carm1 inhibitor  (Merck KGaA)

Journal: Aging Cell

Article Title: Coactivator Associated Arginine Methyltransferase 1 Modulates Cartilage Degeneration and Chondrocyte Apoptosis in Osteoarthritis by Regulating ERK1 /2 Signaling Pathway

doi: 10.1111/acel.70122

Figure Lengend Snippet: CARM1 is up‐regulated in the articular cartilage of osteoarthritis patients, osteoarthritis mice and aged mice. (a) Clinical preoperative and postoperative X‐ray plain film scanning of patients. (b–e) Safranin O‐Fast Green, Alcian Blue, CARM1 Immunofluorescent staining, Statistical analysis of the percentage of CARM1 + chondrocytes, the OARSI grade, and Mankin score of normal and OA cartilage tissues ( n = 6 per group). (f, g) Western blot analysis and quantification of CARM1, MMP13, and COL2A1 in normal and OA cartilage tissues, with GAPDH as the endogenous control. (h, i) Western blot analysis and quantification of CARM1, MMP13, and COL2A1 in Sham and DMM groups, with GAPDH as the endogenous control. (j–m) Safranin O‐Fast Green, Alcian Blue, and CARM1 Immunofluorescent staining, and Statistical analysis of the percentage of CARM1 + chondrocytes and the OARSI and Mankin score of cartilage from Sham and DMM groups ( n = 6 per group). (n–q) Safranin O‐Fast Green staining, Alcian Blue staining, and CARM1 immunofluorescent staining were performed on cartilage samples from the 6‐, 12‐, and 18‐month groups ( n = 6 per group), followed by statistical analysis of the percentage of CARM1 + chondrocytes, as well as OARSI and Mankin scores. Data are presented as the mean ± SD; * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: To study CARM1's role, CARM1 inhibitor (6 μL of 5 ng/mL; Med Chem Express) and recombinant lentivirus (6 μL of 10 8 PFU/mL; Hanbio) for CARM1 over‐expression were injected into the intra‐articular cavity of 12‐week‐old male C57BL/6 mice after DMM.

Techniques: Staining, Western Blot, Control

Journal: Aging Cell

Article Title: Coactivator Associated Arginine Methyltransferase 1 Modulates Cartilage Degeneration and Chondrocyte Apoptosis in Osteoarthritis by Regulating ERK1 /2 Signaling Pathway

doi: 10.1111/acel.70122

Figure Lengend Snippet: Inhibition of CARM1 inhibited the decrease of anabolism, the increase of catabolism and the apoptosis of ATDC5 induced by IL‐1β. (a–c) The protein and mRNA expression levels of CARM1, MMP13, ACAN, Cleaved Caspase3 and Caspase3 were measured by Western blot, densitometric quantification of Western blot, and RT‐qPCR assay (without Cleaved Caspase3) in ATDC5 cells treated with IL‐1β (20 ng/mL) or CARM1 inhibitor (1 or 5 ng/mL) for 24 h. (d) CARM1, ACAN and MMP13 immunofluorescent staining of ATDC5 treated with IL‐1β (20 ng/mL) or CARM1 inhibitor (1 or 5 ng/mL) for 24 h. (e, f) Apoptotic ATDC5 stained by annexin V and PI and analyzed by flow cytometry after treatment with IL‐1β (20 ng/mL) or CARM1 inhibitor (1 or 5 ng/mL) for 24 h, ATDC5 without treatment were used as the negative control. Data are presented as the mean ± SD; * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: To study CARM1's role, CARM1 inhibitor (6 μL of 5 ng/mL; Med Chem Express) and recombinant lentivirus (6 μL of 10 8 PFU/mL; Hanbio) for CARM1 over‐expression were injected into the intra‐articular cavity of 12‐week‐old male C57BL/6 mice after DMM.

