50), and TAB2 (Proteintech, 14410-1-AP, 1:200). .. Then, cells were incubated with fluorescenceconjugated secondary antibodies (Yeasen Biotechnology) at 37 °C for 1 h. DAPI was used to stain the nucleus.

    Article Title: TAB2 deficiency induces dilated cardiomyopathy by promoting mitochondrial calcium overload in human iPSC-derived cardiomyocytes
    Article Snippet: .. The membrane was then sealed with 5% skim milk before the primary antibody was incubated overnight, including TAB2 (1:1000, 14410-1-AP, Proteintech, China), RIPK (1:1000, 17519-1-AP, Proteintech, China), MCU (1:1000, ab272488, Abcam, USA), SERCA2 (1:1000, #9580, Cell signaling Technology, USA), P-AMPK (1:1000, ab39400, Abcam, USA), P-CaMKII (1:1000, #12716, Cell Signaling Technology, USA) and GAPDH (1:1000, 60004-1-lg, Proteintech, CHINA). .. The second antibody (HRP-conjugated Affinipure goat Anti-Mouse IgG H&L (HRP), SA00001-1, 1:2000; HRP-conjugated Affinipure goat Anti-Rabbit IgG H&L (HRP), SA00001-2, 1:2000, Proteintech, CHINA) was incubated at room temperature for 2 h on the second day.

    Fluorescence:

    Article Title: USP25 Inhibits Neuroinflammatory Responses After Cerebral Ischemic Stroke by Deubiquitinating TAB2
    Article Snippet: After blocking with 5% BSA for 30 min at 37 °C, brain sections were stained with primary antibodies against USP25 (Santa Cruz Biotechnology, sc‐398414, 1:50), NeuN (Abcam, ab177487, 1:200), GFAP (Santa Cruz Biotechnology, sc‐33673), Iba‐1 (Cell Signaling Technology, 17198S, 1:200), TNF‐α (Proteintech, 60291‐1‐Ig, 1:50), and TAB2 (Proteintech, 14410‐1‐AP, 1:200) overnight at 4 °C. .. Thereafter, brain sections were incubated with fluorescence‐conjugated secondary antibodies (Yeasen Biotechnology) at 37 °C for 1 h. For cell staining, cells were fixed in 4% PFA for 15 min and then incubated in 0.5% Triton X‐100 for 20 min. After blocking with 5% BSA at 37 °C for 30 min, cells were stained with primary antibodies against p65 (Cell Signaling Technology, 8242S, 1:200), USP25 (Santa Cruz Biotechnology, sc‐398414, 1:50), and TAB2 (Proteintech, 14410‐1‐AP, 1:200). .. Then, cells were incubated with fluorescence‐conjugated secondary antibodies (Yeasen Biotechnology) at 37 °C for 1 h. DAPI was used to stain the nucleus.

    Article Title: USP25 Inhibits Neuroinflammatory Responses After Cerebral Ischemic Stroke by Deubiquitinating TAB2.
    Article Snippet: After blocking with 5% BSA for 30 min at 37 °C, brain sections were stained with primary antibodies against USP25 (Santa Cruz Biotechnology, sc-398414, 1:50), NeuN (Abcam, ab177487, 1:200), GFAP (Santa Cruz Biotechnology, sc-33673), Iba-1 (Cell Signaling Technology, 17198S, 1:200), TNF-α (Proteintech, 60291-1-Ig, 1:50), and TAB2 (Proteintech, 14410-1-AP, 1:200) overnight at 4 °C. .. Thereafter, brain sections were incubated with fluorescence-conjugated secondary antibodies (Yeasen Biotechnology) at 37 °C for 1 h. For cell staining, cells were fixed in 4% PFA for 15 min and then incubated in 0.5% Triton X-100 for 20 min. After blocking with 5% BSA at 37 °C for 30 min, cells were stained with primary antibodies against p65 (Cell Signaling Technology, 8242S, 1:200), USP25 (Santa Cruz Biotechnology, sc-398414, 1:50), and TAB2 (Proteintech, 14410-1-AP, 1:200). .. Then, cells were incubated with fluorescenceconjugated secondary antibodies (Yeasen Biotechnology) at 37 °C for 1 h. DAPI was used to stain the nucleus.

    Membrane:

    Article Title: TAB2 deficiency induces dilated cardiomyopathy by promoting mitochondrial calcium overload in human iPSC-derived cardiomyocytes.
    Article Snippet: .. The membrane was then sealed with 5% skim milk before the primary antibody was incubated overnight, including TAB2 (1:1000, 14410-1-AP, Proteintech, China), RIPK (1:1000, 17519-1-AP, Proteintech, China), MCU (1:1000, ab272488, Abcam, USA), SERCA2 (1:1000, #9580, Cell signaling Technology, USA), P-AMPK (1:1000, ab39400, Abcam, USA), P-CaMKII (1:1000, #12716, Cell Signaling Technology, USA) and GAPDH (1:1000, 60004-1-lg, Proteintech, CHINA). .. The second antibody (HRP-conjugated Affinipure goat Anti-Mouse IgG H&L (HRP), SA00001-1, 1:2000; HRP-conjugated Affinipure goat Anti-Rabbit IgG H&L (HRP), SA00001-2, 1:2000, Proteintech, CHINA) was incubated at room temperature for 2 h on the second day.

    Article Title: TAB2 deficiency induces dilated cardiomyopathy by promoting mitochondrial calcium overload in human iPSC-derived cardiomyocytes
    Article Snippet: .. The membrane was then sealed with 5% skim milk before the primary antibody was incubated overnight, including TAB2 (1:1000, 14410-1-AP, Proteintech, China), RIPK (1:1000, 17519-1-AP, Proteintech, China), MCU (1:1000, ab272488, Abcam, USA), SERCA2 (1:1000, #9580, Cell signaling Technology, USA), P-AMPK (1:1000, ab39400, Abcam, USA), P-CaMKII (1:1000, #12716, Cell Signaling Technology, USA) and GAPDH (1:1000, 60004-1-lg, Proteintech, CHINA). .. The second antibody (HRP-conjugated Affinipure goat Anti-Mouse IgG H&L (HRP), SA00001-1, 1:2000; HRP-conjugated Affinipure goat Anti-Rabbit IgG H&L (HRP), SA00001-2, 1:2000, Proteintech, CHINA) was incubated at room temperature for 2 h on the second day.



