array comparative genomic hybridization (acgh) 180k Search Results


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<t>SNP</t> calling failure rate in association with DLR. SNP calling data were extracted from a . Agilent 180 K <t>aCGH/SNP</t> array, and b . Agilent 400 K aCGH/SNP array. SNP calling failure rate increased significantly when DLR is greater than 0.2 (**, p < 0.01). No significant difference (NS) between samples of DLR 0.2–0.3 and DLR > 0.3
180 K Acgh/Snp Array, supplied by Agilent technologies, 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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<t>SNP</t> calling failure rate in association with DLR. SNP calling data were extracted from a . Agilent 180 K <t>aCGH/SNP</t> array, and b . Agilent 400 K aCGH/SNP array. SNP calling failure rate increased significantly when DLR is greater than 0.2 (**, p < 0.01). No significant difference (NS) between samples of DLR 0.2–0.3 and DLR > 0.3
Sureprint G3 Human Cgh Microarray Kit, supplied by Agilent technologies, 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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<t>SNP</t> calling failure rate in association with DLR. SNP calling data were extracted from a . Agilent 180 K <t>aCGH/SNP</t> array, and b . Agilent 400 K aCGH/SNP array. SNP calling failure rate increased significantly when DLR is greater than 0.2 (**, p < 0.01). No significant difference (NS) between samples of DLR 0.2–0.3 and DLR > 0.3
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<t>SNP</t> calling failure rate in association with DLR. SNP calling data were extracted from a . Agilent 180 K <t>aCGH/SNP</t> array, and b . Agilent 400 K aCGH/SNP array. SNP calling failure rate increased significantly when DLR is greater than 0.2 (**, p < 0.01). No significant difference (NS) between samples of DLR 0.2–0.3 and DLR > 0.3
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Expression <t>microarray</t> analysis at the subacute phase of Fe-NTA-induced renal carcinogenesis sorts out mitochondrial and iron metabolisms as candidate responsible pathways in Brca1 MUT(L63X/+) rat. (A) Results of hierarchical clustering and GO term analysis for the genes differentially expressed between WT and Brca1 MUT at 3 weeks in the Fe-NTA-induced renal carcinogenesis protocol (refer to ). (B) Renal Brca1 expression during the subacute phase of Fe-NTA-induced renal carcinogenesis protocol with qPCR (left panel; means ± SD) and immunoblot analysis (right panels). (C) Examples of altered metabolisms and mitochondrial dysfunction with expression microarray analysis specifically in the kidney of Brca1 MUT rats during the subacute phase of Fe-NTA-induced renal carcinogenesis (n = 3; * P < 0.05, ** P < 0.01, *** P < 0.001 vs wild-type Fe-NTA renal carcinogenesis protocol at 3 weeks). Refer to text for details.
Sureprint G3 Rat Cgh 4 × 180k Microarray, G4826a#27064, supplied by Agilent technologies, 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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Expression <t>microarray</t> analysis at the subacute phase of Fe-NTA-induced renal carcinogenesis sorts out mitochondrial and iron metabolisms as candidate responsible pathways in Brca1 MUT(L63X/+) rat. (A) Results of hierarchical clustering and GO term analysis for the genes differentially expressed between WT and Brca1 MUT at 3 weeks in the Fe-NTA-induced renal carcinogenesis protocol (refer to ). (B) Renal Brca1 expression during the subacute phase of Fe-NTA-induced renal carcinogenesis protocol with qPCR (left panel; means ± SD) and immunoblot analysis (right panels). (C) Examples of altered metabolisms and mitochondrial dysfunction with expression microarray analysis specifically in the kidney of Brca1 MUT rats during the subacute phase of Fe-NTA-induced renal carcinogenesis (n = 3; * P < 0.05, ** P < 0.01, *** P < 0.001 vs wild-type Fe-NTA renal carcinogenesis protocol at 3 weeks). Refer to text for details.
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Expression <t>microarray</t> analysis at the subacute phase of Fe-NTA-induced renal carcinogenesis sorts out mitochondrial and iron metabolisms as candidate responsible pathways in Brca1 MUT(L63X/+) rat. (A) Results of hierarchical clustering and GO term analysis for the genes differentially expressed between WT and Brca1 MUT at 3 weeks in the Fe-NTA-induced renal carcinogenesis protocol (refer to ). (B) Renal Brca1 expression during the subacute phase of Fe-NTA-induced renal carcinogenesis protocol with qPCR (left panel; means ± SD) and immunoblot analysis (right panels). (C) Examples of altered metabolisms and mitochondrial dysfunction with expression microarray analysis specifically in the kidney of Brca1 MUT rats during the subacute phase of Fe-NTA-induced renal carcinogenesis (n = 3; * P < 0.05, ** P < 0.01, *** P < 0.001 vs wild-type Fe-NTA renal carcinogenesis protocol at 3 weeks). Refer to text for details.
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Expression <t>microarray</t> analysis at the subacute phase of Fe-NTA-induced renal carcinogenesis sorts out mitochondrial and iron metabolisms as candidate responsible pathways in Brca1 MUT(L63X/+) rat. (A) Results of hierarchical clustering and GO term analysis for the genes differentially expressed between WT and Brca1 MUT at 3 weeks in the Fe-NTA-induced renal carcinogenesis protocol (refer to ). (B) Renal Brca1 expression during the subacute phase of Fe-NTA-induced renal carcinogenesis protocol with qPCR (left panel; means ± SD) and immunoblot analysis (right panels). (C) Examples of altered metabolisms and mitochondrial dysfunction with expression microarray analysis specifically in the kidney of Brca1 MUT rats during the subacute phase of Fe-NTA-induced renal carcinogenesis (n = 3; * P < 0.05, ** P < 0.01, *** P < 0.001 vs wild-type Fe-NTA renal carcinogenesis protocol at 3 weeks). Refer to text for details.
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Image Search Results