Techniques: Inhibition, Expressing, Western Blot, Quantitative RT-PCR, Staining, Flow Cytometry, Negative Control

Journal: Aging Cell

Article Title: Coactivator Associated Arginine Methyltransferase 1 Modulates Cartilage Degeneration and Chondrocyte Apoptosis in Osteoarthritis by Regulating ERK1 /2 Signaling Pathway

doi: 10.1111/acel.70122

Figure Lengend Snippet: Inhibition of CARM1 attenuated DMM‐induced osteoarthritis development. (a) Schematic diagram of the process of building OA model and inhibiting CARM1 in mice. (b–d) Representative images of Safranin O‐Fast Green and Alcian Blue staining, with the corresponding OARSI and Mankin scores, were collected from Sham, DMM, and DMM + CARM1 inhibitor groups ( n = 6 per group). (e) IHC staining of CARM1, ACAN and MMP13 and TUNEL staining from Sham, DMM, and DMM + CARM1 inhibitor groups ( n = 6 per group). (f–i) Statistical analysis of the percentage of CARM1 + , ACAN + , MMP13 + , and apoptotic chondrocytes in articular cartilage of samples shown in D. Data are presented as the mean ± SD; * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: To study CARM1's role, CARM1 inhibitor (6 μL of 5 ng/mL; Med Chem Express) and recombinant lentivirus (6 μL of 10 8 PFU/mL; Hanbio) for CARM1 over‐expression were injected into the intra‐articular cavity of 12‐week‐old male C57BL/6 mice after DMM.

Techniques: Inhibition, Staining, Immunohistochemistry, TUNEL Assay

Journal: Aging Cell

Article Title: Coactivator Associated Arginine Methyltransferase 1 Modulates Cartilage Degeneration and Chondrocyte Apoptosis in Osteoarthritis by Regulating ERK1 /2 Signaling Pathway

doi: 10.1111/acel.70122

Figure Lengend Snippet: Over‐expression of CARM1 aggravated the decrease of anabolism, the increase of catabolism and the apoptosis of ATDC5. (a, b) The protein levels of CARM1, MMP13, ACAN, Cleaved Caspase3 and Caspase3 were detected and quantified by WB assay in ATDC5 transfected with CARM1 over‐expression lentivirus. (c) The mRNA levels of apoptosis marker Caspase3 and ECM‐related biomarkers ACAN and MMP13 in ATDC5 transfected with CARM1 over‐expression lentivirus. (d) CARM1, ACAN, and MMP13 immunofluorescent staining of ATDC5 transfected with CARM1 over‐expression lentivirus. (e) Representative images show TUNEL staining assay in ATDC5 transfected with CARM1 over‐expression lentivirus. (f) Quantitative analysis shows the total numbers of TUNEL positive in ATDC5 transfected with CARM1 over‐expression lentivirus. (g) Flow cytometry analysis and (h) quantification in ATDC5 transfected with CARM1 over‐expression lentivirus. (i) Representative images show Alcian Blue staining assay in ATDC5 transfected with CARM1 over‐expression lentivirus. Data are presented as the mean ± SD; * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: To study CARM1's role, CARM1 inhibitor (6 μL of 5 ng/mL; Med Chem Express) and recombinant lentivirus (6 μL of 10 8 PFU/mL; Hanbio) for CARM1 over‐expression were injected into the intra‐articular cavity of 12‐week‐old male C57BL/6 mice after DMM.

Techniques: Over Expression, Transfection, Marker, Staining, TUNEL Assay, Flow Cytometry

Journal: Aging Cell

Article Title: Coactivator Associated Arginine Methyltransferase 1 Modulates Cartilage Degeneration and Chondrocyte Apoptosis in Osteoarthritis by Regulating ERK1 /2 Signaling Pathway

doi: 10.1111/acel.70122

Figure Lengend Snippet: CARM1 over‐expression exacerbated OA‐related degeneration in DMM‐induced mice. (a) Schematic diagram of the process of building OA model and over‐expressing CARM1 in mice. (b) Representative images of Safranin O‐Fast Green and Alcian Blue staining and (c, d) the corresponding OARSI and Mankin scores from Sham, DMM, DMM + LV‐NC, DMM + LV‐CARM1, and DMM + LV‐CARM1 + CARM1 inhibitor groups ( n = 6 per group). (e) IHC staining of CARM1, ACAN and MMP13 and TUNEL staining from Sham, DMM, DMM + LV‐NC, DMM + LV‐CARM1, and DMM + LV‐CARM1 + CARM1 inhibitor groups ( n = 6 per group). (f–i) Statistical analysis of the percentage of CARM1 + , ACAN + , MMP13 + , and apoptotic chondrocytes in articular cartilage of samples shown in D. Data have presented as the mean ± SD; ns: not significant, * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: To study CARM1's role, CARM1 inhibitor (6 μL of 5 ng/mL; Med Chem Express) and recombinant lentivirus (6 μL of 10 8 PFU/mL; Hanbio) for CARM1 over‐expression were injected into the intra‐articular cavity of 12‐week‐old male C57BL/6 mice after DMM.