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    (A) CFIm25 overexpression increases <t>TAB2</t> and TBL1XR1 mRNA expression after STM infection, assessed by RT-qPCR analysis in control and CFIm25-OE macrophages at 2 and 6 hours postinfection with STM (n = 3). Data are presented as means ± SD (n = 3); *, P < 0.05; **, P < 0.01. (B) Sequence of primers used for RT-qPCR analysis of TAB2 and TBL1XR1 APA. (C) Schematic representation of the long/total TAB2 and TBL1XR1 transcript regions targeted for RT-qPCR to assess APA and mRNA expression.
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    a The HEK-293T cells were transiently transfected with mock (pcDNA, a control vector), Myc-PYCR1 or <t>Flag-TAB2,</t> as indicated. An IP assay was performed with an anti-Flag antibody, followed by an immunoblotting (IB) assay with anti-Flag or anti-Myc antibodies. b The HEK-293T cells were transiently transfected with mock, Flag-PYCR1, Myc-TAK1 or Flag-TAB2, as indicated. An IP assay was performed with an anti-Myc antibody, followed by an IB assay with anti-Flag or anti-Myc antibodies. c A schematic model illustrating the role of PYCR1 in the regulation of TRAF6-mediated signaling pathways. PYCR1 interacts with TAB2 and increases the interaction between TAK1 and TAB2. This complex enhances the TRAF6-mediated polyubiquitination of TAK1. d The A549 lung cancer cells were transiently transfected with Flag-PYCR1, and treated with or without LPS, as indicated. An IP assay was performed with anti-IgG or anti-Flag antibodies, followed by an IB assay with anti-Flag, anti-IRAK1, anti-TRAF6, anti-TAK1, anti-TAB2 or anti-ECSIT antibodies. e The H1299 cells were transfected with mock or Flag-PYCR1 and stimulated with or without LPS, as indicated. An IB assay was performed with anti-Flag, anti-TAK1, anti-pho-TAK1, anti-IKKs, anti-pho-IKKs, anti-p65, anti-pho-p65 and anti-GAPDH antibodies. f The A549 cells were transfected with mock or different concentrations of Flag-PYCR1, as indicated. The cells were stimulated with or without LPS for 6 h, as indicated. An NF-κB dual-luciferase assay was performed. The results are presented as mean ± s.d. ( n = 5). ** P < 0.01, *** P < 0.001. g , Based on the differential magnitude of PYCR1, TAB2, TAK1 and TRAF6 expression, 42 patients with NSCLC were categorized into two groups: those with upregulated PYCR1, TAB2, TAK1 and TRAF6 ( n = 9, red boxes) and those with downregulated PYCR1, TAB2, TAK1 and TRAF6 ( n = 6, green boxes). h – v The GSEA was conducted between the nine patients with upregulated PYCR1, TAB2, TAK1 and TRAF6 (PYCR1 up TAB2 up TAK1 up TRAF6 up NSCLCs, red) and the six patients with downregulated PYCR1, TAB2, TAK1 and TRAF6 (PYCR1 down TAB2 down TAK1 down TRAF6 down NSCLCs, green); the gene sets related to cancer modules (in h – n ) cancer meta signature ( o ) and EGFR signaling (in p – v ) are represented (Module 32 ( h ) Module 239 ( i ) Module 83 ( j ) Module 151 ( k ) Module 8 ( l ) Module 114 ( m ) Module 159 ( n ) Cancer meta signature ( o ) ERBB1 receptor proximal pathway ( p ) RIOK1 and RIOK2 in EGFR and PI3K-mediated tumorigenesis ( q ) Raf activation ( r ); Erk pathway ( s ); PI3K AKT pathway ( t ) PI3K PLC TRK pathway ( u ); mTOR4 pathway ( v )). Bottom: a heat map associated with the Cancer meta signature (in o ) and the ERBB1 receptor proximal pathway (in p ) are shown. The NES and nominal P value are indicated in the inner panel. w A schematic model of how PYCR1 regulates TLR-mediated signaling for the activation of NF-κB.
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    a The HEK-293T cells were transiently transfected with mock (pcDNA, a control vector), Myc-PYCR1 or <t>Flag-TAB2,</t> as indicated. An IP assay was performed with an anti-Flag antibody, followed by an immunoblotting (IB) assay with anti-Flag or anti-Myc antibodies. b The HEK-293T cells were transiently transfected with mock, Flag-PYCR1, Myc-TAK1 or Flag-TAB2, as indicated. An IP assay was performed with an anti-Myc antibody, followed by an IB assay with anti-Flag or anti-Myc antibodies. c A schematic model illustrating the role of PYCR1 in the regulation of TRAF6-mediated signaling pathways. PYCR1 interacts with TAB2 and increases the interaction between TAK1 and TAB2. This complex enhances the TRAF6-mediated polyubiquitination of TAK1. d The A549 lung cancer cells were transiently transfected with Flag-PYCR1, and treated with or without LPS, as indicated. An IP assay was performed with anti-IgG or anti-Flag antibodies, followed by an IB assay with anti-Flag, anti-IRAK1, anti-TRAF6, anti-TAK1, anti-TAB2 or anti-ECSIT antibodies. e The H1299 cells were transfected with mock or Flag-PYCR1 and stimulated with or without LPS, as indicated. An IB assay was performed with anti-Flag, anti-TAK1, anti-pho-TAK1, anti-IKKs, anti-pho-IKKs, anti-p65, anti-pho-p65 and anti-GAPDH antibodies. f The A549 cells were transfected with mock or different concentrations of Flag-PYCR1, as indicated. The cells were stimulated with or without LPS for 6 h, as indicated. An NF-κB dual-luciferase assay was performed. The results are presented as mean ± s.d. ( n = 5). ** P < 0.01, *** P < 0.001. g , Based on the differential magnitude of PYCR1, TAB2, TAK1 and TRAF6 expression, 42 patients with NSCLC were categorized into two groups: those with upregulated PYCR1, TAB2, TAK1 and TRAF6 ( n = 9, red boxes) and those with downregulated PYCR1, TAB2, TAK1 and TRAF6 ( n = 6, green boxes). h – v