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Proteintech tnfr1
Autophagy limits CAR‐T cell‐mediated cytotoxicity by suppressing TNF‐α induced apoptosis. (A) Volcano plot showing varied genes in Nalm6 cells with the addition of vehicle (as control) and autophinib (log 2 FC > 1 and P < 0.05). (B) Volcano plot showing varied genes between sgControl and indicated RB1CC1 KO Nalm6 cells (log 2 FC > 1 and P < 0.05). (C) KEGG pathway enrichment analysis of varied genes identified in RNA sequencing for Nalm6 cells treated with vehicle (as control) and autophinib. (D) Western blotting showing the expression levels of Caspase‐8, Cleaved caspase‐8, Caspase‐9, Cleaved caspase‐9 and p62 proteins after the addition of vehicle (as control), autophinib and SAR405 in Nalm6 and Raji cells when co‐cultured with or without CD19 CAR‐T cells. GAPDH was used as a loading control. (E) Western blotting showing the expression levels of Caspase‐8, Cleaved caspase‐8, Caspase‐9, Cleaved caspase‐9 and p62 proteins in sgControl and indicated gene‐KO (sgBECN1, sgRB1CC1) Nalm6 and Raji cells when co‐cultured with or without CD19 CAR‐T cells. GAPDH was used as a loading control. (F) Expression of TNFRSF1A mRNA by RT‐qPCR and <t>TNFR1</t> protein by western blotting in Nalm6 and Raji cells after addition of vehicle (as control), autophinib and SAR405 ( n = 3). Values are shown as the mean ± SD. Statistical differences among three groups in each cell line are calculated with one‐way ANOVA with tests. (G‐H) Cytotoxic analysis of sgControl and indicated gene‐KO (sgTNFRSF1A) Nalm6 and Raji cells co‐cultured with CD19 CAR‐T cells (E:T ratio = 1:4) when treated with vehicle (as control), autophinib and SAR405 and then with or without TNF‐block ( n = 3). Values are shown as the mean ± SD. Statistical differences are calculated with two‐way ANOVA with tests. (I) Cytotoxic analysis of sgControl and indicated gene‐KO (sgBECN1, sgRB1CC1, sgTNFRSF1A) Nalm6 and Raji cells co‐cultured with CD19 CAR‐T cells (E: T ratio = 1: 4) when treated with or without TNF block ( n = 3). Values are shown as the mean ± SD. Statistical differences are calculated with two‐way ANOVA with tests. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0,001; ns: not significant. Abbreviations: ANOVA analysis of variance; CAR‐T chimeric antigen receptor T; E:T effector:target; FC fold change; FC fold change; KO knockout; KEGG Kyoto Encyclopedia of Genes and Genomes; RT‐qPCR real‐time quantitative polymerase chain reaction; ns: not significant; SD standard deviation; sg single guide; TNF tumor necrosis factor; TNFR1 tumor necrosis factor receptor 1.
Tnfr1, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 116 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 95 stars, based on 116 article reviews
tnfr1 - by Bioz Stars, 2026-10
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1) Product Images from "Targeting autophagy overcomes cancer‐intrinsic resistance to CAR‐T immunotherapy in B‐cell malignancies"

Article Title: Targeting autophagy overcomes cancer‐intrinsic resistance to CAR‐T immunotherapy in B‐cell malignancies

