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Millipore cdk13 antibody
Cdk13 Antibody, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/cdk13 antibody/product/Millipore
Average 90 stars, based on 1 article reviews

cdk13 antibody - by Bioz Stars, 2026-05

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(a) Dot plot showing editing levels of differentially edited recoding sites in genes in ESCC and CTRL. (b) Amino acid preferences of differentially edited recoding sites in genes. (c) Heatmap showing RNA editing levels of recoding genes containing at least one differentially edited recoding site. (d) Sanger sequencing chromatograms for two differentially edited recoding sites at position 1984 in NBPF8 and position 308 in CDK13 . The orange box highlights the peak of adenosine or guanosine. Edited nucleotide was shaded in red. (e,f) Kaplan-Meier curves for survival of high RNA A-to-I editing (e) and expression (f) versus low CDK13 editing and expression cohorts in NM and M ESCC, respectively. NM: nonmetastatic, M: metastatic. P values were assessed by Cox regression. (g) Overall RNA A-to-I editing levels of CDK13 across ESCC and paired CTRL samples, and across NM and M ESCC, respectively. (h) CDK13 expression across ESCC and CTRL, and NM and M samples. (i) RNA A-to-I editing in CDK13 in two groups of high and low CDK13 expression based on the mean. (j) Correlation analysis of RNA A-to-I editing and expression of CDK13 . (k) Expression of ADARs across samples of ESCC and CTRL. Significant differences were assessed by the Wilcoxon test.

Journal: bioRxiv

Article Title: The RNA Editome of Esophageal Squamous Cell Carcinoma Identifies an ADAR1-CDK13 Editing Feedback Loop Mediating cGAS–STING Activation in Early Tumorigenesis

doi: 10.64898/2026.01.29.701210

Figure Lengend Snippet: (a) Dot plot showing editing levels of differentially edited recoding sites in genes in ESCC and CTRL. (b) Amino acid preferences of differentially edited recoding sites in genes. (c) Heatmap showing RNA editing levels of recoding genes containing at least one differentially edited recoding site. (d) Sanger sequencing chromatograms for two differentially edited recoding sites at position 1984 in NBPF8 and position 308 in CDK13 . The orange box highlights the peak of adenosine or guanosine. Edited nucleotide was shaded in red. (e,f) Kaplan-Meier curves for survival of high RNA A-to-I editing (e) and expression (f) versus low CDK13 editing and expression cohorts in NM and M ESCC, respectively. NM: nonmetastatic, M: metastatic. P values were assessed by Cox regression. (g) Overall RNA A-to-I editing levels of CDK13 across ESCC and paired CTRL samples, and across NM and M ESCC, respectively. (h) CDK13 expression across ESCC and CTRL, and NM and M samples. (i) RNA A-to-I editing in CDK13 in two groups of high and low CDK13 expression based on the mean. (j) Correlation analysis of RNA A-to-I editing and expression of CDK13 . (k) Expression of ADARs across samples of ESCC and CTRL. Significant differences were assessed by the Wilcoxon test.

Article Snippet: The membrane was blocked with 5% non-fat milk powder in 1 × TBST for 1-2 hours at RT, followed by overnight incubation (∼16 h) at 4°C refrigerator with primary antibody against ADAR1 (Santa Cruz, sc-73408; 1:200 dilution) or CDK13 (Bethyl, A301-458A-BL; 1:2000 dilution).