Techniques: Over Expression, Expressing, Staining, Immunohistochemistry, TUNEL Assay

Journal: Aging Cell

Article Title: Coactivator Associated Arginine Methyltransferase 1 Modulates Cartilage Degeneration and Chondrocyte Apoptosis in Osteoarthritis by Regulating ERK1 /2 Signaling Pathway

doi: 10.1111/acel.70122

Figure Lengend Snippet: CARM1 accelerates OA‐related degeneration by interacting and phosphorylating ERK1/2. (a, b) Western blotting and quantification of ERK1/2 and p‐ERK1/2 in normal and OA cartilage tissues, with GAPDH as the endogenous control. (c) CARM1 and ERK1/2 proteins immunoprecipitated from ATDC5 with anti‐CARM1 and anti‐ERK1/2 antibodies, respectively, were analyzed with WB. (d) After IL‐1β (20 ng/mL) treatment of ATDC5 cells, immunofluorescence co‐localization revealed the expression and localization of CARM1 (green) and p‐ERK1/2 (red). (e–g) Western blotting, densitometric quantification of Western blot and RT‐qPCR (without Cleaved Caspase3) analysis shows the levels of ERK1/2, p‐ERK1/2, CARM1, ACAN, MMP13, Cleaved Caspase3 and Caspase3 proteins in IL‐1β‐treated ATDC5 treated with 5 ng/mL CARM1 inhibitor, 0.5 μM SCH772984 (ERK1/2 inhibitor) or co‐treatment with CARM1 inhibitor and 0.5 μM SCH772984. (h–j) Western blotting and RT‐qPCR (without Cleaved Caspase3) analysis show the levels of ERK1/2, p‐ERK1/2, CARM1, ACAN, MMP13, Cleaved Caspase3, and Caspase3 in IL‐1β‐treated ATDC5 treated with CARM1 over‐expression lentivirus, 0.5 μM SCH772984 (ERK1/2 inhibitor) or co‐treatment with CARM1 over‐expression lentivirus and 0.5uM SCH772984. (k) A graphical representation of the hypothesized mechanism by which CARM1 alleviates OA. Data are presented as the mean ± SD; ns: not significant, * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: To study CARM1's role, CARM1 inhibitor (6 μL of 5 ng/mL; Med Chem Express) and recombinant lentivirus (6 μL of 10 8 PFU/mL; Hanbio) for CARM1 over‐expression were injected into the intra‐articular cavity of 12‐week‐old male C57BL/6 mice after DMM.

Techniques: Western Blot, Control, Immunoprecipitation, Immunofluorescence, Expressing, Quantitative RT-PCR, Over Expression

Journal: Plants

Article Title: New Epigenetic Modifier Inhibitors Enhance Microspore Embryogenesis in Bread Wheat

doi: 10.3390/plants13060772

Figure Lengend Snippet: Effect of 24 h stress treatment in SM liquid medium with 0.4 µM TSA (L-0.4TSA), chaetocin (L-0.4Chaetocin), a CARM1 inhibitor (L-CARM1I), aurora kinase inhibitor II (L-0.4AUKI-II), and hesperadin (L-0.4Hesperdin) on the percentages of microspores, bicellular structures, tricellular structures (both pollen-like and tricellular), and tetracellular and multicellular embryogenic structures after 2, 4, and 10 days in culture (2dC, 4dC, and 10dC, respectively) in wheat cultivars ( A ) Pavon and ( B ) Caramba. L-CM = control in SM liquid medium; L-CM + DMSO = control DMSO in SM liquid medium with 1% DMSO.