The GSEA was conducted between the nine patients with upregulated PYCR1, TAB2, TAK1 and TRAF6 (PYCR1 up TAB2 up TAK1 up TRAF6 up NSCLCs, red) and the six patients with downregulated PYCR1, TAB2, TAK1 and TRAF6 (PYCR1 down TAB2 down TAK1 down TRAF6 down NSCLCs, green); the gene sets related to cancer modules (in h – n ) cancer meta signature ( o ) and EGFR signaling (in p – v ) are represented (Module 32 ( h ) Module 239 ( i ) Module 83 ( j ) Module 151 ( k ) Module 8 ( l ) Module 114 ( m ) Module 159 ( n ) Cancer meta signature ( o ) ERBB1 receptor proximal pathway ( p ) RIOK1 and RIOK2 in EGFR and PI3K-mediated tumorigenesis ( q ) Raf activation ( r ); Erk pathway ( s ); PI3K AKT pathway ( t ) PI3K PLC TRK pathway ( u ); mTOR4 pathway ( v )). Bottom: a heat map associated with the Cancer meta signature (in o ) and the ERBB1 receptor proximal pathway (in p ) are shown. The NES and nominal P value are indicated in the inner panel. w A schematic model of how PYCR1 regulates TLR-mediated signaling for the activation of NF-κB.
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    93
    Proteintech anti tab2 antibody
    a The HEK-293T cells were transiently transfected with mock (pcDNA, a control vector), Myc-PYCR1 or <t>Flag-TAB2,</t> as indicated. An IP assay was performed with an anti-Flag antibody, followed by an immunoblotting (IB) assay with anti-Flag or anti-Myc antibodies. b The HEK-293T cells were transiently transfected with mock, Flag-PYCR1, Myc-TAK1 or Flag-TAB2, as indicated. An IP assay was performed with an anti-Myc antibody, followed by an IB assay with anti-Flag or anti-Myc antibodies. c A schematic model illustrating the role of PYCR1 in the regulation of TRAF6-mediated signaling pathways. PYCR1 interacts with TAB2 and increases the interaction between TAK1 and TAB2. This complex enhances the TRAF6-mediated polyubiquitination of TAK1. d The A549 lung cancer cells were transiently transfected with Flag-PYCR1, and treated with or without LPS, as indicated. An IP assay was performed with anti-IgG or anti-Flag antibodies, followed by an IB assay with anti-Flag, anti-IRAK1, anti-TRAF6, anti-TAK1, anti-TAB2 or anti-ECSIT antibodies. e The H1299 cells were transfected with mock or Flag-PYCR1 and stimulated with or without LPS, as indicated. An IB assay was performed with anti-Flag, anti-TAK1, anti-pho-TAK1, anti-IKKs, anti-pho-IKKs, anti-p65, anti-pho-p65 and anti-GAPDH antibodies. f The A549 cells were transfected with mock or different concentrations of Flag-PYCR1, as indicated. The cells were stimulated with or without LPS for 6 h, as indicated. An NF-κB dual-luciferase assay was performed. The results are presented as mean ± s.d. ( n = 5). ** P < 0.01, *** P < 0.001. g , Based on the differential magnitude of PYCR1, TAB2, TAK1 and TRAF6 expression, 42 patients with NSCLC were categorized into two groups: those with upregulated PYCR1, TAB2, TAK1 and TRAF6 ( n = 9, red boxes) and those with downregulated PYCR1, TAB2, TAK1 and TRAF6 ( n = 6, green boxes). h – v The GSEA was conducted between the nine patients with upregulated PYCR1, TAB2, TAK1 and TRAF6 (PYCR1 up TAB2 up TAK1 up TRAF6 up NSCLCs, red) and the six patients with downregulated PYCR1, TAB2, TAK1 and TRAF6 (PYCR1 down TAB2 down TAK1 down TRAF6 down NSCLCs, green); the gene sets related to cancer modules (in h – n ) cancer meta signature ( o ) and EGFR signaling (in p – v ) are represented (Module 32 ( h ) Module 239 ( i ) Module 83 ( j ) Module 151 ( k ) Module 8 ( l ) Module 114 ( m ) Module 159 ( n ) Cancer meta signature ( o ) ERBB1 receptor proximal pathway ( p ) RIOK1 and RIOK2 in EGFR and PI3K-mediated tumorigenesis ( q ) Raf activation ( r ); Erk pathway ( s ); PI3K AKT pathway ( t ) PI3K PLC TRK pathway ( u ); mTOR4 pathway ( v )). Bottom: a heat map associated with the Cancer meta signature (in o ) and the ERBB1 receptor proximal pathway (in p ) are shown. The NES and nominal P value are indicated in the inner panel. w A schematic model of how PYCR1 regulates TLR-mediated signaling for the activation of NF-κB.
    Anti Tab2 Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/tab2/TAB2+Polyclonal+antibody/pm40999870-347-6-46
    Average 93 stars, based on 1 article reviews
    anti tab2 antibody - by Bioz Stars, 2026-10
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    anti tab2 mouse monoclonal  (Santa Cruz Biotechnology)
    93
    Santa Cruz Biotechnology anti tab2 mouse monoclonal
    a The HEK-293T cells were transiently transfected with mock (pcDNA, a control vector), Myc-PYCR1 or <t>Flag-TAB2,</t> as indicated. An IP assay was performed with an anti-Flag antibody, followed by an immunoblotting (IB) assay with anti-Flag or anti-Myc antibodies. b The HEK-293T cells were transiently transfected with mock, Flag-PYCR1, Myc-TAK1 or Flag-TAB2, as indicated. An IP assay was performed with an anti-Myc antibody, followed by an IB assay with anti-Flag or anti-Myc antibodies. c A schematic model illustrating the role of PYCR1 in the regulation of TRAF6-mediated signaling pathways. PYCR1 interacts with TAB2 and increases the interaction between TAK1 and TAB2. This complex enhances the TRAF6-mediated polyubiquitination of TAK1. d The A549 lung cancer cells were transiently transfected with Flag-PYCR1, and treated with or without LPS, as indicated. An IP assay was performed with anti-IgG or anti-Flag antibodies, followed by an IB assay with anti-Flag, anti-IRAK1, anti-TRAF6, anti-TAK1, anti-TAB2 or