Techniques: Sequencing, Expressing

$(a) Correlation of the RNA editing rates (upper panel) or RNA editing events (lower panel) in CDK13 with the expression of ADAR1, ADAR2, and ADAR3 . (b) Illustration of RNA immunoprecipitation (RIP) using KYSE30 and KYSE150 cells. Cells were collected and then equally split into three parts for agarose-conjugated antibody incubation, followed by washing and RNA extraction. (c) Immunoblotting examining ADAR1 abundance in distinct fractions of ADAR1 immunoprecipitation. GAPDH was used as loading control. Abbreviations represent CE: crude extract; SN: supernatant; IP: Immunoprecipitation. (d) Distribution of peaks (KYSE30 and KYSE150) and DRS across genomics elements. (e) Circos plot showing the hg38 genomic landscape of A-to-I editing events. From outermost to innermost, tracks 1-5 showed the editing densities (sites per million base pairs) in tumor (red bars) versus adjacent normal (blue bars) tissues for exons, introns, UTRs, ncRNAs, and intergenic regions, respectively; tracks 6-7 displayed scatter plots of peak scores for KYSE30 and KYSE150 cell lines. Peaks were annotated according to its genomic location, with red dots (exonic), blue (intronic), green (regulatory), and grey (intergenic). The inner links showed the genes correlated with ADAR in A-to-I editing, and the link to CDK13 was highlighted. (f) Distribution of RNA editing sites across genomics elements in two KYSE cells. (g) Distribution of RNA editing sites resided in different elements of protein-coding RNAs. (h) Counts of A-to-I DRS within or outside peaks. (i) Relative expression of ADAR1 and ADAR2 in siRNA ADAR1 , ADAR2 or control (Scramble) knockdown cells. Error bars represent ±S.D. of the mean from two technical replicates . (j) Sanger sequencing chromatograms for two recoding sites CDK13 Q103R ( CDK13 c.A308G ) and NBPF8 I662V ( NBPF8 c.A1984G ) were examined from cDNA of siRNA ADAR1 , ADAR2 or Scramble knockdown cells. (k) RNA secondary structure of unedited (upper panel) and edited (low panel) sequence surrounding c.A308G in CDK13 .$

Journal: bioRxiv

Article Title: The RNA Editome of Esophageal Squamous Cell Carcinoma Identifies an ADAR1-CDK13 Editing Feedback Loop Mediating cGAS–STING Activation in Early Tumorigenesis

doi: 10.64898/2026.01.29.701210

Figure Lengend Snippet: (a) Correlation of the RNA editing rates (upper panel) or RNA editing events (lower panel) in CDK13 with the expression of ADAR1, ADAR2, and ADAR3 . (b) Illustration of RNA immunoprecipitation (RIP) using KYSE30 and KYSE150 cells. Cells were collected and then equally split into three parts for agarose-conjugated antibody incubation, followed by washing and RNA extraction. (c) Immunoblotting examining ADAR1 abundance in distinct fractions of ADAR1 immunoprecipitation. GAPDH was used as loading control. Abbreviations represent CE: crude extract; SN: supernatant; IP: Immunoprecipitation. (d) Distribution of peaks (KYSE30 and KYSE150) and DRS across genomics elements. (e) Circos plot showing the hg38 genomic landscape of A-to-I editing events. From outermost to innermost, tracks 1-5 showed the editing densities (sites per million base pairs) in tumor (red bars) versus adjacent normal (blue bars) tissues for exons, introns, UTRs, ncRNAs, and intergenic regions, respectively; tracks 6-7 displayed scatter plots of peak scores for KYSE30 and KYSE150 cell lines. Peaks were annotated according to its genomic location, with red dots (exonic), blue (intronic), green (regulatory), and grey (intergenic). The inner links showed the genes correlated with ADAR in A-to-I editing, and the link to CDK13 was highlighted. (f) Distribution of RNA editing sites across genomics elements in two KYSE cells. (g) Distribution of RNA editing sites resided in different elements of protein-coding RNAs. (h) Counts of A-to-I DRS within or outside peaks. (i) Relative expression of ADAR1 and ADAR2 in siRNA ADAR1 , ADAR2 or control (Scramble) knockdown cells. Error bars represent ±S.D. of the mean from two technical replicates . (j) Sanger sequencing chromatograms for two recoding sites CDK13 Q103R ( CDK13 c.A308G ) and NBPF8 I662V ( NBPF8 c.A1984G ) were examined from cDNA of siRNA ADAR1 , ADAR2 or Scramble knockdown cells. (k) RNA secondary structure of unedited (upper panel) and edited (low panel) sequence surrounding c.A308G in CDK13 .

