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igf2  (R&D Systems)


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    Structured Review

    R&D Systems igf2
    Igf2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 48 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/igf2+protein/us12606639-1424-14-15?v=R%26D+Systems
    Average 93 stars, based on 48 article reviews
    igf2 - by Bioz Stars, 2026-08
    93/100 stars

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    PTN regulates endometrial stromal cell decidualization through <t>the</t> <t>IGF-2</t> signaling axis. (A) PPI network of PTN, IGF-2, IGFBP1, LIF, PRL, and other decidualization-related genes. (B) The expression levels of PTN and its interacting partners (IGF-2, WNT4, PRL, IGFBP1, and LIF) in the RIF (left) and RPL (right) datasets. (C) Expressions of decidualization-related genes (including IGFBP1 , LIF , PRL , and WNT4 ) in NC or si PTN hESCs after treatment with control vehicle, cAMP, and IGF-2 via RT-qPCR (n = 9). (D) Immunoblotting for PTN, IGFBP1, and PRL expression levels with control vehicle, cAMP, and IGF-2. (E) ELISA for IGF-2 levels with control vehicle, cAMP, and IGF-2. (F) Schematic diagram of the experiments performed using the different treatments of hESCs. Data are presented as mean ± SEM and analyzed using t-test or one-way ANOVA test. * compared with NC treated with control vehicle, # compared with si PTN treated with control vehicle, $ compared with si PTN treated with control cAMP (NS, no significant difference; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ####p < 0.0001, $p < 0.05, $$p < 0.01, $$$p < 0.001, $$$$p< 0.0001). PPI, protein–protein interaction; RIF, recurrent implantation failure; RPL, recurrent pregnancy loss; hESCs, human endometrial stromal cells; cAMP, cyclic adenosine monophosphate.
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    PTN regulates endometrial stromal cell decidualization through <t>the</t> <t>IGF-2</t> signaling axis. (A) PPI network of PTN, IGF-2, IGFBP1, LIF, PRL, and other decidualization-related genes. (B) The expression levels of PTN and its interacting partners (IGF-2, WNT4, PRL, IGFBP1, and LIF) in the RIF (left) and RPL (right) datasets. (C) Expressions of decidualization-related genes (including IGFBP1 , LIF , PRL , and WNT4 ) in NC or si PTN hESCs after treatment with control vehicle, cAMP, and IGF-2 via RT-qPCR (n = 9). (D) Immunoblotting for PTN, IGFBP1, and PRL expression levels with control vehicle, cAMP, and IGF-2. (E) ELISA for IGF-2 levels with control vehicle, cAMP, and IGF-2. (F) Schematic diagram of the experiments performed using the different treatments of hESCs. Data are presented as mean ± SEM and analyzed using t-test or one-way ANOVA test. * compared with NC treated with control vehicle, # compared with si PTN treated with control vehicle, $ compared with si PTN treated with control cAMP (NS, no significant difference; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ####p < 0.0001, $p < 0.05, $$p < 0.01, $$$p < 0.001, $$$$p< 0.0001). PPI, protein–protein interaction; RIF, recurrent implantation failure; RPL, recurrent pregnancy loss; hESCs, human endometrial stromal cells; cAMP, cyclic adenosine monophosphate.
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    Musashi Engineering Inc igf2 mrna binding proteins
    <t>IGF2BP1</t> limits IRF1 -dependent transcription by preventing MDM2 <t>mRNA</t> decay. a C5 tumors and IGF2BP1 -depleted cells show inversed enrichment of IRF1 -TFT gene sets. GSEA was performed upon log 2 FC ranking of C5 to non-C5 tumors (blue) and IGF2BP1 knockdown in ES-2 cells (yellow) using C3:TFT gene sets. b Phenotype rescue experiment of IGF2BP1 depletion and co-depletion of IRF1 in ES-2 cells analyzed by Western blotting (left) and flow cytometry (right) using indicated antibodies. Vinculin (VCL) served as loading control. c IRF1 protein turnover was monitored in ES-2 cells by Western blotting upon IGF2BP1 depletion and emetine treatment (100 µM) to block translation. d MDM2 mRNA turnover was monitored in ES-2 cells by qRT-PCR upon IGF2BP1 depletion and actinomycin D treatment (5 µM). e RNA-immunoprecipitation (RIP) using GFP antibodies in ES-2 