cell line molt16 Search Results


94
DSMZ cell line molt16
Fig. 3. The role of SETD2 in tumor suppression and apoptosis. A) RNA-sequencing analysis of normalized FPKM values (TARGET) showing decreased expression of SETD2 in CNS3 diagnosis patients compared to CNS1 diagnosis samples. (Significance calculated by one-way ANOVA comparing the mean of all groups to the mean of the control group (CNS1), displayed as adjusted p-value. *p < 0.05). B) RNA-sequencing correlation analysis of SETD2 and TP53 (FPKM) showing a negative correlation (r = −0.694, **p=<0.01) and MDM2 showing a positive correlation (r = 0.623, *p=<0.05) in CNS relapsed T-ALL patients (TARGET). (Correlation was calculated using Pearson correlation coefficients, two-tailed with 95% confidence interval). C) String diagram showing protein-protein interactions directly and indirectly experimentally linking SETD2 with TP53, MDM2, BCLX, BCL2, NANOG, SOX2, OCT4, SIRT1 and EP300. D) mRNA expression levels (fold change versus empty vector control) of MDM2, TP53, MYCC, SOX2, NANOG, and OCT4 24 h after SETD2 overexpression by transfection in <t>MOLT16</t> cells. E) mRNA expression levels (displayed as normalized fold change) of SETD2 overexpression in T-ALL cell lines MOLT16, SUP-T1, CCL-119 has a negative correlation with TP53 (r = −0.709, p = ns), and a positive correlation with SOX2 (r = 0.881, p = ns), NANOG (r = 0.844, p = ns) and OCT4 (r = 0.896, p = ns). (Correlation was calculated using Pearson correlation coefficients, two-tailed with 95% confidence interval). F) Expression levels of BCL2 and BCLX isoforms after SETD2 overexpression in T- ALL cell lines (MOLT16, SUP-T1 and CCL-119) normalized to empty vector control (Significance calculated by multiple two-tailed, unpaired Student’s t-test with Holm-ˇSíd´ak correction for multiple comparisons, displayed as adjusted p-value, *p < 0.05 **p < 0.01).
Cell Line Molt16, supplied by DSMZ, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Hayashibara Biochemical Laboratories hel cell line
Fig. 3. The role of SETD2 in tumor suppression and apoptosis. A) RNA-sequencing analysis of normalized FPKM values (TARGET) showing decreased expression of SETD2 in CNS3 diagnosis patients compared to CNS1 diagnosis samples. (Significance calculated by one-way ANOVA comparing the mean of all groups to the mean of the control group (CNS1), displayed as adjusted p-value. *p < 0.05). B) RNA-sequencing correlation analysis of SETD2 and TP53 (FPKM) showing a negative correlation (r = −0.694, **p=<0.01) and MDM2 showing a positive correlation (r = 0.623, *p=<0.05) in CNS relapsed T-ALL patients (TARGET). (Correlation was calculated using Pearson correlation coefficients, two-tailed with 95% confidence interval). C) String diagram showing protein-protein interactions directly and indirectly experimentally linking SETD2 with TP53, MDM2, BCLX, BCL2, NANOG, SOX2, OCT4, SIRT1 and EP300. D) mRNA expression levels (fold change versus empty vector control) of MDM2, TP53, MYCC, SOX2, NANOG, and OCT4 24 h after SETD2 overexpression by transfection in <t>MOLT16</t> cells. E) mRNA expression levels (displayed as normalized fold change) of SETD2 overexpression in T-ALL cell lines MOLT16, SUP-T1, CCL-119 has a negative correlation with TP53 (r = −0.709, p = ns), and a positive correlation with SOX2 (r = 0.881, p = ns), NANOG (r = 0.844, p = ns) and OCT4 (r = 0.896, p = ns). (Correlation was calculated using Pearson correlation coefficients, two-tailed with 95% confidence interval). F) Expression levels of BCL2 and BCLX isoforms after SETD2 overexpression in T- ALL cell lines (MOLT16, SUP-T1 and CCL-119) normalized to empty vector control (Significance calculated by multiple two-tailed, unpaired Student’s t-test with Holm-ˇSíd´ak correction for multiple comparisons, displayed as adjusted p-value, *p < 0.05 **p < 0.01).
Hel Cell Line, supplied by Hayashibara Biochemical Laboratories, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
CEM Corporation cell lines cem/c2
Fig. 3. The role of SETD2 in tumor suppression and apoptosis. A) RNA-sequencing analysis of normalized FPKM values (TARGET) showing decreased expression of SETD2 in CNS3 diagnosis patients compared to CNS1 diagnosis samples. (Significance calculated by one-way ANOVA comparing the mean of all groups to the mean of the control group (CNS1), displayed as adjusted p-value. *p < 0.05). B) RNA-sequencing correlation analysis of SETD2 and TP53 (FPKM) showing a negative correlation (r = −0.694, **p=<0.01) and MDM2 showing a positive correlation (r = 0.623, *p=<0.05) in CNS relapsed T-ALL patients (TARGET). (Correlation was calculated using Pearson correlation coefficients, two-tailed with 95% confidence interval). C) String diagram showing protein-protein interactions directly and indirectly experimentally linking SETD2 with TP53, MDM2, BCLX, BCL2, NANOG, SOX2, OCT4, SIRT1 and EP300. D) mRNA expression levels (fold change versus empty vector control) of MDM2, TP53, MYCC, SOX2, NANOG, and OCT4 24 h after SETD2 overexpression by transfection in <t>MOLT16</t> cells. E) mRNA expression levels (displayed as normalized fold change) of SETD2 overexpression in T-ALL cell lines MOLT16, SUP-T1, CCL-119 has a negative correlation with TP53 (r = −0.709, p = ns), and a positive correlation with SOX2 (r = 0.881, p = ns), NANOG (r = 0.844, p = ns) and OCT4 (r = 0.896, p = ns). (Correlation was calculated using Pearson correlation coefficients, two-tailed with 95% confidence interval). F) Expression levels of BCL2 and BCLX isoforms after SETD2 overexpression in T- ALL cell lines (MOLT16, SUP-T1 and CCL-119) normalized to empty vector control (Significance calculated by multiple two-tailed, unpaired Student’s t-test with Holm-ˇSíd´ak correction for multiple comparisons, displayed as adjusted p-value, *p < 0.05 **p < 0.01).
Cell Lines Cem/C2, supplied by CEM Corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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95