Article Snippet: Two histone methylation inhibitors, HMTase Inhibitor II Chaetocin (Merck KGaA, Darmstadt, Germany) and a CARM1 inhibitor (Merck KGaA, Darmstadt, Germany), and two histone phosphorylation inhibitors, aurora kinase inhibitor II (AUKI-II) (Merck KGaA, Darmstadt, Germany) and hesperadin (Merck KGaA, Darmstadt, Germany), were assayed at 0.4 μM (L-0.4Chaetocin, L-0.4CARM1I, L-0.4AUKI-II, and L-0.4Hesperadin, respectively).

Techniques: Control

Journal: Oncology Reports

Article Title: RPF2 mediates the CARM1‑MYCN axis to promote chemotherapy resistance in colorectal cancer cells

doi: 10.3892/or.2023.8670

Figure Lengend Snippet: Molecular mechanism exploration and animal experiments in vivo . (A) Intracellular expression of ABCB1, MYCN and CARM1 was detected by western blotting. Expression of ABCB1 was significantly increased in the RPF2 group (P<0.05) and decreased in the shRPF2i group (P<0.01). expression of MYCN was significantly increased in the RPF2 group (P<0.015 and decreased in the shRPF2i group (P<0.05). While the expression of CARM1 did not seem to be affected (P>0.05). (B) Co-immunoprecipitation found the presence of CARM1 co-immunoprecipitation with MYCN and that the formation of CARM1-MYCN complex was increased in the RPF2 group and decreased in the shRPF2i group. (C) After cisplatin treatment, the tumor volume as well as the mass of the mice in the shRPF2i group decreased relative to the shCtrl group. (weight: P<0.001; volume: P<0.01). *P<0.05; **P<0.01; ***P<0.001; ns, not significant. ABC, ATP-binding cassette; MYCN, N-myc proto-oncogene protein; CARM1, coactivator-associated arginine methyltransferase 1; sh, short hairpin; RPF2, ribosome production factor 2 homolog.

Article Snippet: N-myc proto-oncogene protein (MYCN; cat. no. 84406; Cell Signaling Technology, Inc.), Histone H3 (cat. no. 4499; Cell Signaling Technology, Inc.), Alexa Fluor 555 labelled donkey anti-rabbit IgG (H+L; cat. no. A0453; Beyotime Institute of Biotechnology), Alexa Fluor 647 labelled goat anti-mouse IgG (H+L; A0473; Beyotime Institute of Biotechnology), CARM1 Inhibitor (cat. no. 217531; MilliporeSigma).

Techniques: In Vivo, Expressing, Western Blot, Immunoprecipitation, Binding Assay

Journal: Oncology Reports

Article Title: RPF2 mediates the CARM1‑MYCN axis to promote chemotherapy resistance in colorectal cancer cells

doi: 10.3892/or.2023.8670

Figure Lengend Snippet: Functional recovery and validation experiments in vitro . (A) RKO cell viability at 0 h after plate spreading was detected using MTS reagent as a control. Normal serum-containing medium, CARM1 inhibitor (2 µg/ml) + serum-containing medium, cisplatin (21 µM) + serum-containing medium and CARM1 inhibitor (2 µg/ml) + cisplatin (21 µM) + serum-containing medium were added to the plates, respectively. cell viability was detected after incubation for 24 h at 37°C, respectively. There was no significant difference in the growth of the cell groups after incubation with CARM1 inhibitor alone (P>0.05). After CARM1 inhibition, cisplatin resistance was suppressed in all groups of cells. The degree of cisplatin resistance in the RPF2 group after CARM1 inhibition was not significantly different from the remaining two groups. (B) After CARM1 inhibitor incubation followed by cisplatin incubation, the number of cell clone-forming lines was significantly lower compared with the direct addition of cisplatin and there was no longer a significant difference in the RPF2 group compared with the other two groups. (C) The results of protein blotting suggested that the CARM1 inhibitor successfully reduced CARM1 expression in the cells. At the same time, ABCB1 and MYCN expression was similarly inhibited. RPF2 expression was unchanged. ****P<0.0001; ns, not significant. MTS, 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium; CARM1, coactivator-associated arginine methyltransferase 1; RPF2, ribosome production factor 2 homolog; ABC, ATP-binding cassette; MYCN, N-myc proto-oncogene protein; sh, short hairpin.