with IGF2BP1 deletion and re-expression of GFP- IGF2BP1 . GFP served as negative control. Cells were treated with indicated compounds and concentrations or DMSO as negative control 24 h before the RIP experiment. Associated transcripts were quantified by qRT-PCR relative to inputs, controls and H2AC12. f The endogenous MDM2 -3’UTR was deleted by CRISPR/Cas9 in ES-2 cells (left). Cells were analyzed by Western blotting (middle) and flow cytometry (right) upon IGF2BP1 knockdown. g Schematic depicts IGF2BP1 -directed control of IRF1 -dependent transcription via MDM2 . Error bars indicate s.d. for N ≥ 3 experiments. Statistical significance was assessed using Chi-squared comparison ( c , d ) or an unpaired two-tailed t test ( e , f )
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    R&D Systems recombinant mouse igf2
    <t>IGF2BP1</t> limits IRF1 -dependent transcription by preventing MDM2 <t>mRNA</t> decay. a C5 tumors and IGF2BP1 -depleted cells show inversed enrichment of IRF1 -TFT gene sets. GSEA was performed upon log 2 FC ranking of C5 to non-C5 tumors (blue) and IGF2BP1 knockdown in ES-2 cells (yellow) using C3:TFT gene sets. b Phenotype rescue experiment of IGF2BP1 depletion and co-depletion of IRF1 in ES-2 cells analyzed by Western blotting (left) and flow cytometry (right) using indicated antibodies. Vinculin (VCL) served as loading control. c IRF1 protein turnover was monitored in ES-2 cells by Western blotting upon IGF2BP1 depletion and emetine treatment (100 µM) to block translation. d MDM2 mRNA turnover was monitored in ES-2 cells by qRT-PCR upon IGF2BP1 depletion and actinomycin D treatment (5 µM). e RNA-immunoprecipitation (RIP) using GFP antibodies in ES-2 with IGF2BP1 deletion and re-expression of GFP- IGF2BP1 . GFP served as negative control. Cells were treated with indicated compounds and concentrations or DMSO as negative control 24 h before the RIP experiment. Associated transcripts were quantified by qRT-PCR relative to inputs, controls and H2AC12. f The endogenous MDM2 -3’UTR was deleted by CRISPR/Cas9 in ES-2 cells (left). Cells were analyzed by Western blotting (middle) and flow cytometry (right) upon IGF2BP1 knockdown. g Schematic depicts IGF2BP1 -directed control of IRF1 -dependent transcription via MDM2 . Error bars indicate s.d. for N ≥ 3 experiments. Statistical significance was assessed using Chi-squared comparison ( c , d ) or an unpaired two-tailed t test ( e , f )
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    R&D Systems mouse insulin growth factor ii
    <t>IGF2BP1</t> limits IRF1 -dependent transcription by preventing MDM2 <t>mRNA</t> decay. a C5 tumors and IGF2BP1 -depleted cells show inversed enrichment of IRF1 -TFT gene sets. GSEA was performed upon log 2 FC ranking of C5 to non-C5 tumors (blue) and IGF2BP1 knockdown in ES-2 cells (yellow) using C3:TFT gene sets. b Phenotype rescue experiment of IGF2BP1 depletion and co-depletion of IRF1 in ES-2 cells analyzed by Western blotting (left) and flow cytometry (right) using indicated antibodies. Vinculin (VCL) served as loading control. c IRF1 protein turnover was monitored in ES-2 cells by Western blotting upon IGF2BP1 depletion and emetine treatment (100 µM) to block translation. d MDM2 mRNA turnover was monitored in ES-2 cells by qRT-PCR upon IGF2BP1 depletion and actinomycin D treatment (5 µM). e RNA-immunoprecipitation (RIP) using GFP antibodies in ES-2 with IGF2BP1 deletion and re-expression of GFP- IGF2BP1 . GFP served as negative control. Cells were treated with indicated compounds and concentrations or DMSO as negative control 24 h before the RIP experiment. Associated transcripts were quantified by qRT-PCR relative to inputs, controls and H2AC12. f The endogenous MDM2 -3’UTR was deleted by CRISPR/Cas9 in ES-2 cells (left). Cells were analyzed by Western blotting (middle) and flow cytometry (right) upon IGF2BP1 knockdown. g Schematic depicts IGF2BP1 -directed control of IRF1 -dependent transcription via MDM2 . Error bars indicate s.d. for N ≥ 3 experiments. Statistical significance was assessed using Chi-squared comparison ( c , d ) or an unpaired two-tailed t test ( e , f )
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    Image Search Results


