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microarray analysis partek genomics suite (v6.6)  (Partek)

 
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    Partek microarray analysis partek genomics suite (v6.6)
    Microarray Analysis Partek Genomics Suite (V6.6), 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/result/microarray analysis partek genomics suite (v6.6)/product/Partek
    Average 90 stars, based on 1 article reviews
    microarray analysis partek genomics suite (v6.6) - by Bioz Stars, 2026-06
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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 <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 <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 <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 <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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    Partek partek microarray suite
    (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