Article Snippet: N-myc proto-oncogene protein (MYCN; cat. no. 84406; Cell Signaling Technology, Inc.), Histone H3 (cat. no. 4499; Cell Signaling Technology, Inc.), Alexa Fluor 555 labelled donkey anti-rabbit IgG (H+L; cat. no. A0453; Beyotime Institute of Biotechnology), Alexa Fluor 647 labelled goat anti-mouse IgG (H+L; A0473; Beyotime Institute of Biotechnology), CARM1 Inhibitor (cat. no. 217531; MilliporeSigma).

Techniques: Functional Assay, Biomarker Discovery, In Vitro, Control, Incubation, Inhibition, Expressing, Binding Assay

Journal: Cancer Research Communications

Article Title: Targeting Fatty Acid Reprogramming Suppresses CARM1-expressing Ovarian Cancer

doi: 10.1158/2767-9764.crc-23-0030

Figure Lengend Snippet: FIGURE 1 CARM1 regulates genes involved in FA metabolism. A, Expression of CARM1 and a loading control β-actin in control and CARM1 knockout (KO) A1847 cells determined by immunoblot. B, Scatter plot of KEGG pathway analysis for genes upregulated in wildtype compared with CARM1 KO A1847 cells (WT/KO >2, FDR < 0.05). Dot size represents gene number, color represents P value. P values were calculated by KEGG analysis.

Article Snippet: SCD1 inhibitor CAY10566 (#HY15823) and CARM1 inhibitor EZM2302 (#HY-111109) were purchased from MCE.

Techniques: Expressing, Control, Knock-Out, Western Blot

Journal: Cancer Research Communications

Article Title: Targeting Fatty Acid Reprogramming Suppresses CARM1-expressing Ovarian Cancer

doi: 10.1158/2767-9764.crc-23-0030

Figure Lengend Snippet: FIGURE 2 CARM1 enhances SCD1 expression by recruiting XBP1s to their promoters independently of its enzymatic activity. A, ChIP-seq track of

Article Snippet: SCD1 inhibitor CAY10566 (#HY15823) and CARM1 inhibitor EZM2302 (#HY-111109) were purchased from MCE.

Techniques: Expressing, Activity Assay, ChIP-sequencing

Journal: Cancer Research Communications

Article Title: Targeting Fatty Acid Reprogramming Suppresses CARM1-expressing Ovarian Cancer

doi: 10.1158/2767-9764.crc-23-0030

Figure Lengend Snippet: FIGURE 3 CARM1 promotes MUFA synthesis. A, Volcano plot illustrating the changes of metabolite levels in wildtype or CARM1 KO A1847 cells detected by LC/MS. Red dots and green dots indicate metabolites significantly upregulated or downregulated in wildtype compared with knockout

Article Snippet: SCD1 inhibitor CAY10566 (#HY15823) and CARM1 inhibitor EZM2302 (#HY-111109) were purchased from MCE.

Techniques: Liquid Chromatography with Mass Spectroscopy, Knock-Out

Journal: Cancer Research Communications

Article Title: Targeting Fatty Acid Reprogramming Suppresses CARM1-expressing Ovarian Cancer

doi: 10.1158/2767-9764.crc-23-0030

Figure Lengend Snippet: FIGURE 4 CARM1 expression sensitizes cells to SCD1 inhibition. Sensitivity of control and CARM1 KO A1847 cells to SCD1 inhibitor CAY10566 determined by colony formation assay (A), which was quantified as dose response curves (B). Sensitivity of control and CARM1-overexpressing CAVO3 cells to SCD1 inhibitor CAY10566 determined by colony formation assay (C), which was quantified as dose–response curves (D). E, Sensitivity of the

Article Snippet: SCD1 inhibitor CAY10566 (#HY15823) and CARM1 inhibitor EZM2302 (#HY-111109) were purchased from MCE.

Techniques: Expressing, Inhibition, Control, Colony Assay

Journal: Cancer Research Communications

Article Title: Targeting Fatty Acid Reprogramming Suppresses CARM1-expressing Ovarian Cancer

doi: 10.1158/2767-9764.crc-23-0030

Figure Lengend Snippet: FIGURE 5 CARM1 KO sensitizes cells to saturated FA. Sensitivity of control and CARM1 KO A1847 cells to BSA conjugated palmitate FA determined

Article Snippet: SCD1 inhibitor CAY10566 (#HY15823) and CARM1 inhibitor EZM2302 (#HY-111109) were purchased from MCE.