    PTN regulates endometrial stromal cell decidualization through the IGF-2 signaling axis. (A) PPI network of PTN, IGF-2, IGFBP1, LIF, PRL, and other decidualization-related genes. (B) The expression levels of PTN and its interacting partners (IGF-2, WNT4, PRL, IGFBP1, and LIF) in the RIF (left) and RPL (right) datasets. (C) Expressions of decidualization-related genes (including IGFBP1 , LIF , PRL , and WNT4 ) in NC or si PTN hESCs after treatment with control vehicle, cAMP, and IGF-2 via RT-qPCR (n = 9). (D) Immunoblotting for PTN, IGFBP1, and PRL expression levels with control vehicle, cAMP, and IGF-2. (E) ELISA for IGF-2 levels with control vehicle, cAMP, and IGF-2. (F) Schematic diagram of the experiments performed using the different treatments of hESCs. Data are presented as mean ± SEM and analyzed using t-test or one-way ANOVA test. * compared with NC treated with control vehicle, # compared with si PTN treated with control vehicle, $ compared with si PTN treated with control cAMP (NS, no significant difference; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ####p < 0.0001, $p < 0.05, $$p < 0.01, $$$p < 0.001, $$$$p< 0.0001). PPI, protein–protein interaction; RIF, recurrent implantation failure; RPL, recurrent pregnancy loss; hESCs, human endometrial stromal cells; cAMP, cyclic adenosine monophosphate.

    Journal: Frontiers in Immunology

    Article Title: PTN/IGF-2 signaling modulates endometrial decidualization and immune cell trafficking to facilitate pregnancy maintenance

    doi: 10.3389/fimmu.2026.1790942

    Figure Lengend Snippet: PTN regulates endometrial stromal cell decidualization through the IGF-2 signaling axis. (A) PPI network of PTN, IGF-2, IGFBP1, LIF, PRL, and other decidualization-related genes. (B) The expression levels of PTN and its interacting partners (IGF-2, WNT4, PRL, IGFBP1, and LIF) in the RIF (left) and RPL (right) datasets. (C) Expressions of decidualization-related genes (including IGFBP1 , LIF , PRL , and WNT4 ) in NC or si PTN hESCs after treatment with control vehicle, cAMP, and IGF-2 via RT-qPCR (n = 9). (D) Immunoblotting for PTN, IGFBP1, and PRL expression levels with control vehicle, cAMP, and IGF-2. (E) ELISA for IGF-2 levels with control vehicle, cAMP, and IGF-2. (F) Schematic diagram of the experiments performed using the different treatments of hESCs. Data are presented as mean ± SEM and analyzed using t-test or one-way ANOVA test. * compared with NC treated with control vehicle, # compared with si PTN treated with control vehicle, $ compared with si PTN treated with control cAMP (NS, no significant difference; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ####p < 0.0001, $p < 0.05, $$p < 0.01, $$$p < 0.001, $$$$p< 0.0001). PPI, protein–protein interaction; RIF, recurrent implantation failure; RPL, recurrent pregnancy loss; hESCs, human endometrial stromal cells; cAMP, cyclic adenosine monophosphate.