DSMZ cell lines
Fig. 3. The role of SETD2 in tumor suppression and apoptosis. A) RNA-sequencing analysis of normalized FPKM values (TARGET) showing decreased expression of SETD2 in CNS3 diagnosis patients compared to CNS1 diagnosis samples. (Significance calculated by one-way ANOVA comparing the mean of all groups to the mean of the control group (CNS1), displayed as adjusted p-value. *p < 0.05). B) RNA-sequencing correlation analysis of SETD2 and TP53 (FPKM) showing a negative correlation (r = −0.694, **p=<0.01) and MDM2 showing a positive correlation (r = 0.623, *p=<0.05) in CNS relapsed T-ALL patients (TARGET). (Correlation was calculated using Pearson correlation coefficients, two-tailed with 95% confidence interval). C) String diagram showing protein-protein interactions directly and indirectly experimentally linking SETD2 with TP53, MDM2, BCLX, BCL2, NANOG, SOX2, OCT4, SIRT1 and EP300. D) mRNA expression levels (fold change versus empty vector control) of MDM2, TP53, MYCC, SOX2, NANOG, and OCT4 24 h after SETD2 overexpression by transfection in <t>MOLT16</t> cells. E) mRNA expression levels (displayed as normalized fold change) of SETD2 overexpression in T-ALL cell lines MOLT16, SUP-T1, CCL-119 has a negative correlation with TP53 (r = −0.709, p = ns), and a positive correlation with SOX2 (r = 0.881, p = ns), NANOG (r = 0.844, p = ns) and OCT4 (r = 0.896, p = ns). (Correlation was calculated using Pearson correlation coefficients, two-tailed with 95% confidence interval). F) Expression levels of BCL2 and BCLX isoforms after SETD2 overexpression in T- ALL cell lines (MOLT16, SUP-T1 and CCL-119) normalized to empty vector control (Significance calculated by multiple two-tailed, unpaired Student’s t-test with Holm-ˇSíd´ak correction for multiple comparisons, displayed as adjusted p-value, *p < 0.05 **p < 0.01).
Cell Lines, supplied by DSMZ, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
CEM Corporation t-all cell lines ccrf-cem
Fig. 3. The role of SETD2 in tumor suppression and apoptosis. A) RNA-sequencing analysis of normalized FPKM values (TARGET) showing decreased expression of SETD2 in CNS3 diagnosis patients compared to CNS1 diagnosis samples. (Significance calculated by one-way ANOVA comparing the mean of all groups to the mean of the control group (CNS1), displayed as adjusted p-value. *p < 0.05). B) RNA-sequencing correlation analysis of SETD2 and TP53 (FPKM) showing a negative correlation (r = −0.694, **p=<0.01) and MDM2 showing a positive correlation (r = 0.623, *p=<0.05) in CNS relapsed T-ALL patients (TARGET). (Correlation was calculated using Pearson correlation coefficients, two-tailed with 95% confidence interval). C) String diagram showing protein-protein interactions directly and indirectly experimentally linking SETD2 with TP53, MDM2, BCLX, BCL2, NANOG, SOX2, OCT4, SIRT1 and EP300. D) mRNA expression levels (fold change versus empty vector control) of MDM2, TP53, MYCC, SOX2, NANOG, and OCT4 24 h after SETD2 overexpression by transfection in <t>MOLT16</t> cells. E) mRNA expression levels (displayed as normalized fold change) of SETD2 overexpression in T-ALL cell lines MOLT16, SUP-T1, CCL-119 has a negative correlation with TP53 (r = −0.709, p = ns), and a positive correlation with SOX2 (r = 0.881, p = ns), NANOG (r = 0.844, p = ns) and OCT4 (r = 0.896, p = ns). (Correlation was calculated using Pearson correlation coefficients, two-tailed with 95% confidence interval). F) Expression levels of BCL2 and BCLX isoforms after SETD2 overexpression in T- ALL cell lines (MOLT16, SUP-T1 and CCL-119) normalized to empty vector control (Significance calculated by multiple two-tailed, unpaired Student’s t-test with Holm-ˇSíd´ak correction for multiple comparisons, displayed as adjusted p-value, *p < 0.05 **p < 0.01).
T All Cell Lines Ccrf Cem, supplied by CEM Corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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96
DSMZ authentication leukemia cell lines
Fig. 3. The role of SETD2 in tumor suppression and apoptosis. A) RNA-sequencing analysis of normalized FPKM values (TARGET) showing decreased expression of SETD2 in CNS3 diagnosis patients compared to CNS1 diagnosis samples. (Significance calculated by one-way ANOVA comparing the mean of all groups to the mean of the control group (CNS1), displayed as adjusted p-value. *p < 0.05). B) RNA-sequencing correlation analysis of SETD2 and TP53 (FPKM) showing a negative correlation (r = −0.694, **p=<0.01) and MDM2 showing a positive correlation (r = 0.623, *p=<0.05) in CNS relapsed T-ALL patients (TARGET). (Correlation was calculated using Pearson correlation coefficients, two-tailed with 95% confidence interval). C) String diagram showing protein-protein interactions directly and indirectly experimentally linking SETD2 with TP53, MDM2, BCLX, BCL2, NANOG, SOX2, OCT4, SIRT1 and EP300. D) mRNA expression levels (fold change versus empty vector control) of MDM2, TP53, MYCC, SOX2, NANOG, and OCT4 24 h after SETD2 overexpression by transfection in <t>MOLT16</t> cells. E) mRNA expression levels (displayed as normalized fold change) of SETD2 overexpression in T-ALL cell lines MOLT16, SUP-T1, CCL-119 has a negative correlation with TP53 (r = −0.709, p = ns), and a positive correlation with SOX2 (r = 0.881, p = ns), NANOG (r = 0.844, p = ns) and OCT4 (r = 0.896, p = ns). (Correlation was calculated using Pearson correlation coefficients, two-tailed with 95% confidence interval). F) Expression levels of BCL2 and BCLX isoforms after SETD2 overexpression in T- ALL cell lines (MOLT16, SUP-T1 and CCL-119) normalized to empty vector control (Significance calculated by multiple two-tailed, unpaired Student’s t-test with Holm-ˇSíd´ak correction for multiple comparisons, displayed as adjusted p-value, *p < 0.05 **p < 0.01).
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Image Search Results


