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cdna microarray partek genomics suite 6.6  (Partek)

 
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    Partek cdna microarray partek genomics suite 6.6
    Cdna Microarray Partek Genomics Suite 6.6, supplied by Partek, 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/partek+microarray+suite/cdna+microarray+partek+genomics+suite+6+6/pm24059308-2-1-4
    Average 90 stars, based on 1 article reviews
    cdna microarray partek genomics suite 6.6 - by Bioz Stars, 2026-11
    90/100 stars

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    Article Title: Establishing genomic/transcriptomic links between Alzheimer's disease and type 2 diabetes mellitus by meta-analysis approach.
    Article Snippet: Meta-analysis methods exist for combining multiple microarray datasets.. However, there are a wide range of issues associated with microarray meta-analysis and a limited ability to compare the performance of different metaanalysis methods.. Using cDNA microarray technology (Partek Genomics Suite 6.6) and global pathway analysis with Ingenuity Pathway Analysis tool (IPA, Inc), we examined the transcript level in type 2 diabetes mellitus (T2DM) and Alzheimer’s disease (AD) patients and controls.



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    (A) IPA assay of CASZ1b targets in SY5Y cells determined by <t>microarray</t> showed gene enrichment in the categories of molecular and cellular functions with a key subcategory being cell growth and proliferation (threshold represents p=0.05). (B) GSEA assay indicated the positive enrichment of genes involved neurological system process (left panel), and negative enrichment of genes regulated by MYC (right panel). NES, normalized enrichment score; Nom, nominal; FDR, false discovery rate. (C) Transcriptional activity assay of cytoplasmic localized K37A mutant and loss of NuRD binding mutant L31A in SY5Y cells by realtime PCR. a, Left panel: western blot analysis of CASZ1b and mutant proteins from SY5YtetCASZ1b and CASZ1b mutant cells after 24 h Tet treatment; right panel: realtime PCR analysis of CASZ1b and mutant mRNA levels from SY5YtetCASZ1b and CASZ1b mutant cells after 24 h Tet treatment. b-f, realtime PCR result verified the regulation of TH, NGFR, CD9, MYC and KIT by CASZ1b in SY5Y cells after 24 h Tet treatment. Compared to wild type CASZ1b, K37 almost completely lost transcriptional activity at regulating all these genes in SY5Y cells (data are shown as means ± S.E.M., *: p<0.05). Compared to wild type CASZ1b, L37 significantly decreased transcriptional activity at regulating TH, NGFR and MYC, but had a slight increase at regulating CD9 and no effect on KIT (data are shown as means ± S.E.M., *: p<0.05).
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    (A) IPA assay of CASZ1b targets in SY5Y cells determined by microarray showed gene enrichment in the categories of molecular and cellular functions with a key subcategory being cell growth and proliferation (threshold represents p=0.05). (B) GSEA assay indicated the positive enrichment of genes involved neurological system process (left panel), and negative enrichment of genes regulated by MYC (right panel). NES, normalized enrichment score; Nom, nominal; FDR, false discovery rate. (C) Transcriptional activity assay of cytoplasmic localized K37A mutant and loss of NuRD binding mutant L31A in SY5Y cells by realtime PCR. a, Left panel: western blot analysis of CASZ1b and mutant proteins from SY5YtetCASZ1b and CASZ1b mutant cells after 24 h Tet treatment; right panel: realtime PCR analysis of CASZ1b and mutant mRNA levels from SY5YtetCASZ1b and CASZ1b mutant cells after 24 h Tet treatment. b-f, realtime PCR result verified the regulation of TH, NGFR, CD9, MYC and KIT by CASZ1b in SY5Y cells after 24 h Tet treatment. Compared to wild type CASZ1b, K37 almost completely lost transcriptional activity at regulating all these genes in SY5Y cells (data are shown as means ± S.E.M., *: p<0.05). Compared to wild type CASZ1b, L37 significantly decreased transcriptional activity at regulating TH, NGFR and MYC, but had a slight increase at regulating CD9 and no effect on KIT (data are shown as means ± S.E.M., *: p<0.05).

    Journal: Oncogene

    Article Title: Identification of CASZ1 nuclear export signal (NES) reveals potential mechanisms for loss of CASZ1 tumor suppressor activity in neuroblastoma

    doi: 10.1038/onc.2016.179

    Figure Lengend Snippet: (A) IPA assay of CASZ1b targets in SY5Y cells determined by microarray showed gene enrichment in the categories of molecular and cellular functions with a key subcategory being cell growth and proliferation (threshold represents p=0.05). (B) GSEA assay indicated the positive enrichment of genes involved neurological system process (left panel), and negative enrichment of genes regulated by MYC (right panel). NES, normalized enrichment score; Nom, nominal; FDR, false discovery rate. (C) Transcriptional activity assay of cytoplasmic localized K37A mutant and loss of NuRD binding mutant L31A in SY5Y cells by realtime PCR. a, Left panel: western blot analysis of CASZ1b and mutant proteins from SY5YtetCASZ1b and CASZ1b mutant cells after 24 h Tet treatment; right panel: realtime PCR analysis of CASZ1b and mutant mRNA levels from SY5YtetCASZ1b and CASZ1b mutant cells after 24 h Tet treatment. b-f, realtime PCR result verified the regulation of TH, NGFR, CD9, MYC and KIT by CASZ1b in SY5Y cells after 24 h Tet treatment. Compared to wild type CASZ1b, K37 almost completely lost transcriptional activity at regulating all these genes in SY5Y cells (data are shown as means ± S.E.M., *: p<0.05). Compared to wild type CASZ1b, L37 significantly decreased transcriptional activity at regulating TH, NGFR and MYC, but had a slight increase at regulating CD9 and no effect on KIT (data are shown as means ± S.E.M., *: p<0.05).

    Article Snippet: Gene set enrich analysis (GSEA) ( , ) was performed using the whole gene list generated by uploading the raw microarray data to Partek Genomics Suite 6.6.

    Techniques: Microarray, Activity Assay, Mutagenesis, Binding Assay, Western Blot