Journal: Cancer Communications

doi: 10.1002/cac2.12525

Autophagy limits CAR‐T cell‐mediated cytotoxicity by suppressing TNF‐α induced apoptosis. (A) Volcano plot showing varied genes in Nalm6 cells with the addition of vehicle (as control) and autophinib (log 2 FC > 1 and P < 0.05). (B) Volcano plot showing varied genes between sgControl and indicated RB1CC1 KO Nalm6 cells (log 2 FC > 1 and P < 0.05). (C) KEGG pathway enrichment analysis of varied genes identified in RNA sequencing for Nalm6 cells treated with vehicle (as control) and autophinib. (D) Western blotting showing the expression levels of Caspase‐8, Cleaved caspase‐8, Caspase‐9, Cleaved caspase‐9 and p62 proteins after the addition of vehicle (as control), autophinib and SAR405 in Nalm6 and Raji cells when co‐cultured with or without CD19 CAR‐T cells. GAPDH was used as a loading control. (E) Western blotting showing the expression levels of Caspase‐8, Cleaved caspase‐8, Caspase‐9, Cleaved caspase‐9 and p62 proteins in sgControl and indicated gene‐KO (sgBECN1, sgRB1CC1) Nalm6 and Raji cells when co‐cultured with or without CD19 CAR‐T cells. GAPDH was used as a loading control. (F) Expression of TNFRSF1A mRNA by RT‐qPCR and TNFR1 protein by western blotting in Nalm6 and Raji cells after addition of vehicle (as control), autophinib and SAR405 ( n = 3). Values are shown as the mean ± SD. Statistical differences among three groups in each cell line are calculated with one‐way ANOVA with tests. (G‐H) Cytotoxic analysis of sgControl and indicated gene‐KO (sgTNFRSF1A) Nalm6 and Raji cells co‐cultured with CD19 CAR‐T cells (E:T ratio = 1:4) when treated with vehicle (as control), autophinib and SAR405 and then with or without TNF‐block ( n = 3). Values are shown as the mean ± SD. Statistical differences are calculated with two‐way ANOVA with tests. (I) Cytotoxic analysis of sgControl and indicated gene‐KO (sgBECN1, sgRB1CC1, sgTNFRSF1A) Nalm6 and Raji cells co‐cultured with CD19 CAR‐T cells (E: T ratio = 1: 4) when treated with or without TNF block ( n = 3). Values are shown as the mean ± SD. Statistical differences are calculated with two‐way ANOVA with tests. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0,001; ns: not significant. Abbreviations: ANOVA analysis of variance; CAR‐T chimeric antigen receptor T; E:T effector:target; FC fold change; FC fold change; KO knockout; KEGG Kyoto Encyclopedia of Genes and Genomes; RT‐qPCR real‐time quantitative polymerase chain reaction; ns: not significant; SD standard deviation; sg single guide; TNF tumor necrosis factor; TNFR1 tumor necrosis factor receptor 1.
Figure Legend Snippet: Autophagy limits CAR‐T cell‐mediated cytotoxicity by suppressing TNF‐α induced apoptosis. (A) Volcano plot showing varied genes in Nalm6 cells with the addition of vehicle (as control) and autophinib (log 2 FC > 1 and P < 0.05). (B) Volcano plot showing varied genes between sgControl and indicated RB1CC1 KO Nalm6 cells (log 2 FC > 1 and P < 0.05). (C) KEGG pathway enrichment analysis of varied genes identified in RNA sequencing for Nalm6 cells treated with vehicle (as control) and autophinib. (D) Western blotting showing the expression levels of Caspase‐8, Cleaved caspase‐8, Caspase‐9, Cleaved caspase‐9 and p62 proteins after the addition of vehicle (as control), autophinib and SAR405 in Nalm6 and Raji cells when co‐cultured with or without CD19 CAR‐T cells. GAPDH was used as a loading control. (E) Western blotting showing the expression levels of Caspase‐8, Cleaved caspase‐8, Caspase‐9, Cleaved caspase‐9 and p62 proteins in sgControl and indicated gene‐KO (sgBECN1, sgRB1CC1) Nalm6 and Raji cells when co‐cultured with or without CD19 CAR‐T cells. GAPDH was used as a loading control. (F) Expression of TNFRSF1A mRNA by RT‐qPCR and TNFR1 protein by western blotting in Nalm6 and Raji cells after addition of vehicle (as control), autophinib and SAR405 ( n = 3). Values are shown as the mean ± SD. Statistical differences among three groups in each cell line are calculated with one‐way ANOVA with tests. (G‐H) Cytotoxic analysis of sgControl and indicated gene‐KO (sgTNFRSF1A) Nalm6 and Raji cells co‐cultured with CD19 CAR‐T cells (E:T ratio = 1:4) when treated with vehicle (as control), autophinib and SAR405 and then with or without TNF‐block ( n = 3). Values are shown as the mean ± SD. Statistical differences are calculated with two‐way ANOVA with tests. (I) Cytotoxic analysis of sgControl and indicated gene‐KO (sgBECN1, sgRB1CC1, sgTNFRSF1A) Nalm6 and Raji cells co‐cultured with CD19 CAR‐T cells (E: T ratio = 1: 4) when treated with or without TNF block ( n = 3). Values are shown as the mean ± SD. Statistical differences are calculated with two‐way ANOVA with tests. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0,001; ns: not significant. Abbreviations: ANOVA analysis of variance; CAR‐T chimeric antigen receptor T; E:T effector:target; FC fold change; FC fold change; KO knockout; KEGG Kyoto Encyclopedia of Genes and Genomes; RT‐qPCR real‐time quantitative polymerase chain reaction; ns: not significant; SD standard deviation; sg single guide; TNF tumor necrosis factor; TNFR1 tumor necrosis factor receptor 1.