Techniques: Expressing, RNA Immunoprecipitation, Incubation, RNA Extraction, Western Blot, Immunoprecipitation, Control, Knockdown, Sequencing

(a) Relative CDK13 expression in two stable shRNA knockdown and control KYSE30 cell lines (left) and Western blot of CDK13 in the same cell lines (right); asterisks indicate CDK13. (b) Volcano plot showing differential gene expression upon CDK13 knockdown in KYSE30 cells, with ADAR family members highlighted. (c) Expression of representative ISGs in ESCC versus control (top) and in primary versus metastatic tumors (bottom). (d) Regression analysis of six ISGs with CDK13 RNA A-to-I editing and CDK13 expression. (e) Schematic illustration of ADAR1/CDK13 regulation in ESCC prognosis. Data are mean ± S.D.; significance was assessed by Student’s t-test. Asterisks denote significance (*p < 0.05, **p < 0.01, ***p < 0.001).

Journal: bioRxiv

Article Title: The RNA Editome of Esophageal Squamous Cell Carcinoma Identifies an ADAR1-CDK13 Editing Feedback Loop Mediating cGAS–STING Activation in Early Tumorigenesis

doi: 10.64898/2026.01.29.701210

Figure Lengend Snippet: (a) Relative CDK13 expression in two stable shRNA knockdown and control KYSE30 cell lines (left) and Western blot of CDK13 in the same cell lines (right); asterisks indicate CDK13. (b) Volcano plot showing differential gene expression upon CDK13 knockdown in KYSE30 cells, with ADAR family members highlighted. (c) Expression of representative ISGs in ESCC versus control (top) and in primary versus metastatic tumors (bottom). (d) Regression analysis of six ISGs with CDK13 RNA A-to-I editing and CDK13 expression. (e) Schematic illustration of ADAR1/CDK13 regulation in ESCC prognosis. Data are mean ± S.D.; significance was assessed by Student’s t-test. Asterisks denote significance (*p < 0.05, **p < 0.01, ***p < 0.001).

Techniques: Expressing, shRNA, Knockdown, Control, Western Blot, Gene Expression

(a) Reduced CDK13 signal in stable shRNA knockdown KYSE30 cells compared with controls. rRNA-depleted reads were separated by strand and normalized to CPM. (b) Volcano plot of differentially expressed genes (DEG2) in CDK13 knockdown versus control cells. DEG2 were defined as log2FC > 0.5 or < −0.5 with FDR < 0.05. Blue and red dots indicate down- and up-regulated DEG2, respectively. (c) Volcano plot of differentially phosphorylated sites (DPS). DPS were defined as log2FC > 1.5 or < −1.5 with p < 0.05. Blue and red dots represent hypo- and hyper-phosphorylated sites, respectively. (d) DEG2 is significantly enriched in immune response, cytoskeleton, and interferon signaling pathways. (e) Heatmap showing fold changes (logFC) of genes related to cGAS – STING activation, cytoskeleton regulation, STING trafficking, and interferon-stimulated gene (ISG) readout upon CDK13 knockdown in KYSE30 cells. (f) Venn diagram of DEG2 and hypo-phosphorylated sites, and the top 10 GO terms enriched among non-DEG2 DPS ranked by FDR. FDR was controlled at 5%. Blue and orange bars indicate GO terms enriched in proteins containing up- and down-phosphorylated sites, respectively. (g) Dot plot of Reactome pathways enriched for down-regulated DPS. (h) Potential CDK13 targets involved in ADAR1-dependent RNA editing. Twenty-two proteins containing 28 DPS were identified with the canonical proline residue directly following the phosphorylated amino acid . (i) Sequence conservation surrounding phosphorylated residues (±7 amino acids). Colors indicate amino acid chemistry, and bits represent residue conservation. (j) Venn diagram integrating four datasets: ADAR1-binding genes (from overlapping peaks), RNA editing-correlated genes (DEG1 and editing-correlated), DEG2, and down-regulated DPS.

