Guido Plotz
www.kgu.de
0000-0001-5314-9739
Goethe University Frankfurt
45 papers found
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High Expression of Casein Kinase 2 Alpha Is Responsible for Enhanced Phosphorylation of DNA Mismatch Repair Protein MLH1 and Increased Tumor Mutation Rates in Colorectal Cancer
SPTAN1 Expression Predicts Treatment and Survival Outcomes in Colorectal Cancer
Investigation of the Wilson gene ATP7B transcriptional start site and the effect of core promoter alterations
Alternative AKT2 splicing produces protein lacking the hydrophobic motif regulatory region
Expression and secretion of the pro‑inflammatory cytokine IL‑8 is increased in colorectal cancer cells following the knockdown of non‑erythroid spectrin αII
Validation of an in Vitro Mismatch Repair Assay Used in the Functional Characterization of Mismatch Repair Variants
Downregulation of SPTAN1 is related to MLH1 deficiency and metastasis in colorectal cancer
Analysis of MUTYH alternative transcript expression, promoter function, and the effect of human genetic variants
Diagnostic yield and clinical utility of a comprehensive gene panel for hereditary tumor syndromes
DNA mismatch repair activity of MutLα is regulated by CK2-dependent phosphorylation of MLH1 (S477)
Evaluation of MLH1 variants of unclear significance
Phosphorylation-dependent signaling controls degradation of DNA mismatch repair protein PMS2
Elucidating the clinical significance of two PMS2 missense variants coexisting in a family fulfilling hereditary cancer criteria
Loss of MLH1 sensitizes colon cancer cells to DNA-PKcs inhibitor KU60648
Functional testing strategy for coding genetic variants of unclear significance in MLH1 in Lynch syndrome diagnosis
Exome sequencing identifiesMUTYHmutations in a family with colorectal cancer and an atypical phenotype
Promoter Methylation of MLH1, PMS2, MSH2 and p16 Is a Phenomenon of Advanced-Stage HCCs
Reduced migration of MLH1 deficient colon cancer cells depends on SPTAN1
Refining the role ofpms2in Lynch syndrome: germline mutational analysis improved by comprehensive assessment of variants
Expression Defect Size among Unclassified MLH1 Variants Determines Pathogenicity in Lynch Syndrome Diagnosis
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