Techniques Used: Control, RNA Sequencing, Western Blot, Expressing, Cell Culture, Quantitative RT-PCR, Blocking Assay, Knock-Out, Real-time Polymerase Chain Reaction, Standard Deviation

STAT1/IRF1 axis mediates the upregulation of CXCL10 and CXCL11 induced by autophagy targeting. (A‐B) Western blotting showing the expression levels of STAT1, pSTAT1, and IRF1 proteins in Nalm6 and Raji cells after the addition of autophagy inhibitors or the knockout of RB1CC1 ( n = 3). GAPDH was used as a loading control. The histograms showing the expression of STAT1 and IRF1 mRNA by RT‐qPCR quantification. Values are shown as the mean ± SD. Statistical differences are calculated with one‐way ANOVA tests. (C‐D) Western blotting showing the expression levels of STAT1 and IRF1 proteins in Nalm6 and Raji cells after the addition of autophagy inhibitors and the silencing of STAT1 ( n = 3). GAPDH was used as a loading control. The histograms showing the expression of STAT1 and IRF1 mRNA by RT‐qPCR quantification. Values are shown as the mean ± SD. Statistical differences are calculated with one‐way ANOVA tests. (E‐F) Expression of CXCL10 and CXCL11 mRNA by RT‐qPCR and ELISA quantification of CXCL10 and CXCL11 protein levels in the supernatants of shControl, shSTAT1 and shIRF1 Nalm6 and Raji cells ( n = 3). Values are shown as the mean ± SD. Statistical differences are calculated with two‐way ANOVA tests. (G‐H) ChIP‐qPCR showing the binding of STAT1 and IRF1 to the promoter region of CXCL10 and CXCL11 ( n = 3). Values are shown as the mean ± SD. Statistical differences for each cell line are calculated with unpaired Student's t tests. (I) Graphic abstract: in the proposed model, inhibition of cancer cell‐autonomous autophagy leads to accumulation of cytosolic DNA, which thereby not only suppresses cancer cell survival by inducing TNFR1‐TNF‐α mediated apoptosis but also promotes the CAR‐T cell recruitment in tumor microenvironment via STAT1/IRF1‐dependent activation of chemokine signaling. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0,001; ns: not significant. Abbreviations: ANOVA analysis of variance; CAR‐T, chimeric antigen receptor T; ChIP, chromatin immunoprecipitation; CXCL CXC, chemokine ligand; ELISA, enzyme‐linked immunosorbent assay; FC, fold change; IRF, interferon regulatory factor; ns: not significant; RT‐qPCR, real‐time quantitative polymerase chain reaction; SD, standard deviation; sh short hairpin; STAT, signal transducers and activators of transcription.
Figure Legend Snippet: STAT1/IRF1 axis mediates the upregulation of CXCL10 and CXCL11 induced by autophagy targeting. (A‐B) Western blotting showing the expression levels of STAT1, pSTAT1, and IRF1 proteins in Nalm6 and Raji cells after the addition of autophagy inhibitors or the knockout of RB1CC1 ( n = 3). GAPDH was used as a loading control. The histograms showing the expression of STAT1 and IRF1 mRNA by RT‐qPCR quantification. Values are shown as the mean ± SD. Statistical differences are calculated with one‐way ANOVA tests. (C‐D) Western blotting showing the expression levels of STAT1 and IRF1 proteins in Nalm6 and Raji cells after the addition of autophagy inhibitors and the silencing of STAT1 ( n = 3). GAPDH was used as a loading control. The histograms showing the expression of STAT1 and IRF1 mRNA by RT‐qPCR quantification. Values are shown as the mean ± SD. Statistical differences are calculated with one‐way ANOVA tests. (E‐F) Expression of CXCL10 and CXCL11 mRNA by RT‐qPCR and ELISA quantification of CXCL10 and CXCL11 protein levels in the supernatants of shControl, shSTAT1 and shIRF1 Nalm6 and Raji cells ( n = 3). Values are shown as the mean ± SD. Statistical differences are calculated with two‐way ANOVA tests. (G‐H) ChIP‐qPCR showing the binding of STAT1 and IRF1 to the promoter region of CXCL10 and CXCL11 ( n = 3). Values are shown as the mean ± SD. Statistical differences for each cell line are calculated with unpaired Student's t tests. (I) Graphic abstract: in the proposed model, inhibition of cancer cell‐autonomous autophagy leads to accumulation of cytosolic DNA, which thereby not only suppresses cancer cell survival by inducing TNFR1‐TNF‐α mediated apoptosis but also promotes the CAR‐T cell recruitment in tumor microenvironment via STAT1/IRF1‐dependent activation of chemokine signaling. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0,001; ns: not significant. Abbreviations: ANOVA analysis of variance; CAR‐T, chimeric antigen receptor T; ChIP, chromatin immunoprecipitation; CXCL CXC, chemokine ligand; ELISA, enzyme‐linked immunosorbent assay; FC, fold change; IRF, interferon regulatory factor; ns: not significant; RT‐qPCR, real‐time quantitative polymerase chain reaction; SD, standard deviation; sh short hairpin; STAT, signal transducers and activators of transcription.