anti-ECSIT antibodies. e The H1299 cells were transfected with mock or Flag-PYCR1 and stimulated with or without LPS, as indicated. An IB assay was performed with anti-Flag, anti-TAK1, anti-pho-TAK1, anti-IKKs, anti-pho-IKKs, anti-p65, anti-pho-p65 and anti-GAPDH antibodies. f The A549 cells were transfected with mock or different concentrations of Flag-PYCR1, as indicated. The cells were stimulated with or without LPS for 6 h, as indicated. An NF-κB dual-luciferase assay was performed. The results are presented as mean ± s.d. ( n = 5). ** P < 0.01, *** P < 0.001. g , Based on the differential magnitude of PYCR1, TAB2, TAK1 and TRAF6 expression, 42 patients with NSCLC were categorized into two groups: those with upregulated PYCR1, TAB2, TAK1 and TRAF6 ( n = 9, red boxes) and those with downregulated PYCR1, TAB2, TAK1 and TRAF6 ( n = 6, green boxes). h – v The GSEA was conducted between the nine patients with upregulated PYCR1, TAB2, TAK1 and TRAF6 (PYCR1 up TAB2 up TAK1 up TRAF6 up NSCLCs, red) and the six patients with downregulated PYCR1, TAB2, TAK1 and TRAF6 (PYCR1 down TAB2 down TAK1 down TRAF6 down NSCLCs, green); the gene sets related to cancer modules (in h – n ) cancer meta signature ( o ) and EGFR signaling (in p – v ) are represented (Module 32 ( h ) Module 239 ( i ) Module 83 ( j ) Module 151 ( k ) Module 8 ( l ) Module 114 ( m ) Module 159 ( n ) Cancer meta signature ( o ) ERBB1 receptor proximal pathway ( p ) RIOK1 and RIOK2 in EGFR and PI3K-mediated tumorigenesis ( q ) Raf activation ( r ); Erk pathway ( s ); PI3K AKT pathway ( t ) PI3K PLC TRK pathway ( u ); mTOR4 pathway ( v )). Bottom: a heat map associated with the Cancer meta signature (in o ) and the ERBB1 receptor proximal pathway (in p ) are shown. The NES and nominal P value are indicated in the inner panel. w A schematic model of how PYCR1 regulates TLR-mediated signaling for the activation of NF-κB.
    Anti Tab2 Mouse Monoclonal, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/tab2/TAB2+Antibody/pmc12459955-306-6-9
    Average 93 stars, based on 1 article reviews
    anti tab2 mouse monoclonal - by Bioz Stars, 2026-10
    93/100 stars
    		  Buy from Supplier
    anti tab2  (Santa Cruz Biotechnology)
    93
    Santa Cruz Biotechnology anti tab2
    a The HEK-293T cells were transiently transfected with mock (pcDNA, a control vector), Myc-PYCR1 or <t>Flag-TAB2,</t> as indicated. An IP assay was performed with an anti-Flag antibody, followed by an immunoblotting (IB) assay with anti-Flag or anti-Myc antibodies. b The HEK-293T cells were transiently transfected with mock, Flag-PYCR1, Myc-TAK1 or Flag-TAB2, as indicated. An IP assay was performed with an anti-Myc antibody, followed by an IB assay with anti-Flag or anti-Myc antibodies. c A schematic model illustrating the role of PYCR1 in the regulation of TRAF6-mediated signaling pathways. PYCR1 interacts with TAB2 and increases the interaction between TAK1 and TAB2. This complex enhances the TRAF6-mediated polyubiquitination of TAK1. d The A549 lung cancer cells were transiently transfected with Flag-PYCR1, and treated with or without LPS, as indicated. An IP assay was performed with anti-IgG or anti-Flag antibodies, followed by an IB assay with anti-Flag, anti-IRAK1, anti-TRAF6, anti-TAK1, anti-TAB2 or anti-ECSIT antibodies. e The H1299 cells were transfected with mock or Flag-PYCR1 and stimulated with or without LPS, as indicated. An IB assay was performed with anti-Flag, anti-TAK1, anti-pho-TAK1, anti-IKKs, anti-pho-IKKs, anti-p65, anti-pho-p65 and anti-GAPDH antibodies. f The A549 cells were transfected with mock or different concentrations of Flag-PYCR1, as indicated. The cells were stimulated with or without LPS for 6 h, as indicated. An NF-κB dual-luciferase assay was performed. The results are presented as mean ± s.d. ( n = 5). ** P < 0.01, *** P < 0.001. g , Based on the differential magnitude of PYCR1, TAB2, TAK1 and TRAF6 expression, 42 patients with NSCLC were categorized into two groups: those with upregulated PYCR1, TAB2, TAK1 and TRAF6 ( n = 9, red boxes) and those with downregulated PYCR1, TAB2, TAK1 and TRAF6 ( n = 6, green boxes). h – v The GSEA was conducted between the nine patients with upregulated PYCR1, TAB2, TAK1 and TRAF6 (PYCR1 up TAB2 up TAK1 up TRAF6 up NSCLCs, red) and the six patients with downregulated PYCR1, TAB2, TAK1 and TRAF6 (PYCR1 down TAB2 down TAK1 down TRAF6 down NSCLCs, green); the gene sets related to cancer modules (in h – n ) cancer meta signature ( o ) and EGFR signaling (in p – v ) are represented (Module 32 ( h ) Module 239 ( i ) Module 83 ( j ) Module 151 ( k ) Module 8 ( l ) Module 114 ( m ) Module 159 ( n ) Cancer meta signature ( o ) ERBB1 receptor proximal pathway ( p ) RIOK1 and RIOK2 in EGFR and PI3K-mediated tumorigenesis ( q ) Raf activation ( r ); Erk pathway ( s ); PI3K AKT pathway ( t ) PI3K PLC TRK pathway ( u ); mTOR4 pathway ( v )). Bottom: a heat map associated with the Cancer meta signature (in o ) and the ERBB1 receptor proximal pathway (in p ) are shown. The NES and nominal P value are indicated in the inner panel. w A schematic model of how PYCR1 regulates TLR-mediated signaling for the activation of NF-κB.
    Anti Tab2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/tab2/TAB2+Antibody/pmc12459955-35-2-6
    Average 93 stars, based on 1 article reviews
    anti tab2 - by Bioz Stars, 2026-10
    93/100 stars
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    Image Search Results