    Article Snippet: The remaining cells were digested with trypsin and inoculated into a new culture dish, and they were treated with control vehicle or IGF-2 (50 ng/mL, R&D Systems, Minneapolis, MN, USA, 292-G2) for 48 h and then collected for quantitative real-time polymerase chain reaction (qRT-PCR).

    Techniques: Expressing, Control, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay

    IGF-2 promotes decidualization and rescues decidualization defects caused by PTN deficiency. (A) Schematic diagram of the experiments performed using the different treatments of ESCs isolated from endometrium of RIF and RPL patients. (B, C) RT-qPCR analysis of levels of decidualization-related genes in ESCs isolated from endometrium of RIF (B) and RPL (C) patients after IGF-2 (50 ng/mL) treatment for 48 h (n = 9). (D) The flowchart depicts the steps involved in establishing a mouse model of intrauterine perfusion with siRNA-mediated knockdown of PTN and then supplemented with IGF-2 (50 ng/mL) through tail vein injection. (E) Expression of PTN after Ptn knockdown and supplemented with control vehicle or IGF-2 (50 ng/mL) in the mouse endometrium, measured by immunofluorescence, and quantitative analysis of immunofluorescence was performed (n = 6). (F) RT-qPCR analysis of levels of decidualization-related genes after Ptn knockdown and supplemented with control vehicle or IGF-2 (50 ng/mL) in the mouse endometrium (n = 6). Data are presented as mean ± SEM and analyzed using t-test or one-way ANOVA test. * compared with NC treated with control vehicle, # compared with si PTN treated with control vehicle (NS, no significant difference; *p < 0.05, **p < 0.01, ***p < 0.001, ****p< 0.0001, ## p < 0.01, ### p < 0.001, #### p < 0.0001). ESCs, endometrial stromal cells; PPI, protein–protein interaction; RIF, recurrent implantation failure.

    Journal: Frontiers in Immunology

    Article Title: PTN/IGF-2 signaling modulates endometrial decidualization and immune cell trafficking to facilitate pregnancy maintenance

    doi: 10.3389/fimmu.2026.1790942

    Figure Lengend Snippet: IGF-2 promotes decidualization and rescues decidualization defects caused by PTN deficiency. (A) Schematic diagram of the experiments performed using the different treatments of ESCs isolated from endometrium of RIF and RPL patients. (B, C) RT-qPCR analysis of levels of decidualization-related genes in ESCs isolated from endometrium of RIF (B) and RPL (C) patients after IGF-2 (50 ng/mL) treatment for 48 h (n = 9). (D) The flowchart depicts the steps involved in establishing a mouse model of intrauterine perfusion with siRNA-mediated knockdown of PTN and then supplemented with IGF-2 (50 ng/mL) through tail vein injection. (E) Expression of PTN after Ptn knockdown and supplemented with control vehicle or IGF-2 (50 ng/mL) in the mouse endometrium, measured by immunofluorescence, and quantitative analysis of immunofluorescence was performed (n = 6). (F) RT-qPCR analysis of levels of decidualization-related genes after Ptn knockdown and supplemented with control vehicle or IGF-2 (50 ng/mL) in the mouse endometrium (n = 6). Data are presented as mean ± SEM and analyzed using t-test or one-way ANOVA test. * compared with NC treated with control vehicle, # compared with si PTN treated with control vehicle (NS, no significant difference; *p < 0.05, **p < 0.01, ***p < 0.001, ****p< 0.0001, ## p < 0.01, ### p < 0.001, #### p < 0.0001). ESCs, endometrial stromal cells; PPI, protein–protein interaction; RIF, recurrent implantation failure.

    Article Snippet: The remaining cells were digested with trypsin and inoculated into a new culture dish, and they were treated with control vehicle or IGF-2 (50 ng/mL, R&D Systems, Minneapolis, MN, USA, 292-G2) for 48 h and then collected for quantitative real-time polymerase chain reaction (qRT-PCR).