Techniques Used: Western Blot, Expressing, Knock-Out, Control, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, ChIP-qPCR, Binding Assay, Inhibition, Activation Assay, Chromatin Immunoprecipitation, Real-time Polymerase Chain Reaction, Standard Deviation

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CCK-8 Assay:

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Multiple Displacement Amplification:

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Real-time Polymerase Chain Reaction:

Article Title: Rhoifolin inhibits ferroptosis and alleviates pulmonary arterial hypertension via the TNF-α/TNF-R1/CASP8/CASP3 pathway.
Article Snippet: Background: Pulmonary arterial hypertension (PAH) is a fatal disease driven by progressive vascular remodeling.. Emerging evidence links ferroptosis, an iron-dependent form of regulated cell death, to PAH pathogenesis, suggesting that inhibiting ferroptosis is a promising therapeutic strategy.. Rhoifolin (ROF), a natural flavonoid with multiple bioactivities, has not been studied in PAH.

SYBR Green Assay:

Article Title: Rhoifolin inhibits ferroptosis and alleviates pulmonary arterial hypertension via the TNF-α/TNF-R1/CASP8/CASP3 pathway.
Article Snippet: Background: Pulmonary arterial hypertension (PAH) is a fatal disease driven by progressive vascular remodeling.. Emerging evidence links ferroptosis, an iron-dependent form of regulated cell death, to PAH pathogenesis, suggesting that inhibiting ferroptosis is a promising therapeutic strategy.. Rhoifolin (ROF), a natural flavonoid with multiple bioactivities, has not been studied in PAH.

Live Cell Imaging:

Article Title: Rhoifolin inhibits ferroptosis and alleviates pulmonary arterial hypertension via the TNF-α/TNF-R1/CASP8/CASP3 pathway.
Article Snippet: Background: Pulmonary arterial hypertension (PAH) is a fatal disease driven by progressive vascular remodeling.. Emerging evidence links ferroptosis, an iron-dependent form of regulated cell death, to PAH pathogenesis, suggesting that inhibiting ferroptosis is a promising therapeutic strategy.. Rhoifolin (ROF), a natural flavonoid with multiple bioactivities, has not been studied in PAH.

Electrophoresis:

Article Title: Rhoifolin inhibits ferroptosis and alleviates pulmonary arterial hypertension via the TNF-α/TNF-R1/CASP8/CASP3 pathway.
Article Snippet: Background: Pulmonary arterial hypertension (PAH) is a fatal disease driven by progressive vascular remodeling.. Emerging evidence links ferroptosis, an iron-dependent form of regulated cell death, to PAH pathogenesis, suggesting that inhibiting ferroptosis is a promising therapeutic strategy.. Rhoifolin (ROF), a natural flavonoid with multiple bioactivities, has not been studied in PAH.