    (A) CFIm25 overexpression increases TAB2 and TBL1XR1 mRNA expression after STM infection, assessed by RT-qPCR analysis in control and CFIm25-OE macrophages at 2 and 6 hours postinfection with STM (n = 3). Data are presented as means ± SD (n = 3); *, P < 0.05; **, P < 0.01. (B) Sequence of primers used for RT-qPCR analysis of TAB2 and TBL1XR1 APA. (C) Schematic representation of the long/total TAB2 and TBL1XR1 transcript regions targeted for RT-qPCR to assess APA and mRNA expression.

    Journal: bioRxiv

    Article Title: The Alternative Polyadenylation Factor CFIm25 Orchestrates Macrophage Antibacterial Immunity by Amplifying TAB2-Mediated MAPK and NF-κB Signaling During Salmonella Infection

    doi: 10.64898/2026.02.26.707986

    Figure Lengend Snippet: (A) CFIm25 overexpression increases TAB2 and TBL1XR1 mRNA expression after STM infection, assessed by RT-qPCR analysis in control and CFIm25-OE macrophages at 2 and 6 hours postinfection with STM (n = 3). Data are presented as means ± SD (n = 3); *, P < 0.05; **, P < 0.01. (B) Sequence of primers used for RT-qPCR analysis of TAB2 and TBL1XR1 APA. (C) Schematic representation of the long/total TAB2 and TBL1XR1 transcript regions targeted for RT-qPCR to assess APA and mRNA expression.

    Article Snippet: Antibodies used in this study included CFIm25 (Proteintech, 10322-1-AP), LL-37 (Santa Cruz, sc-166770), phosphorylated NF-κB P65 (Ser536) (Cell Signaling, 3033), NF-κB P65 (Cell Signaling, 8242), TAB2 (Cell Signaling, 3744), TBL1XR1 (Novus, NBP1-86996), phosphorylated STAT1 (Tyr701) (Cell Signaling, 9167), STAT1 (Cell Signaling, 14994), phosphorylated STAT3(Tyr705) (Cell Signaling, 9145), STAT3 (Cell Signaling, 4904), IκBα (Cell Signaling, 4814), phosphorylated P38(Thr180/Tyr182) (Cell Signaling, 4511), P38 (Cell Signaling, 9212), CD163 (Proteintech 68218-1-g), histone H3 (Cell Signaling, 9715), and GAPDH (Santa Cruz SC3233).

    Techniques: Over Expression, Expressing, Infection, Quantitative RT-PCR, Control, Sequencing

    (A-B) RT-qPCR analysis of the log2 ratio of long/total TAB2 (A) and TBL1XR1 (B) mRNA isoforms in control and CFIm25-OE macrophages at two and six hours postinfection, normalized to GAPDH. (C) Western blot analysis of CFIm25, HLA-DR, CD 163, and the indicated immune signaling proteins (“P”, protein; “p”, phosphorylated form) in control and CFIm25-OE macrophages at two and six hours postinfection, with GAPDH as the loading control. (D) Quantification of changes of the indicated proteins in Western blots of samples from control and CFIm25-OE macrophages at two and six hours postinfection, with values normalized to GAPDH. (E) Representative Western blot showing nuclear and cytoplasmic distribution of NF-κB subunits in control and CFIm25-OE macrophages two and six hours postinfection, assessed by fractionation and immunoblotting. Data from all quantifications are presented as means ± SD from three independent experiments. *, P < 0.05; **, P < 0.01.

    Journal: bioRxiv

    Article Title: The Alternative Polyadenylation Factor CFIm25 Orchestrates Macrophage Antibacterial Immunity by Amplifying TAB2-Mediated MAPK and NF-κB Signaling During Salmonella Infection

    doi: 10.64898/2026.02.26.707986

    Figure Lengend Snippet: (A-B) RT-qPCR analysis of the log2 ratio of long/total TAB2 (A) and TBL1XR1 (B) mRNA isoforms in control and CFIm25-OE macrophages at two and six hours postinfection, normalized to GAPDH. (C) Western blot analysis of CFIm25, HLA-DR, CD 163, and the indicated immune signaling proteins (“P”, protein; “p”, phosphorylated form) in control and CFIm25-OE macrophages at two and six hours postinfection, with GAPDH as the loading control. (D) Quantification of changes of the indicated proteins in Western blots of samples from control and CFIm25-OE macrophages at two and six hours postinfection, with values normalized to GAPDH. (E) Representative Western blot showing nuclear and cytoplasmic distribution of NF-κB subunits in control and CFIm25-OE macrophages two and six hours postinfection, assessed by fractionation and immunoblotting. Data from all quantifications are presented as means ± SD from three independent experiments. *, P < 0.05; **, P < 0.01.