SNP calling failure rate in association with DLR. SNP calling data were extracted from a . Agilent 180 K aCGH/SNP array, and b . Agilent 400 K aCGH/SNP array. SNP calling failure rate increased significantly when DLR is greater than 0.2 (**, p < 0.01). No significant difference (NS) between samples of DLR 0.2–0.3 and DLR > 0.3

Journal: Molecular Cytogenetics

Article Title: Analytical validation and chromosomal distribution of regions of homozygosity by oligonucleotide array comparative genomic hybridization from normal prenatal and postnatal case series

doi: 10.1186/s13039-019-0424-6

Figure Lengend Snippet: SNP calling failure rate in association with DLR. SNP calling data were extracted from a . Agilent 180 K aCGH/SNP array, and b . Agilent 400 K aCGH/SNP array. SNP calling failure rate increased significantly when DLR is greater than 0.2 (**, p < 0.01). No significant difference (NS) between samples of DLR 0.2–0.3 and DLR > 0.3

Article Snippet: SNP calling data were extracted from a . Agilent 180 K aCGH/SNP array, and b . Agilent 400 K aCGH/SNP array.

Techniques:

Expression microarray analysis at the subacute phase of Fe-NTA-induced renal carcinogenesis sorts out mitochondrial and iron metabolisms as candidate responsible pathways in Brca1 MUT(L63X/+) rat. (A) Results of hierarchical clustering and GO term analysis for the genes differentially expressed between WT and Brca1 MUT at 3 weeks in the Fe-NTA-induced renal carcinogenesis protocol (refer to ). (B) Renal Brca1 expression during the subacute phase of Fe-NTA-induced renal carcinogenesis protocol with qPCR (left panel; means ± SD) and immunoblot analysis (right panels). (C) Examples of altered metabolisms and mitochondrial dysfunction with expression microarray analysis specifically in the kidney of Brca1 MUT rats during the subacute phase of Fe-NTA-induced renal carcinogenesis (n = 3; * P < 0.05, ** P < 0.01, *** P < 0.001 vs wild-type Fe-NTA renal carcinogenesis protocol at 3 weeks). Refer to text for details.

Journal: Redox Biology

Article Title: BRCA1 haploinsufficiency promotes chromosomal amplification under Fenton reaction-based carcinogenesis through ferroptosis-resistance

doi: 10.1016/j.redox.2022.102356

Figure Lengend Snippet: Expression microarray analysis at the subacute phase of Fe-NTA-induced renal carcinogenesis sorts out mitochondrial and iron metabolisms as candidate responsible pathways in Brca1 MUT(L63X/+) rat. (A) Results of hierarchical clustering and GO term analysis for the genes differentially expressed between WT and Brca1 MUT at 3 weeks in the Fe-NTA-induced renal carcinogenesis protocol (refer to ). (B) Renal Brca1 expression during the subacute phase of Fe-NTA-induced renal carcinogenesis protocol with qPCR (left panel; means ± SD) and immunoblot analysis (right panels). (C) Examples of altered metabolisms and mitochondrial dysfunction with expression microarray analysis specifically in the kidney of Brca1 MUT rats during the subacute phase of Fe-NTA-induced renal carcinogenesis (n = 3; * P < 0.05, ** P < 0.01, *** P < 0.001 vs wild-type Fe-NTA renal carcinogenesis protocol at 3 weeks). Refer to text for details.

Article Snippet: We labeled DNA from 16 rat primary RCCs (4 in wild-type without metastasis, 4 in wild-type with pulmonary metastasis, 4 in Brca1-MUT rat without metastasis, and 4 in Brca1-MUT rat with pulmonary metastasis; randomly selected from RCC samples of appropriate size [diameter >15 mm] without massive necrosis and obtained by scheduled autopsy; ) with Cy-5 and the corresponding control DNA with Cy-3, which were applied to the aCGH microarray slides (SurePrint G3 Rat CGH 4 × 180k Microarray, G4826A#27064, Agilent Technologies, Santa Clara, CA) according to the Agilent Oligonucleotide Array-Based CGH for Genomic DNA Analysis protocol Ver.7.3.

Techniques: Expressing, Microarray, Western Blot