Journal: bioRxiv

Article Title: The RNA Editome of Esophageal Squamous Cell Carcinoma Identifies an ADAR1-CDK13 Editing Feedback Loop Mediating cGAS–STING Activation in Early Tumorigenesis

doi: 10.64898/2026.01.29.701210

Figure Lengend Snippet: (a) Reduced CDK13 signal in stable shRNA knockdown KYSE30 cells compared with controls. rRNA-depleted reads were separated by strand and normalized to CPM. (b) Volcano plot of differentially expressed genes (DEG2) in CDK13 knockdown versus control cells. DEG2 were defined as log2FC > 0.5 or < −0.5 with FDR < 0.05. Blue and red dots indicate down- and up-regulated DEG2, respectively. (c) Volcano plot of differentially phosphorylated sites (DPS). DPS were defined as log2FC > 1.5 or < −1.5 with p < 0.05. Blue and red dots represent hypo- and hyper-phosphorylated sites, respectively. (d) DEG2 is significantly enriched in immune response, cytoskeleton, and interferon signaling pathways. (e) Heatmap showing fold changes (logFC) of genes related to cGAS – STING activation, cytoskeleton regulation, STING trafficking, and interferon-stimulated gene (ISG) readout upon CDK13 knockdown in KYSE30 cells. (f) Venn diagram of DEG2 and hypo-phosphorylated sites, and the top 10 GO terms enriched among non-DEG2 DPS ranked by FDR. FDR was controlled at 5%. Blue and orange bars indicate GO terms enriched in proteins containing up- and down-phosphorylated sites, respectively. (g) Dot plot of Reactome pathways enriched for down-regulated DPS. (h) Potential CDK13 targets involved in ADAR1-dependent RNA editing. Twenty-two proteins containing 28 DPS were identified with the canonical proline residue directly following the phosphorylated amino acid . (i) Sequence conservation surrounding phosphorylated residues (±7 amino acids). Colors indicate amino acid chemistry, and bits represent residue conservation. (j) Venn diagram integrating four datasets: ADAR1-binding genes (from overlapping peaks), RNA editing-correlated genes (DEG1 and editing-correlated), DEG2, and down-regulated DPS.

Techniques: shRNA, Knockdown, Control, Protein-Protein interactions, Activation Assay, Residue, Sequencing, Binding Assay

CDK13 is a downstream target gene for the oncological role of CCNO in LUAD. (A) Heatmap of mRNAs in the H1299 cell line with stable knockdown of CCNO obtained from transcriptome sequencing by hierarchical clustering, identifying that CCNO alters the expression of genes associated with the cell cycle. The signaling pathways of genes altered by CCNO knockdown in cells are detected by microarray analysis. The length of the columns represents the number of genes. (B) Potential molecules bound to Flag- CCNO are obtained by liquid-phase mass spectrometry analysis of the contents of H1299 cells stably overexpressing Flag- CCNO . The height of the column indicates the abundance value of the contents. (C) Correlation analysis of CCNO with CDK13 at the mRNA level in matched LUADs in the GEO dataset. (D) Correlation analysis of CDK13 expression with CCNO in 94 matched LUAD patients by immunohistochemical staining analysis. (E) COIP demonstrates that CDK13 and CCNO can bind to each other intracellularly. (F) Silver staining assay. (G) Immunofluorescence shows that CCNO co-localizes with CDK13 in the nucleus (blue with DAPI means nucleus, green with CCNO antibody and red with CDK13 antibody, 400×). (H) Typical IHC images of CDK13 high and low expression in LUAD and para-tumors (7× and 40×). GSVA, Gene Set Variation Analysis; CCNO , Cyclin O; LC-MS, liquid chromatography tandem mass spectrometry; TPM, transcripts per million; LUAD, lung adenocarcinoma; IgG, immunoglobulin G; GEO, Gene Expression Omnibus; IHC, immunohistochemistry; COIP, co-immunoprecipitation.

