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ttk inhibitor  (MedChemExpress)


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    MedChemExpress ttk inhibitor
    CDKN2A and <t>TTK</t> expression was upregulated in EC tissue. (A) Flowchart showing the identification process of the potential target molecules. The 125 significant genes, involving cell cycle regulators, transcription factors, protein kinase, metabolism enzymes, non-coding RNAs and epigenetic modifiers, were identified by intersecting the 2,038 genes increased in endometrial carcinoma and 786 genes associated with a poor prognosis. (B,C) Expression levels of CDKN2A (C) and TTK (D) were confirmed using data from the GEPIA database (N=91, T=174). CDKN2A, P<8.54e-31; TTK, P<9.81e-46. (E,F) The relationship between patients’ overall survival and messenger RNA expression of CDKN2A (D) and TTK (E) was analyzed using data from the GEPIA database. (F) The correlation between CDKN2A expression and TTK expression was analyzed using TCGA data sets (n=552). CDKN2A, cyclin dependent <t>kinase</t> <t>inhibitor</t> 2A; TTK, tyrosine threonine kinase; EC, endometrial carcinoma; GEPIA, Gene Expression Profiling Interactive Analysis; TCGA, The Cancer Genome Atlas; HPA, Human Protein Atlas.
    Ttk Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ttk inhibitor/product/MedChemExpress
    Average 91 stars, based on 1 article reviews
    ttk inhibitor - by Bioz Stars, 2026-02
    91/100 stars

    Images

    1) Product Images from "High tyrosine threonine kinase expression predicts a poor prognosis: a potential therapeutic target for endometrial carcinoma"

    Article Title: High tyrosine threonine kinase expression predicts a poor prognosis: a potential therapeutic target for endometrial carcinoma

    Journal: Annals of Translational Medicine

    doi: 10.21037/atm-22-5783

    CDKN2A and TTK expression was upregulated in EC tissue. (A) Flowchart showing the identification process of the potential target molecules. The 125 significant genes, involving cell cycle regulators, transcription factors, protein kinase, metabolism enzymes, non-coding RNAs and epigenetic modifiers, were identified by intersecting the 2,038 genes increased in endometrial carcinoma and 786 genes associated with a poor prognosis. (B,C) Expression levels of CDKN2A (C) and TTK (D) were confirmed using data from the GEPIA database (N=91, T=174). CDKN2A, P<8.54e-31; TTK, P<9.81e-46. (E,F) The relationship between patients’ overall survival and messenger RNA expression of CDKN2A (D) and TTK (E) was analyzed using data from the GEPIA database. (F) The correlation between CDKN2A expression and TTK expression was analyzed using TCGA data sets (n=552). CDKN2A, cyclin dependent kinase inhibitor 2A; TTK, tyrosine threonine kinase; EC, endometrial carcinoma; GEPIA, Gene Expression Profiling Interactive Analysis; TCGA, The Cancer Genome Atlas; HPA, Human Protein Atlas.
    Figure Legend Snippet: CDKN2A and TTK expression was upregulated in EC tissue. (A) Flowchart showing the identification process of the potential target molecules. The 125 significant genes, involving cell cycle regulators, transcription factors, protein kinase, metabolism enzymes, non-coding RNAs and epigenetic modifiers, were identified by intersecting the 2,038 genes increased in endometrial carcinoma and 786 genes associated with a poor prognosis. (B,C) Expression levels of CDKN2A (C) and TTK (D) were confirmed using data from the GEPIA database (N=91, T=174). CDKN2A, P<8.54e-31; TTK, P<9.81e-46. (E,F) The relationship between patients’ overall survival and messenger RNA expression of CDKN2A (D) and TTK (E) was analyzed using data from the GEPIA database. (F) The correlation between CDKN2A expression and TTK expression was analyzed using TCGA data sets (n=552). CDKN2A, cyclin dependent kinase inhibitor 2A; TTK, tyrosine threonine kinase; EC, endometrial carcinoma; GEPIA, Gene Expression Profiling Interactive Analysis; TCGA, The Cancer Genome Atlas; HPA, Human Protein Atlas.

    Techniques Used: Expressing, RNA Expression

    Knockdown of TTK increased the sensitivity of EC cells to the TTK inhibitor. (A,B) High expression of TTK enriched the genes associated with nucleolus (A) and RNA processing (B) through a GSEA of TCGA data (n=552). (C) The messenger RNA expression of TTK is represented in a strip chart (N=35, T=552). (D) The relationship between the overall survival and messenger RNA expression of TTK was analyzed using data from the HPA database. (E,F) The suppressing effects of TTK knockdown was identified by Western blot in the EN (E) and AN3-CA (F) cells. (G,H) The growth curve of the EN (G) and AN3-CA (H) cells after TTK knockdown was presented using siNC as the control. P<0.05. (I,J) The TKK inhibitor sensitivity (IC50 of NTRC0066-0) in the EC cell line EN (I) and AN3-CA (J). TTK, tyrosine threonine kinase; GSEA, gene set enrichment analysis; TCGA, The Cancer Genome Atlas; HPA, Human Protein Atlas; NC, negative control.
    Figure Legend Snippet: Knockdown of TTK increased the sensitivity of EC cells to the TTK inhibitor. (A,B) High expression of TTK enriched the genes associated with nucleolus (A) and RNA processing (B) through a GSEA of TCGA data (n=552). (C) The messenger RNA expression of TTK is represented in a strip chart (N=35, T=552). (D) The relationship between the overall survival and messenger RNA expression of TTK was analyzed using data from the HPA database. (E,F) The suppressing effects of TTK knockdown was identified by Western blot in the EN (E) and AN3-CA (F) cells. (G,H) The growth curve of the EN (G) and AN3-CA (H) cells after TTK knockdown was presented using siNC as the control. P<0.05. (I,J) The TKK inhibitor sensitivity (IC50 of NTRC0066-0) in the EC cell line EN (I) and AN3-CA (J). TTK, tyrosine threonine kinase; GSEA, gene set enrichment analysis; TCGA, The Cancer Genome Atlas; HPA, Human Protein Atlas; NC, negative control.

    Techniques Used: Knockdown, Expressing, RNA Expression, Stripping Membranes, Western Blot, Control, Negative Control



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