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sureprint g3 human cgh microarray kit, 4×180k, amadid: 022060  (Agilent technologies)


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    Agilent technologies sureprint g3 human cgh microarray kit, 4×180k, amadid: 022060
    Sureprint G3 Human Cgh Microarray Kit, 4×180k, Amadid: 022060, 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
    https://www.bioz.com/product/180k+sureprint+g3+cgh+microarray/pm38575304-56-10-19
    Average 90 stars, based on 1 article reviews
    sureprint g3 human cgh microarray kit, 4×180k, amadid: 022060 - by Bioz Stars, 2026-09
    90/100 stars

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    Related Articles

    Hybridization:

    Article Title: Dual Molecular Effects of Dominant RORA Mutations Cause Two Variants of Syndromic Intellectual Disability with Either Autism or Cerebellar Ataxia
    Article Snippet: .. Routine genetic testing was performed whenever clinically relevant, including copy-number variation (CNV) analysis by high-resolution array-based comparative genomic hybridization (aCGH) using (1) 180k CytoSure ISCA v2 array (Oxford Gene Technology; individuals 10A–D), (2) 180k SurePrint G3 CGH microarray as described 10 (Agilent; individual 11), or (3) 400k SurePrint G3 CGH microarray, as described 11 (Agilent, individuals 12 and 13). .. Affected individuals with a negative aCGH result underwent whole-exome sequencing (WES) on an Illumina HiSeq platform according to the following paradigms: (1) trio-based clinical diagnostic WES (individuals 1, 2, 6, 7, and 9), (2) trio-based WES in a research laboratory (individuals 3 and 4), or (3) WES of an affected individual followed by single site testing in parental DNA samples (individuals 5 and 8; see Table S1 for further details).

    Microarray:

    Article Title: Dual Molecular Effects of Dominant RORA Mutations Cause Two Variants of Syndromic Intellectual Disability with Either Autism or Cerebellar Ataxia
    Article Snippet: .. Routine genetic testing was performed whenever clinically relevant, including copy-number variation (CNV) analysis by high-resolution array-based comparative genomic hybridization (aCGH) using (1) 180k CytoSure ISCA v2 array (Oxford Gene Technology; individuals 10A–D), (2) 180k SurePrint G3 CGH microarray as described 10 (Agilent; individual 11), or (3) 400k SurePrint G3 CGH microarray, as described 11 (Agilent, individuals 12 and 13). .. Affected individuals with a negative aCGH result underwent whole-exome sequencing (WES) on an Illumina HiSeq platform according to the following paradigms: (1) trio-based clinical diagnostic WES (individuals 1, 2, 6, 7, and 9), (2) trio-based WES in a research laboratory (individuals 3 and 4), or (3) WES of an affected individual followed by single site testing in parental DNA samples (individuals 5 and 8; see Table S1 for further 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 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