Journal: Journal of Thoracic Disease

Article Title: Cyclin O promotes lung cancer progression and cetuximab resistance via cell cycle regulation and CDK13 interaction

doi: 10.21037/jtd-23-437

Figure Lengend Snippet: CDK13 is a downstream target gene for the oncological role of CCNO in LUAD. (A) Heatmap of mRNAs in the H1299 cell line with stable knockdown of CCNO obtained from transcriptome sequencing by hierarchical clustering, identifying that CCNO alters the expression of genes associated with the cell cycle. The signaling pathways of genes altered by CCNO knockdown in cells are detected by microarray analysis. The length of the columns represents the number of genes. (B) Potential molecules bound to Flag- CCNO are obtained by liquid-phase mass spectrometry analysis of the contents of H1299 cells stably overexpressing Flag- CCNO . The height of the column indicates the abundance value of the contents. (C) Correlation analysis of CCNO with CDK13 at the mRNA level in matched LUADs in the GEO dataset. (D) Correlation analysis of CDK13 expression with CCNO in 94 matched LUAD patients by immunohistochemical staining analysis. (E) COIP demonstrates that CDK13 and CCNO can bind to each other intracellularly. (F) Silver staining assay. (G) Immunofluorescence shows that CCNO co-localizes with CDK13 in the nucleus (blue with DAPI means nucleus, green with CCNO antibody and red with CDK13 antibody, 400×). (H) Typical IHC images of CDK13 high and low expression in LUAD and para-tumors (7× and 40×). GSVA, Gene Set Variation Analysis; CCNO , Cyclin O; LC-MS, liquid chromatography tandem mass spectrometry; TPM, transcripts per million; LUAD, lung adenocarcinoma; IgG, immunoglobulin G; GEO, Gene Expression Omnibus; IHC, immunohistochemistry; COIP, co-immunoprecipitation.

Article Snippet: The following antibodies were used: antibody against CCNO (Abcam Cat#ab47682), antibody against HER-2 (Abcam Cat#ab214275), antibody against EGFR (Abcam Cat#52894), antibody against beta Actin (Invitrogen Cat#MA1-140), antibody against CDK13 (Santa Cruz Cat#sc-81837), antibody against P-EGFR (Cell Signaling Cat#2236), antibody against p-HER2 (Cell Signaling Cat#2243), antibody against CDK12 (Cell Signaling Cat#11973), antibody against GAPDH (Cell Signaling Cat#5174), antibody against p-p70s6k (Cell Signaling Cat#97596), antibody against p70s6k (Cell Signaling Cat#9202), antibody against pAKT (Cell Signaling Cat#4060), antibody against AKT (Cell Signaling Cat#4691), and antibody against Anti-Flag Tag (Cell Signaling Cat#147935).

Techniques: Knockdown, Sequencing, Expressing, Protein-Protein interactions, Microarray, Mass Spectrometry, Stable Transfection, Immunohistochemical staining, Staining, Silver Staining, Immunofluorescence, Liquid Chromatography with Mass Spectroscopy, Liquid Chromatography, Gene Expression, Immunohistochemistry, Immunoprecipitation

CCNO promotes tumor cell proliferation and survival through p-EGFR in vivo via CDK13 . (A) Changes in the expression of the EGFR biomarkers p-HER2 , HER2 , p-EGFR , EGFR , p-p70S6K , p70S6K , pAKT , and AKT after CCNO knockdown as detected by western blot. (B) Representative images of IHC staining of p-EGFR in xenograft tumors (200×). (C) CCK8 assays identify proliferation under different treatments in H1299 cells stably overexpressing CCNO . NC, negative control; OE, overexpression; CI, CCNOsi ; S, SR-4835; C, Cetuximab; P, Placebo; CET, Cetuximab; CCNO , Cyclin O; EGFR , epidermal growth factor receptor; HER2 , human epidermal growth factor receptor-2; AKT , protein kinase B; CCK8, Cell Counting Kit-8.