    Article Snippet: Antibodies used in this study included CFIm25 (Proteintech, 10322-1-AP), LL-37 (Santa Cruz, sc-166770), phosphorylated NF-κB P65 (Ser536) (Cell Signaling, 3033), NF-κB P65 (Cell Signaling, 8242), TAB2 (Cell Signaling, 3744), TBL1XR1 (Novus, NBP1-86996), phosphorylated STAT1 (Tyr701) (Cell Signaling, 9167), STAT1 (Cell Signaling, 14994), phosphorylated STAT3(Tyr705) (Cell Signaling, 9145), STAT3 (Cell Signaling, 4904), IκBα (Cell Signaling, 4814), phosphorylated P38(Thr180/Tyr182) (Cell Signaling, 4511), P38 (Cell Signaling, 9212), CD163 (Proteintech 68218-1-g), histone H3 (Cell Signaling, 9715), and GAPDH (Santa Cruz SC3233).

    Techniques: Quantitative RT-PCR, Control, Western Blot, Fractionation

    (A) CFUs recovered at six hours postinfection from Intracellular STM in CFIm25-OE macrophages transfected with control siRNA, TAB2 siRNA, or TBL1XR1 siRNA. (B) Concentrations of TNF-α, IL-12, TGF-β, and IL-10 in culture supernatants from CFIm25-OE macrophages expressing control, TAB2, or TBL1XR1 siRNAs, harvested at six hours postinfection, and measured by ELISA. (C-F) ROS (C), NO (D), arginase activity (E), and lactate (F) levels at six hours postinfection in CFIm25-OE macrophages treated with control, TAB2, or TBL1XR1 siRNA. (G) Flow cytometric analysis of CD80 and CD206 expression at six hours postinfection in CFIm25-OE macrophages treated with control, TAB2, or TBL1XR1 siRNA. (H) Western blot analysis of the indicated NF-κB and MAPK signaling proteins at six hours postinfection in CFIm25-OE macrophages treated with control, TAB2, or TBL1XR1 siRNA, with densitometric quantification from three independent experiments (“P”, protein; “p”, phosphorylated form). Data are presented as means ± SD (n = 3); *, P < 0.05; **, P < 0.01.

    Journal: bioRxiv

    Article Title: The Alternative Polyadenylation Factor CFIm25 Orchestrates Macrophage Antibacterial Immunity by Amplifying TAB2-Mediated MAPK and NF-κB Signaling During Salmonella Infection

    doi: 10.64898/2026.02.26.707986

    Figure Lengend Snippet: (A) CFUs recovered at six hours postinfection from Intracellular STM in CFIm25-OE macrophages transfected with control siRNA, TAB2 siRNA, or TBL1XR1 siRNA. (B) Concentrations of TNF-α, IL-12, TGF-β, and IL-10 in culture supernatants from CFIm25-OE macrophages expressing control, TAB2, or TBL1XR1 siRNAs, harvested at six hours postinfection, and measured by ELISA. (C-F) ROS (C), NO (D), arginase activity (E), and lactate (F) levels at six hours postinfection in CFIm25-OE macrophages treated with control, TAB2, or TBL1XR1 siRNA. (G) Flow cytometric analysis of CD80 and CD206 expression at six hours postinfection in CFIm25-OE macrophages treated with control, TAB2, or TBL1XR1 siRNA. (H) Western blot analysis of the indicated NF-κB and MAPK signaling proteins at six hours postinfection in CFIm25-OE macrophages treated with control, TAB2, or TBL1XR1 siRNA, with densitometric quantification from three independent experiments (“P”, protein; “p”, phosphorylated form). Data are presented as means ± SD (n = 3); *, P < 0.05; **, P < 0.01.

    Article Snippet: Antibodies used in this study included CFIm25 (Proteintech, 10322-1-AP), LL-37 (Santa Cruz, sc-166770), phosphorylated NF-κB P65 (Ser536) (Cell Signaling, 3033), NF-κB P65 (Cell Signaling, 8242), TAB2 (Cell Signaling, 3744), TBL1XR1 (Novus, NBP1-86996), phosphorylated STAT1 (Tyr701) (Cell Signaling, 9167), STAT1 (Cell Signaling, 14994), phosphorylated STAT3(Tyr705) (Cell Signaling, 9145), STAT3 (Cell Signaling, 4904), IκBα (Cell Signaling, 4814), phosphorylated P38(Thr180/Tyr182) (Cell Signaling, 4511), P38 (Cell Signaling, 9212), CD163 (Proteintech 68218-1-g), histone H3 (Cell Signaling, 9715), and GAPDH (Santa Cruz SC3233).

    Techniques: Transfection, Control, Expressing, Enzyme-linked Immunosorbent Assay, Activity Assay, Western Blot