    Techniques: Isolation, Quantitative RT-PCR, Knockdown, Injection, Expressing, Control, Immunofluorescence

    PTN deficiency induces endometrial immune imbalance and leads to adverse pregnancy outcomes, which can be partially reversed by IGF-2. (A) PPI network of PTN, IGF-2, CXCR4, CD4, CD8, CD56, and other immunoregulators. (B, C) Flow cytometry analysis (B) and statistical quantification (C) of cell populations of NK cells and T cells, and the expression levels of CD16, CXCR4, and GZMB in NK cell form the endometrial tissues of NC and si PTN mice treated with control vehicle or IGF-2 (50 ng/mL) (n = 6). (D) The flowchart depicts the steps involved in establishing a mouse model of intrauterine perfusion with siRNA-mediated knockdown of Ptn and then supplemented with IGF-2 (50 ng/mL) through tail vein injection for 2 days; then, these female mice were mated with fertile male mice; analysis of fertility, including pregnancy rate, IF, and fluorescence-activated cell sorting (FACS). were performed at gestational day 13.5. (E) Representative images of uteri from pregnant mice in the NC and si PTN mice treated with control vehicle or IGF-2 (50 ng/mL) at gestational day 13.5 (n = 6) (arrow shows the absorption site). (F) Pregnancy rate (%) in NC and si PTN mice treated with control vehicle or IGF-2 (50 ng/mL) (n = 15). (G) Quantification of embryo numbers (left) and absorption rate (right) per mouse in NC (n = 13) and si PTN mice treated with control vehicle (n = 6) or IGF-2 (50 ng/mL) (n = 11) at gestational day 13.5. Data are presented as mean ± SEM and analyzed using one-way ANOVA test or χ 2 test. * Compared with NC treated with control vehicle, # compared with si PTN treated with control vehicle (NS, no significant difference; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ## p < 0.01, ### p < 0.001, #### p < 0.0001). IF, immunofluorescence.

    Journal: Frontiers in Immunology

    Article Title: PTN/IGF-2 signaling modulates endometrial decidualization and immune cell trafficking to facilitate pregnancy maintenance

    doi: 10.3389/fimmu.2026.1790942

    Figure Lengend Snippet: PTN deficiency induces endometrial immune imbalance and leads to adverse pregnancy outcomes, which can be partially reversed by IGF-2. (A) PPI network of PTN, IGF-2, CXCR4, CD4, CD8, CD56, and other immunoregulators. (B, C) Flow cytometry analysis (B) and statistical quantification (C) of cell populations of NK cells and T cells, and the expression levels of CD16, CXCR4, and GZMB in NK cell form the endometrial tissues of NC and si PTN mice treated with control vehicle or IGF-2 (50 ng/mL) (n = 6). (D) The flowchart depicts the steps involved in establishing a mouse model of intrauterine perfusion with siRNA-mediated knockdown of Ptn and then supplemented with IGF-2 (50 ng/mL) through tail vein injection for 2 days; then, these female mice were mated with fertile male mice; analysis of fertility, including pregnancy rate, IF, and fluorescence-activated cell sorting (FACS). were performed at gestational day 13.5. (E) Representative images of uteri from pregnant mice in the NC and si PTN mice treated with control vehicle or IGF-2 (50 ng/mL) at gestational day 13.5 (n = 6) (arrow shows the absorption site). (F) Pregnancy rate (%) in NC and si PTN mice treated with control vehicle or IGF-2 (50 ng/mL) (n = 15). (G) Quantification of embryo numbers (left) and absorption rate (right) per mouse in NC (n = 13) and si PTN mice treated with control vehicle (n = 6) or IGF-2 (50 ng/mL) (n = 11) at gestational day 13.5. Data are presented as mean ± SEM and analyzed using one-way ANOVA test or χ 2 test. * Compared with NC treated with control vehicle, # compared with si PTN treated with control vehicle (NS, no significant difference; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ## p < 0.01, ### p < 0.001, #### p < 0.0001). IF, immunofluorescence.