Fig. 3. The role of SETD2 in tumor suppression and apoptosis. A) RNA-sequencing analysis of normalized FPKM values (TARGET) showing decreased expression of SETD2 in CNS3 diagnosis patients compared to CNS1 diagnosis samples. (Significance calculated by one-way ANOVA comparing the mean of all groups to the mean of the control group (CNS1), displayed as adjusted p-value. *p < 0.05). B) RNA-sequencing correlation analysis of SETD2 and TP53 (FPKM) showing a negative correlation (r = −0.694, **p=<0.01) and MDM2 showing a positive correlation (r = 0.623, *p=<0.05) in CNS relapsed T-ALL patients (TARGET). (Correlation was calculated using Pearson correlation coefficients, two-tailed with 95% confidence interval). C) String diagram showing protein-protein interactions directly and indirectly experimentally linking SETD2 with TP53, MDM2, BCLX, BCL2, NANOG, SOX2, OCT4, SIRT1 and EP300. D) mRNA expression levels (fold change versus empty vector control) of MDM2, TP53, MYCC, SOX2, NANOG, and OCT4 24 h after SETD2 overexpression by transfection in MOLT16 cells. E) mRNA expression levels (displayed as normalized fold change) of SETD2 overexpression in T-ALL cell lines MOLT16, SUP-T1, CCL-119 has a negative correlation with TP53 (r = −0.709, p = ns), and a positive correlation with SOX2 (r = 0.881, p = ns), NANOG (r = 0.844, p = ns) and OCT4 (r = 0.896, p = ns). (Correlation was calculated using Pearson correlation coefficients, two-tailed with 95% confidence interval). F) Expression levels of BCL2 and BCLX isoforms after SETD2 overexpression in T- ALL cell lines (MOLT16, SUP-T1 and CCL-119) normalized to empty vector control (Significance calculated by multiple two-tailed, unpaired Student’s t-test with Holm-ˇSíd´ak correction for multiple comparisons, displayed as adjusted p-value, *p < 0.05 **p < 0.01).

