about
K-Ras4B phosphorylation at Ser181 is inhibited by calmodulin and modulates K-Ras activity and functionGenetic analysis of Ras signalling pathways in cell proliferation, migration and survival.Discovery of targeting peptides for selective therapy of medullary thyroid carcinoma.Novel SRESPHP peptide mediates specific binding to primary medullary thyroid carcinoma after systemic injection.Loss of p53 induces cell proliferation via Ras-independent activation of the Raf/Mek/Erk signaling pathway.Reversible, interrelated mRNA and miRNA expression patterns in the transcriptome of Rasless fibroblasts: functional and mechanistic implicationsGene therapeutic approaches for medullary thyroid carcinoma treatment.The RET proto-oncogene: a potential target for molecular cancer therapy.A new mode of DNA binding distinguishes Capicua from other HMG-box factors and explains its mutation patterns in cancer.Mechanisms of Disease: cancer targeting and the impact of oncogenic RET for medullary thyroid carcinoma therapy.Clasp2 ensures mitotic fidelity and prevents differentiation of epidermal keratinocytesGenetic analysis of Ras genes in epidermal development and tumorigenesis.Modeling K-Ras-driven lung adenocarcinoma in mice: preclinical validation of therapeutic targets.Using cells devoid of RAS proteins as tools for drug discovery.Tumours with class 3 BRAF mutants are sensitive to the inhibition of activated RAS.Genetic Validation of Cell Proliferation via Ras-Independent Activation of the Raf/Mek/Erk Pathway.Role of MEN2A-derived RET in maintenance and proliferation of medullary thyroid carcinoma.Ras and p53: An unsuspected liaison.Ras in epidermal proliferation.Ras signaling is essential for skin development.A new therapeutic approach in medullary thyroid cancer treatment: inhibition of oncogenic RET signaling by adenoviral vector-mediated expression of a dominant-negative RET mutant.Antitumor capacity of a dominant-negative RET proto-oncogene mutant in a medullary thyroid carcinoma model.Inactivation of Capicua in adult mice causes T-cell lymphoblastic lymphoma.c-RAF Ablation Induces Regression of Advanced Kras/Trp53 Mutant Lung Adenocarcinomas by a Mechanism Independent of MAPK Signaling.H-Ras and K-Ras Oncoproteins Induce Different Tumor Spectra When Driven by the Same Regulatory Sequences.Allele-Specific Mechanisms of Activation of MEK1 Mutants Determine Their Properties.ERF deletion rescues RAS deficiency in mouse embryonic stem cells.The Capicua tumor suppressor: a gatekeeper of Ras signaling in development and cancer.Mutant K-Ras activation of the proapoptotic MST2 pathway is antagonized by wild-type K-Ras.Genetically Engineered Mouse Models of K-Ras-Driven Lung and Pancreatic Tumors: Validation of Therapeutic TargetsTargeting the MAPK Pathway in KRAS-Driven TumorsRequirement for epithelial p38α in KRAS-driven lung tumor progressionComplete Regression of Advanced Pancreatic Ductal Adenocarcinomas upon Combined Inhibition of EGFR and C-RAF
P50
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P50
description
hulumtues
@sq
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Matthias Drosten
@ast
Matthias Drosten
@en
Matthias Drosten
@es
Matthias Drosten
@nl
Matthias Drosten
@sl
type
label
Matthias Drosten
@ast
Matthias Drosten
@en
Matthias Drosten
@es
Matthias Drosten
@nl
Matthias Drosten
@sl
prefLabel
Matthias Drosten
@ast
Matthias Drosten
@en
Matthias Drosten
@es
Matthias Drosten
@nl
Matthias Drosten
@sl
P106
P21
P31
P496
0000-0002-3205-456X