    Article Snippet: The remaining cells were digested with trypsin and inoculated into a new culture dish, and they were treated with control vehicle or IGF-2 (50 ng/mL, R&D Systems, Minneapolis, MN, USA, 292-G2) for 48 h and then collected for quantitative real-time polymerase chain reaction (qRT-PCR).

    Techniques: Flow Cytometry, Expressing, Control, Knockdown, Injection, Fluorescence, FACS, Immunofluorescence

    IGF2BP1 limits IRF1 -dependent transcription by preventing MDM2 mRNA decay. a C5 tumors and IGF2BP1 -depleted cells show inversed enrichment of IRF1 -TFT gene sets. GSEA was performed upon log 2 FC ranking of C5 to non-C5 tumors (blue) and IGF2BP1 knockdown in ES-2 cells (yellow) using C3:TFT gene sets. b Phenotype rescue experiment of IGF2BP1 depletion and co-depletion of IRF1 in ES-2 cells analyzed by Western blotting (left) and flow cytometry (right) using indicated antibodies. Vinculin (VCL) served as loading control. c IRF1 protein turnover was monitored in ES-2 cells by Western blotting upon IGF2BP1 depletion and emetine treatment (100 µM) to block translation. d MDM2 mRNA turnover was monitored in ES-2 cells by qRT-PCR upon IGF2BP1 depletion and actinomycin D treatment (5 µM). e RNA-immunoprecipitation (RIP) using GFP antibodies in ES-2 with IGF2BP1 deletion and re-expression of GFP- IGF2BP1 . GFP served as negative control. Cells were treated with indicated compounds and concentrations or DMSO as negative control 24 h before the RIP experiment. Associated transcripts were quantified by qRT-PCR relative to inputs, controls and H2AC12. f The endogenous MDM2 -3’UTR was deleted by CRISPR/Cas9 in ES-2 cells (left). Cells were analyzed by Western blotting (middle) and flow cytometry (right) upon IGF2BP1 knockdown. g Schematic depicts IGF2BP1 -directed control of IRF1 -dependent transcription via MDM2 . Error bars indicate s.d. for N ≥ 3 experiments. Statistical significance was assessed using Chi-squared comparison ( c , d ) or an unpaired two-tailed t test ( e , f )

    Journal: Signal Transduction and Targeted Therapy

    Article Title: Inhibition of RNA-binding proteins enhances immunotherapy in ovarian cancer

    doi: 10.1038/s41392-025-02515-1

    Figure Lengend Snippet: IGF2BP1 limits IRF1 -dependent transcription by preventing MDM2 mRNA decay. a C5 tumors and IGF2BP1 -depleted cells show inversed enrichment of IRF1 -TFT gene sets. GSEA was performed upon log 2 FC ranking of C5 to non-C5 tumors (blue) and IGF2BP1 knockdown in ES-2 cells (yellow) using C3:TFT gene sets. b Phenotype rescue experiment of IGF2BP1 depletion and co-depletion of IRF1 in ES-2 cells analyzed by Western blotting (left) and flow cytometry (right) using indicated antibodies. Vinculin (VCL) served as loading control. c IRF1 protein turnover was monitored in ES-2 cells by Western blotting upon IGF2BP1 depletion and emetine treatment (100 µM) to block translation. d MDM2 mRNA turnover was monitored in ES-2 cells by qRT-PCR upon IGF2BP1 depletion and actinomycin D treatment (5 µM). e RNA-immunoprecipitation (RIP) using GFP antibodies in ES-2 with IGF2BP1 deletion and re-expression of GFP- IGF2BP1 . GFP served as negative control. Cells were treated with indicated compounds and concentrations or DMSO as negative control 24 h before the RIP experiment. Associated transcripts were quantified by qRT-PCR relative to inputs, controls and H2AC12. f The endogenous MDM2 -3’UTR was deleted by CRISPR/Cas9 in ES-2 cells (left). Cells were analyzed by Western blotting (middle) and flow cytometry (right) upon IGF2BP1 knockdown. g Schematic depicts IGF2BP1 -directed control of IRF1 -dependent transcription via MDM2 . Error bars indicate s.d. for N ≥ 3 experiments. Statistical significance was assessed using Chi-squared comparison ( c , d ) or an unpaired two-tailed t test ( e , f )

    Article Snippet: Previously considered undruggable, oncofetal RBPs enriched in stem cells—such as IGF2 mRNA binding proteins ( IGF2BP1-3 ), LIN-28 RNA binding posttranscriptional regulators ( LIN28A/B ) and Musashi proteins ( MSI1/2 )—have recently emerged as promising strategies for targeted therapies.