Spectrophotometry:

Article Title: Rhoifolin inhibits ferroptosis and alleviates pulmonary arterial hypertension via the TNF-α/TNF-R1/CASP8/CASP3 pathway.
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Polymerase Chain Reaction:

Article Title: Rhoifolin inhibits ferroptosis and alleviates pulmonary arterial hypertension via the TNF-α/TNF-R1/CASP8/CASP3 pathway.
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Incubation:

Article Title: Targeting the DSTYK-ULK1 axis rewires TNFR1 signaling to overcome treatment resistance in lung cancer.
Article Snippet: .. Cells were washed twice in ice-cold PBS, then blocked in ice-cold Tris-balanced salt solution with 0.05% v/v Triton X-100 (TBS-T) supplemented with 10% v/v Bovine Serum Albumin (BSA) (Sigma-Aldrich; #A3059-100G) for >1 h. Cells were incubated in mouse anti-TNFR1 primary antibody overnight (Proteintech; #60192-1-Ig) or anti-c-IAP1 primary antibody (Cell signaling Technology; #7065) at 4 ◦ C 1:1000 and 1:500 in TBS-T with 10% v/v donkey serum. .. To inhibit ULK1, plated cells were treated with 10 μM ULK101 (#HY-114490; MedChemExpress).

Article Title: A SASP-related four-gene signature associated with intervertebral disc degeneration: integrated bioinformatics analysis and validation of pinocembrin as a therapeutic candidate.
Article Snippet: 1 Department of Orthopedic Surgery, The Third Affiliated Hospital, Jiangxi Medical College, First Hospital of Nanchang, Nanchang University, Nanchang, People’s Republic of China 2 Department of Orthopedic Surgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of China 3 Jiangxi Provincial Key Laboratory of Spine and Spinal Cord Diseases, Nanchang 330006, People’s Republic of China 4 Department of Orthopedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, People’s Republic of China 5 Department of Otorhinolaryngology, Nanfang Hospital, Southern Medical University, Guangzhou, People’s Republic of China Abstract Background Cellular senescence and the senescence-associated secretory phenotype (SASP) are increasingly recognized as contributors to intervertebral disc degeneration (IVDD).. However, clinically relevant SASP-related gene signatures and therapeutic implications remain incompletely defined.. Methods Two peripheral whole-blood transcriptomic datasets from GEO (GSE124272 and GSE150408) were integrated.

other:

Article Title: Targeting the DSTYK-ULK1 axis rewires TNFR1 signaling to overcome treatment resistance in lung cancer.
Article Snippet: Phospho-peptide enriched, and non-enriched (full proteome analysis) samples were analyzed by an LC-MS/MS Ultimate 3000 UHLPC System coupled to an Exploris480 mass spectrometer (Thermo Scientific, San Jose, CA), by data dependent analysis (DDA).

Article Title: Intercellular interaction licenses TNFα/IFNγ-induced cancer cell apoptosis through the NF2–YAP–TRAIL pathway
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Cell-Signaling:

Article Title: Granulin+ Macrophages Promote Lineage Plasticity in Prostate Cancer Through Paracrine Signaling Loops.
Article Snippet: .. The primary 887 antibodies used were rabbit anti-TNFRSF1A (Catalog No. 21574-1-AP, Proteintech, 888 Wuhan, China), rabbit anti-N-cadherin (Catalog No. 13116, Cell Signaling Technology, 889 Danvers, MA), rabbit anti-VIM (Catalog No. 5741, Cell Signaling Technology, 890 Danvers, MA), rabbit anti-E-cadherin (Catalog No. 3195, Cell Signaling Technology, 891 Danvers, MA), rabbit anti-ZO-1 (Catalog No. 8193, Cell Signaling Technology, 892 Danvers, MA), and rabbit anti-GAPDH (Catalog No. 5174, Cell Signaling Technology, 893 Danvers, MA). ..

Blocking Assay:

Article Title: A SASP-related four-gene signature associated with intervertebral disc degeneration: integrated bioinformatics analysis and validation of pinocembrin as a therapeutic candidate.
Article Snippet: 1 Department of Orthopedic Surgery, The Third Affiliated Hospital, Jiangxi Medical College, First Hospital of Nanchang, Nanchang University, Nanchang, People’s Republic of China 2 Department of Orthopedic Surgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of China 3 Jiangxi Provincial Key Laboratory of Spine and Spinal Cord Diseases, Nanchang 330006, People’s Republic of China 4 Department of Orthopedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, People’s Republic of China 5 Department of Otorhinolaryngology, Nanfang Hospital, Southern Medical University, Guangzhou, People’s Republic of China Abstract Background Cellular senescence and the senescence-associated secretory phenotype (SASP) are increasingly recognized as contributors to intervertebral disc degeneration (IVDD).. However, clinically relevant SASP-related gene signatures and therapeutic implications remain incompletely defined.. Methods Two peripheral whole-blood transcriptomic datasets from GEO (GSE124272 and GSE150408) were integrated.



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