    a The HEK-293T cells were transiently transfected with mock (pcDNA, a control vector), Myc-PYCR1 or Flag-TAB2, as indicated. An IP assay was performed with an anti-Flag antibody, followed by an immunoblotting (IB) assay with anti-Flag or anti-Myc antibodies. b The HEK-293T cells were transiently transfected with mock, Flag-PYCR1, Myc-TAK1 or Flag-TAB2, as indicated. An IP assay was performed with an anti-Myc antibody, followed by an IB assay with anti-Flag or anti-Myc antibodies. c A schematic model illustrating the role of PYCR1 in the regulation of TRAF6-mediated signaling pathways. PYCR1 interacts with TAB2 and increases the interaction between TAK1 and TAB2. This complex enhances the TRAF6-mediated polyubiquitination of TAK1. d The A549 lung cancer cells were transiently transfected with Flag-PYCR1, and treated with or without LPS, as indicated. An IP assay was performed with anti-IgG or anti-Flag antibodies, followed by an IB assay with anti-Flag, anti-IRAK1, anti-TRAF6, anti-TAK1, anti-TAB2 or anti-ECSIT antibodies. e The H1299 cells were transfected with mock or Flag-PYCR1 and stimulated with or without LPS, as indicated. An IB assay was performed with anti-Flag, anti-TAK1, anti-pho-TAK1, anti-IKKs, anti-pho-IKKs, anti-p65, anti-pho-p65 and anti-GAPDH antibodies. f The A549 cells were transfected with mock or different concentrations of Flag-PYCR1, as indicated. The cells were stimulated with or without LPS for 6 h, as indicated. An NF-κB dual-luciferase assay was performed. The results are presented as mean ± s.d. ( n = 5). ** P < 0.01, *** P < 0.001. g , Based on the differential magnitude of PYCR1, TAB2, TAK1 and TRAF6 expression, 42 patients with NSCLC were categorized into two groups: those with upregulated PYCR1, TAB2, TAK1 and TRAF6 ( n = 9, red boxes) and those with downregulated PYCR1, TAB2, TAK1 and TRAF6 ( n = 6, green boxes). h – v The GSEA was conducted between the nine patients with upregulated PYCR1, TAB2, TAK1 and TRAF6 (PYCR1 up TAB2 up TAK1 up TRAF6 up NSCLCs, red) and the six patients with downregulated PYCR1, TAB2, TAK1 and TRAF6 (PYCR1 down TAB2 down TAK1 down TRAF6 down NSCLCs, green); the gene sets related to cancer modules (in h – n ) cancer meta signature ( o ) and EGFR signaling (in p – v ) are represented (Module 32 ( h ) Module 239 ( i ) Module 83 ( j ) Module 151 ( k ) Module 8 ( l ) Module 114 ( m ) Module 159 ( n ) Cancer meta signature ( o ) ERBB1 receptor proximal pathway ( p ) RIOK1 and RIOK2 in EGFR and PI3K-mediated tumorigenesis ( q ) Raf activation ( r ); Erk pathway ( s ); PI3K AKT pathway ( t ) PI3K PLC TRK pathway ( u ); mTOR4 pathway ( v )). Bottom: a heat map associated with the Cancer meta signature (in o ) and the ERBB1 receptor proximal pathway (in p ) are shown. The NES and nominal P value are indicated in the inner panel. w A schematic model of how PYCR1 regulates TLR-mediated signaling for the activation of NF-κB.

    Journal: Experimental & Molecular Medicine

    Article Title: PYCR1 drives lung cancer progression through functional interactions with EGFR and TLR signaling pathways

    doi: 10.1038/s12276-025-01577-z

    Figure Lengend Snippet: a The HEK-293T cells were transiently transfected with mock (pcDNA, a control vector), Myc-PYCR1 or Flag-TAB2, as indicated. An IP assay was performed with an anti-Flag antibody, followed by an immunoblotting (IB) assay with anti-Flag or anti-Myc antibodies. b The HEK-293T cells were transiently transfected with mock, Flag-PYCR1, Myc-TAK1 or Flag-TAB2, as indicated. An IP assay was performed with an anti-Myc antibody, followed by an IB assay with anti-Flag or anti-Myc antibodies. c A schematic model illustrating the role of PYCR1 in the regulation of TRAF6-mediated signaling pathways. PYCR1 interacts with TAB2 and increases the interaction between TAK1 and TAB2. This complex enhances the TRAF6-mediated polyubiquitination of TAK1. d The A549 lung cancer cells were transiently transfected with Flag-PYCR1, and treated with or without LPS, as indicated. An IP assay was performed with anti-IgG or anti-Flag antibodies, followed by an IB assay with anti-Flag, anti-IRAK1, anti-TRAF6, anti-TAK1, anti-TAB2 or anti-ECSIT antibodies. e The H1299 cells were transfected with mock or Flag-PYCR1 and stimulated with or without LPS, as indicated. An IB assay was performed with anti-Flag, anti-TAK1, anti-pho-TAK1, anti-IKKs, anti-pho-IKKs, anti-p65, anti-pho-p65 and anti-GAPDH antibodies. f The A549 cells were transfected with mock or different concentrations of Flag-PYCR1, as indicated. The cells were stimulated with or without LPS for 6 h, as indicated. An NF-κB dual-luciferase assay was performed. The results are presented as mean ± s.d. ( n = 5). ** P < 0.01, *** P < 0.001. g , Based on the differential magnitude of PYCR1, TAB2, TAK1 and TRAF6 expression, 42 patients with NSCLC were categorized into two groups: those with upregulated PYCR1, TAB2, TAK1 and TRAF6 ( n = 9, red boxes) and those with downregulated PYCR1, TAB2, TAK1 and TRAF6 ( n = 6, green boxes). h – v The GSEA was conducted between the nine patients with upregulated PYCR1, TAB2, TAK1 and TRAF6 (PYCR1 up TAB2 up TAK1 up TRAF6 up NSCLCs, red) and the six patients with downregulated PYCR1, TAB2, TAK1 and TRAF6 (PYCR1 down TAB2 down TAK1 down TRAF6 down NSCLCs, green); the gene sets related to cancer modules (in h – n ) cancer meta signature ( o ) and EGFR signaling (in p – v ) are represented (Module 32 ( h ) Module 239 ( i ) Module 83 ( j ) Module 151 ( k ) Module 8 ( l ) Module 114 ( m ) Module 159 ( n ) Cancer meta signature ( o ) ERBB1 receptor proximal pathway ( p ) RIOK1 and RIOK2 in EGFR and PI3K-mediated tumorigenesis ( q ) Raf activation ( r ); Erk pathway ( s ); PI3K AKT pathway ( t ) PI3K PLC TRK pathway ( u ); mTOR4 pathway ( v )). Bottom: a heat map associated with the Cancer meta signature (in o ) and the ERBB1 receptor proximal pathway (in p ) are shown. The NES and nominal P value are indicated in the inner panel. w A schematic model of how PYCR1 regulates TLR-mediated signaling for the activation of NF-κB.