Techniques: Control

Journal: Cancer Research Communications

Article Title: Targeting Fatty Acid Reprogramming Suppresses CARM1-expressing Ovarian Cancer

doi: 10.1158/2767-9764.crc-23-0030

Figure Lengend Snippet: FIGURE 6 SCD1 inhibition suppresses CARM1-expressing ovarian cancer in vivo. A, Schematic of experimental design for orthotopic xenograft ovarian cancer mouse model using A1847 cells. B and C, Reproductive tracts with tumors from the indicated treatment groups were dissected

Article Snippet: SCD1 inhibitor CAY10566 (#HY15823) and CARM1 inhibitor EZM2302 (#HY-111109) were purchased from MCE.

Techniques: Inhibition, Expressing, In Vivo

Journal: Cancer Discovery

Article Title: BAF Complex Maintains Glioma Stem Cells in Pediatric H3K27M Glioma

doi: 10.1158/2159-8290.CD-21-1491

Figure Lengend Snippet: BAF complex ATPase inhibition and degradation are novel therapeutic strategies in pediatric H3K27M-glioma. A, Heat map of IC 50 values comparing small-molecule inhibitors and a degrader targeting BAF complex members, and its regulators (BRG1/BRM inhibitors: Compounds 11, 12, 14, PFI-3; CARM1 inhibitors: CARM1 inhibitor, TP064; BRD9 inhibitor: I-BRD9; and BRD9 degrader: dBRD9-13) in H3.3K27M ( n = 5), H3.1K27M ( n = 1), and H3WT ( n = 3) pediatric glioma neurosphere models and nonmalignant cell lines ( n = 2, NHA-hTERT: immortalized normal human astrocytes, and Oli Neu: immortalized normal mouse OPCs). B, PRISM analysis of 694 cancer cell lines representing 23 lineages (Broad Institute), treated with a BRG1/BRM inhibitor (Compound 11) at an 8-point dose curve (3-fold dilution, with a maximum of 10 μmol/L) for 5 days. The black dashed line represents the mean AUC computed over cell lines of all lineages. Cancer lineages below this line represent those sensitive to BRG1/BRM inhibition by Compound 11. C, Chemical structures of BRG1/BRM inhibitors (Compounds 11, 12, and 14) and a novel BRG1/BRM degrader (JQ-dS-4). D, Log 2 fold change (FC) of differential proteins (left) as assessed by SILAC of DMSO control (light isotope labeled) and 1 μmol/L JQ-dS-4 (heavy isotope labeled)–treated BT869 H3.3K27M-glioma neurospheres (2 days of treatment). Heat map (right) of BAF complex proteins (with encoding genes shown in parentheses) depleted upon JQ-dS-4 treatment in BT869 neurospheres. E, Immunoblot for BRG1 and BRM protein levels in BT869, HSJD-DIPG007, and SU-DIPGXIIIP* neurospheres treated with novel BRG1/BRM degraders (AU-15330 and JQ-dS-4) at indicated doses and time points. Cleaved PARP was used as a marker for apoptosis. Total H3 and GAPDH served as loading controls. F, Heat map of IC 50 values comparing two BRG1/BRM degraders (JQ-dS-4 and AU-15330) in H3.3K27M ( n = 5), H3.1K27M ( n = 1), and H3WT ( n = 3) pediatric glioma neurosphere models and nonmalignant cell lines ( n = 2, NHA-hTERT: immortalized normal human astrocytes, and Oli Neu: immortalized normal mouse OPCs). G, Dose–response curves for BRG1/BRM degraders (AU-15330 and JQ-dS-4) in H3.3K27M ( n = 5), H3.1K27M ( n = 1), and H3WT ( n = 3) pediatric glioma neurosphere models and nonmalignant cell lines ( n = 2, NHA-hTERT: immortalized normal human astrocytes, and Oli Neu: immortalized normal mouse OPCs).

Article Snippet: CARM1 inhibitors (CARM1 inhibitor and TP064) were purchased from Sigma and Tocris Biosciences, respectively.

Techniques: Inhibition, Multiplex sample analysis, Control, Labeling, Western Blot, Marker