polyclonal rabbit anti tet2 antibody  (Santa Cruz Biotechnology)

Journal: Journal of Hematology & Oncology

Article Title: TET2 and DNMT3A mutations and exceptional response to 4′-thio-2′-deoxycytidine in human solid tumor models

doi: 10.1186/s13045-021-01091-5

Figure Lengend Snippet: Validation of TET2 mutation in NCI-H23 cells by Sanger sequencing, and frequency of TET2 and/or DNMT3A mutations in human malignancies: a TET2 c.5162T > G missense mutation (upper panel; arrow) in NCI-H23 cells versus no alteration at the site in HCT116 cells (lower panel). Shown were all forward strands. b Frequency of TET2 and/or DNMT3A mutations in human malignancies analyzed from cBioPortal. AML, acute myeloid leukemia; CEBPA, CCAAT/enhancer-binding protein alpha; NPM, nucleophosmin; NSCLC, non-small cell lung cancer; NOS, not otherwise specified

Article Snippet: In brief, rabbit monoclonal antibodies to DNMT3A (clone D23G1) and CDKN1A/p21 Waf1/Cip1 (p21, clone 12D1) were obtained from Cell Signaling Technology (Danvers, MA), and rabbit polyclonal antibodies to TET2 (ABE364) was purchased from EMD Millipore (Burlington , MA).

Techniques: Biomarker Discovery, Mutagenesis, Sequencing, Binding Assay

Journal: Journal of Hematology & Oncology

Article Title: TET2 and DNMT3A mutations and exceptional response to 4′-thio-2′-deoxycytidine in human solid tumor models

doi: 10.1186/s13045-021-01091-5

Figure Lengend Snippet: Cell and tumor growth inhibition by T-dCyd treatment in multiple cancer cell lines and xenograft tumor models with and without deleterious TET2 and nonsynonymous DNMT3A mutations: a The cell growth inhibition by increasing concentrations, as indicated, of T-dCyd in NCI-H23 cells with TET2/DNMT3A mutations (black bars) and wildtype SKOV3 cells (gray bars), *** P < 0.0001 compared to vehicle treatment; ns, not significant (left panel). b p21 expression in NCI-H23 cells treated with T-dCyd at 48 h by Western blotting (right panel), * P < 0.05 compared to vehicle. c Cell growth inhibition by 0.5 μM of T-dCyd evaluated by clonogenic assay in mutant groups (black), wildtype group (gray) and other status (dark gray), ** P = 0.007 compared between black bar group and gray/dark-gray bar groups. d Tumor growth delay [(T-C)/C] in the mutant xenograft tumors (black), and wildtype tumors (gray) by T-dCyd treatment (all dosed with 4 mg/kg of T-dCyd). Dotted line indicated 30% of tumor growth delay. C, control; ns, not significant; T, treatment

Article Snippet: In brief, rabbit monoclonal antibodies to DNMT3A (clone D23G1) and CDKN1A/p21 Waf1/Cip1 (p21, clone 12D1) were obtained from Cell Signaling Technology (Danvers, MA), and rabbit polyclonal antibodies to TET2 (ABE364) was purchased from EMD Millipore (Burlington , MA).

Techniques: Inhibition, Expressing, Western Blot, Clonogenic Assay, Mutagenesis, Control

Journal: Journal of Hematology & Oncology

Article Title: TET2 and DNMT3A mutations and exceptional response to 4′-thio-2′-deoxycytidine in human solid tumor models

doi: 10.1186/s13045-021-01091-5

Figure Lengend Snippet: TET2 and DNMT3A mutation status in cancer cell lines

Article Snippet: In brief, rabbit monoclonal antibodies to DNMT3A (clone D23G1) and CDKN1A/p21 Waf1/Cip1 (p21, clone 12D1) were obtained from Cell Signaling Technology (Danvers, MA), and rabbit polyclonal antibodies to TET2 (ABE364) was purchased from EMD Millipore (Burlington , MA).

Techniques: Mutagenesis

Journal: Journal of Hematology & Oncology

Article Title: TET2 and DNMT3A mutations and exceptional response to 4′-thio-2′-deoxycytidine in human solid tumor models

doi: 10.1186/s13045-021-01091-5

Figure Lengend Snippet: Modulation of TET2, DNMT3A and p21 by T-dCyd (4 mg/kg) treatment in vivo

Article Snippet: In brief, rabbit monoclonal antibodies to DNMT3A (clone D23G1) and CDKN1A/p21 Waf1/Cip1 (p21, clone 12D1) were obtained from Cell Signaling Technology (Danvers, MA), and rabbit polyclonal antibodies to TET2 (ABE364) was purchased from EMD Millipore (Burlington , MA).

Techniques: Saline