Journal: Journal of Thoracic Disease

Article Title: Cyclin O promotes lung cancer progression and cetuximab resistance via cell cycle regulation and CDK13 interaction

doi: 10.21037/jtd-23-437

Figure Lengend Snippet: CCNO promotes tumor cell proliferation and survival through p-EGFR in vivo via CDK13 . (A) Changes in the expression of the EGFR biomarkers p-HER2 , HER2 , p-EGFR , EGFR , p-p70S6K , p70S6K , pAKT , and AKT after CCNO knockdown as detected by western blot. (B) Representative images of IHC staining of p-EGFR in xenograft tumors (200×). (C) CCK8 assays identify proliferation under different treatments in H1299 cells stably overexpressing CCNO . NC, negative control; OE, overexpression; CI, CCNOsi ; S, SR-4835; C, Cetuximab; P, Placebo; CET, Cetuximab; CCNO , Cyclin O; EGFR , epidermal growth factor receptor; HER2 , human epidermal growth factor receptor-2; AKT , protein kinase B; CCK8, Cell Counting Kit-8.

Techniques: In Vivo, Expressing, Knockdown, Western Blot, Immunohistochemistry, Stable Transfection, Negative Control, Over Expression, Cell Counting

CCNO activates the p-EGFR signaling pathways via CDK13 in vitro . (A) Typical images of tumors from the different treatment groups 5 weeks after tumor injections. (B,C) The weights (B) and volumes (C) are lower in xenograft tumors with overexpressed CCNO under different treatments. *, P<0.05; **, P<0.01; ****, P<0.0001. NC, negative control; OE, overexpression; SR, SR-4835; S, SR-4835; C, Cetuximab; ns, no significance; CCNO , Cyclin O.

Journal: Journal of Thoracic Disease

Article Title: Cyclin O promotes lung cancer progression and cetuximab resistance via cell cycle regulation and CDK13 interaction

doi: 10.21037/jtd-23-437

Figure Lengend Snippet: CCNO activates the p-EGFR signaling pathways via CDK13 in vitro . (A) Typical images of tumors from the different treatment groups 5 weeks after tumor injections. (B,C) The weights (B) and volumes (C) are lower in xenograft tumors with overexpressed CCNO under different treatments. *, P<0.05; **, P<0.01; ****, P<0.0001. NC, negative control; OE, overexpression; SR, SR-4835; S, SR-4835; C, Cetuximab; ns, no significance; CCNO , Cyclin O.

Techniques: Protein-Protein interactions, In Vitro, Negative Control, Over Expression

CDK13 is a key factor in the oncological effect of CCNO . (A) CCK8 assays identify proliferation under different treatments in H1299 and A549 cells. (B) EdU assays (400×) identify proliferation under different treatments in H1299 and A549 cells. **, P<0.01; ***, P<0.001; ****, P<0.0001. CCK8, Cell Counting Kit-8; NC, negative control; ns, no significance; CCNO si, CCNO knockdown; CCNO , Cyclin O; EdU, 5-Ethynyl-2'-deoxyuridine.

Journal: Journal of Thoracic Disease

Article Title: Cyclin O promotes lung cancer progression and cetuximab resistance via cell cycle regulation and CDK13 interaction

doi: 10.21037/jtd-23-437

Figure Lengend Snippet: CDK13 is a key factor in the oncological effect of CCNO . (A) CCK8 assays identify proliferation under different treatments in H1299 and A549 cells. (B) EdU assays (400×) identify proliferation under different treatments in H1299 and A549 cells. **, P<0.01; ***, P<0.001; ****, P<0.0001. CCK8, Cell Counting Kit-8; NC, negative control; ns, no significance; CCNO si, CCNO knockdown; CCNO , Cyclin O; EdU, 5-Ethynyl-2'-deoxyuridine.

Techniques: Cell Counting, Negative Control, Knockdown

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