    Article Snippet: Anti-NF-κB p65/RelA (A2547) and anti-TAB2 (A9867) antibodies were purchased from ABclonal.

    Techniques: Transfection, Control, Plasmid Preparation, Western Blot, Protein-Protein interactions, Luciferase, Expressing, Activation Assay

    a An experimental protocol for the evaluation of therapeutic effect of a PYCR1 inhibitor, PYCR1-IN-1, in WT H1299 (50 cells per well), H460 (50 cells per well) and A549 (250 cells per well) cells. After the stabilization of tumor spheroids for 2 days, the spheroids were treated with 10 μM PYCR1-IN-1, treated with vehicle (DMSO, 0.1% v/v concentration), Pam3CSK4 (3 μg/ml), HKLM (10 7 /ml), Poly(I:C) (5 μg/ml), LPS (5 μg/ml) or EGF (10 ng/ml) and incubated for different times, as indicated. b , c The H1299-derived tumor spheroid formation and growth were evaluated using phase-contrast microscopy (scale bar, 100 μm) ( b , phase-contrast microscopy images). The spheroid sizes were measured using ImageJ Software. The error bars represent ± s.d. ( n = 7) (in c , spheroid sizes). * P < 0.05, ** P < 0.01, *** P < 0.001: # P < 0.05, ## P < 0.01, ### P < 0.001, H1299 spheroids treated without PYCR1-IN-1 versus H1299 spheroids treated with PYCR1-IN-1. d , e H460-derived tumor spheroid formation and growth were evaluated using phase-contrast microscopy (scale bar, 100 μm) ( d , phase-contrast microscopy images). The spheroid sizes were measured using ImageJ Software. The error bars represent ± s.d. ( n = 7) (in e , spheroid sizes). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001: # P < 0.05, ## P < 0.01, ### P < 0.001, #### P < 0.0001, H460 spheroids treated without PYCR1-IN-1 versus H460 spheroids treated with PYCR1-IN-1. f , g A549-derived tumor spheroid formation and growth were evaluated using phase-contrast microscopy (scale bar, 100 μm) ( f , phase-contrast microscopy images). The spheroid sizes were measured using ImageJ Software. The error bars represent ± s.d. ( n = 7) (in g , spheroid sizes). * P < 0.05, ** P < 0.01, *** P < 0.001: # P < 0.05, ## P < 0.01, ### P < 0.001, A549 spheroids treated without PYCR1-IN-1 versus A549 spheroids treated with PYCR1-IN-1. h , i A schematic representation of the therapeutic target in EGFR- ( h ) or TLR-driven ( i ) lung cancer progression. PYCR1 interacts with USP11, resulting in the deubiquitination and subsequent stabilization of EGFR in h . PYCR1 interacts with TLR-mediated signaling molecules, such as IRAK1, TRAF6, TAB2 and ECSIT, leading to increased ROS production and enhanced NF-κB activity in i .

    Journal: Experimental & Molecular Medicine

    Article Title: PYCR1 drives lung cancer progression through functional interactions with EGFR and TLR signaling pathways

    doi: 10.1038/s12276-025-01577-z

    Figure Lengend Snippet: a An experimental protocol for the evaluation of therapeutic effect of a PYCR1 inhibitor, PYCR1-IN-1, in WT H1299 (50 cells per well), H460 (50 cells per well) and A549 (250 cells per well) cells. After the stabilization of tumor spheroids for 2 days, the spheroids were treated with 10 μM PYCR1-IN-1, treated with vehicle (DMSO, 0.1% v/v concentration), Pam3CSK4 (3 μg/ml), HKLM (10 7 /ml), Poly(I:C) (5 μg/ml), LPS (5 μg/ml) or EGF (10 ng/ml) and incubated for different times, as indicated. b , c The H1299-derived tumor spheroid formation and growth were evaluated using phase-contrast microscopy (scale bar, 100 μm) ( b , phase-contrast microscopy images). The spheroid sizes were measured using ImageJ Software. The error bars represent ± s.d. ( n = 7) (in c , spheroid sizes). * P < 0.05, ** P < 0.01, *** P < 0.001: # P < 0.05, ## P < 0.01, ### P < 0.001, H1299 spheroids treated without PYCR1-IN-1 versus H1299 spheroids treated with PYCR1-IN-1. d , e H460-derived tumor spheroid formation and growth were evaluated using phase-contrast microscopy (scale bar, 100 μm) ( d , phase-contrast microscopy images). The spheroid sizes were measured using ImageJ Software. The error bars represent ± s.d. ( n = 7) (in e , spheroid sizes). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001: # P < 0.05, ## P < 0.01, ### P < 0.001, #### P < 0.0001, H460 spheroids treated without PYCR1-IN-1 versus H460 spheroids treated with PYCR1-IN-1. f , g A549-derived tumor spheroid formation and growth were evaluated using phase-contrast microscopy (scale bar, 100 μm) ( f , phase-contrast microscopy images). The spheroid sizes were measured using ImageJ Software. The error bars represent ± s.d. ( n = 7) (in g , spheroid sizes). * P < 0.05, ** P < 0.01, *** P < 0.001: # P < 0.05, ## P < 0.01, ### P < 0.001, A549 spheroids treated without PYCR1-IN-1 versus A549 spheroids treated with PYCR1-IN-1. h , i A schematic representation of the therapeutic target in EGFR- ( h ) or TLR-driven ( i ) lung cancer progression. PYCR1 interacts with USP11, resulting in the deubiquitination and subsequent stabilization of EGFR in h . PYCR1 interacts with TLR-mediated signaling molecules, such as IRAK1, TRAF6, TAB2 and ECSIT, leading to increased ROS production and enhanced NF-κB activity in i .

    Article Snippet: Anti-NF-κB p65/RelA (A2547) and anti-TAB2 (A9867) antibodies were purchased from ABclonal.

    Techniques: Concentration Assay, Incubation, Derivative Assay, Microscopy, Software, Activity Assay