Journal: Experimental cell research

Article Title: The CNS microenvironment promotes leukemia cell survival by disrupting tumor suppression and cell cycle regulation in pediatric T-cell acute lymphoblastic leukemia.

doi: 10.1016/j.yexcr.2024.114015

Figure Lengend Snippet: Fig. 3. The role of SETD2 in tumor suppression and apoptosis. A) RNA-sequencing analysis of normalized FPKM values (TARGET) showing decreased expression of SETD2 in CNS3 diagnosis patients compared to CNS1 diagnosis samples. (Significance calculated by one-way ANOVA comparing the mean of all groups to the mean of the control group (CNS1), displayed as adjusted p-value. *p < 0.05). B) RNA-sequencing correlation analysis of SETD2 and TP53 (FPKM) showing a negative correlation (r = −0.694, **p=<0.01) and MDM2 showing a positive correlation (r = 0.623, *p=<0.05) in CNS relapsed T-ALL patients (TARGET). (Correlation was calculated using Pearson correlation coefficients, two-tailed with 95% confidence interval). C) String diagram showing protein-protein interactions directly and indirectly experimentally linking SETD2 with TP53, MDM2, BCLX, BCL2, NANOG, SOX2, OCT4, SIRT1 and EP300. D) mRNA expression levels (fold change versus empty vector control) of MDM2, TP53, MYCC, SOX2, NANOG, and OCT4 24 h after SETD2 overexpression by transfection in MOLT16 cells. E) mRNA expression levels (displayed as normalized fold change) of SETD2 overexpression in T-ALL cell lines MOLT16, SUP-T1, CCL-119 has a negative correlation with TP53 (r = −0.709, p = ns), and a positive correlation with SOX2 (r = 0.881, p = ns), NANOG (r = 0.844, p = ns) and OCT4 (r = 0.896, p = ns). (Correlation was calculated using Pearson correlation coefficients, two-tailed with 95% confidence interval). F) Expression levels of BCL2 and BCLX isoforms after SETD2 overexpression in T- ALL cell lines (MOLT16, SUP-T1 and CCL-119) normalized to empty vector control (Significance calculated by multiple two-tailed, unpaired Student’s t-test with Holm-ˇSíd´ak correction for multiple comparisons, displayed as adjusted p-value, *p < 0.05 **p < 0.01).

Article Snippet: T-ALL cell line MOLT16 (Leibniz Institute DSMZ) was cultured in suspension in IMDM (Gibco) with 10% FBS.

Techniques: RNA Sequencing, Expressing, Biomarker Discovery, Control, Two Tailed Test, Protein-Protein interactions, Plasmid Preparation, Over Expression, Transfection