    Techniques: Knockdown, Western Blot, Flow Cytometry, Control, Blocking Assay, Quantitative RT-PCR, RNA Immunoprecipitation, Expressing, Negative Control, CRISPR, Comparison, Two Tailed Test

    IGF2BP1 controls PD-L1 mRNA turnover in a 3’UTR-dependent manner. a Volcano plot of IRF1 -driven transcription (TFT: IRF1 _01) upon IGF2BP1 depletion in ES-2 cells. Transcripts with significant fold change (log 2 FC > 2; FDR < 0.05) are labeled by color. b Western blot of IGF2BP1 depleted ES-2 cells with indicated antibodies. Quantifications are shown below panels. c PD-L1 mRNA turnover was monitored in ES-2 cells by qRT-PCR upon IGF2BP1 depletion and actinomycin D treatment (5 µM). d RIP analyses using ES-2 cell extracts and treatments were performed as described in (Fig. ). e The endogenous PD-L1 -3’UTR was deleted by CRISPR/Cas9 in ES-2 cells (left). Cells were analyzed by Western blotting (middle) and flow cytometry (right) upon IGF2BP1 knockdown as indicated. Error bars indicate s.d. of N ≥ 3 experiments. Statistical significance was assessed using Chi-squared comparison (c) or an unpaired two-tailed t test ( b , d , e ). f Schematic depicts IGF2BP1 -directed post-transcriptional control of PD-L1 expression, uncoupling it from IRF1 -dependent transcription

    Journal: Signal Transduction and Targeted Therapy

    Article Title: Inhibition of RNA-binding proteins enhances immunotherapy in ovarian cancer

    doi: 10.1038/s41392-025-02515-1

    Figure Lengend Snippet: IGF2BP1 controls PD-L1 mRNA turnover in a 3’UTR-dependent manner. a Volcano plot of IRF1 -driven transcription (TFT: IRF1 _01) upon IGF2BP1 depletion in ES-2 cells. Transcripts with significant fold change (log 2 FC > 2; FDR < 0.05) are labeled by color. b Western blot of IGF2BP1 depleted ES-2 cells with indicated antibodies. Quantifications are shown below panels. c PD-L1 mRNA turnover was monitored in ES-2 cells by qRT-PCR upon IGF2BP1 depletion and actinomycin D treatment (5 µM). d RIP analyses using ES-2 cell extracts and treatments were performed as described in (Fig. ). e The endogenous PD-L1 -3’UTR was deleted by CRISPR/Cas9 in ES-2 cells (left). Cells were analyzed by Western blotting (middle) and flow cytometry (right) upon IGF2BP1 knockdown as indicated. Error bars indicate s.d. of N ≥ 3 experiments. Statistical significance was assessed using Chi-squared comparison (c) or an unpaired two-tailed t test ( b , d , e ). f Schematic depicts IGF2BP1 -directed post-transcriptional control of PD-L1 expression, uncoupling it from IRF1 -dependent transcription

    Article Snippet: Previously considered undruggable, oncofetal RBPs enriched in stem cells—such as IGF2 mRNA binding proteins ( IGF2BP1-3 ), LIN-28 RNA binding posttranscriptional regulators ( LIN28A/B ) and Musashi proteins ( MSI1/2 )—have recently emerged as promising strategies for targeted therapies.

    Techniques: Labeling, Western Blot, Quantitative RT-PCR, CRISPR, Flow Cytometry, Knockdown, Comparison, Two Tailed Test, Control, Expressing