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Michaela Reissland (1991-)

Biochemikerin

Name	Michaela Reissland
Zeit	1991- (Lebensdaten)
Ort	Deutschland
Geschlecht	weiblich
Akademischer Grad bzw. Titel	Dr.
Beruf	Biochemikerin (charakteristischer Beruf)
Weitere Angaben	Dissertation an der Graduate School of Life Sciences, Section Biomedicine, der Univ. Würzburg (2023)
Quelle	USP10 is a de novo tumour-specific regulator of β-Catenin and contributes to cancer stem cell maintenance and tumour progression - 2024 researchgate: https://www.researchgate.net/profile/Michaela-Reissland (Stand: 09.07.2024)
Datensatztyp	Person
GND-Nummer	1335116346
Datensatz-ID	1335116346
Beteiligt an alle anzeigen USP10 is a de novo tumour-specific regulator of β-Catenin and contributes to cancer stem cell maintenance and tumour progression USP28 enables oncogenic transformation of respiratory cells, and its inhibition potentiates molecular therapy targeting mutant EGFR, BRAF and PI3K RNF4~RGMb~BMP6 axis required for osteogenic differentiation and cancer cell survival PTEN mutant non-small cell lung cancer require ATM to suppress pro-apoptotic signalling and evade radiotherapy Implementation of CRISPR/Cas9 Genome Editing to Generate Murine Lung Cancer Models That Depict the Mutational Landscape of Human Disease Inhibition of USP28 overcomes Cisplatin-resistance of squamous tumors by suppression of the Fanconi anemia pathway PTEN mutant non-small cell lung cancer require ATM to suppress pro-apoptotic signalling and evade radiotherapy USP28 enables oncogenic transformation of respiratory cells, and its inhibition potentiates molecular therapy targeting mutant EGFR, BRAF and PI3K Maintaining protein stability of ∆Np63 via USP28 is required by squamous cancer cells USP28 enables oncogenic transformation of respiratory cells and its inhibition potentiates molecular therapy targeting mutant EGFR, BRAF and PI3K Maintaining protein stability of ∆Np63 via USP28 is required by squamous cancer cells

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Michaela Reissland (1991-)

USP10 is a de novo tumour-specific regulator of β-Catenin and contributes to cancer stem cell maintenance and tumour progression

USP28 enables oncogenic transformation of respiratory cells, and its inhibition potentiates molecular therapy targeting mutant EGFR, BRAF and PI3K

RNF4~RGMb~BMP6 axis required for osteogenic differentiation and cancer cell survival

PTEN mutant non-small cell lung cancer require ATM to suppress pro-apoptotic signalling and evade radiotherapy

Implementation of CRISPR/Cas9 Genome Editing to Generate Murine Lung Cancer Models That Depict the Mutational Landscape of Human Disease

Inhibition of USP28 overcomes Cisplatin-resistance of squamous tumors by suppression of the Fanconi anemia pathway

PTEN mutant non-small cell lung cancer require ATM to suppress pro-apoptotic signalling and evade radiotherapy

USP28 enables oncogenic transformation of respiratory cells, and its inhibition potentiates molecular therapy targeting mutant EGFR, BRAF and PI3K

Maintaining protein stability of ∆Np63 via USP28 is required by squamous cancer cells

USP28 enables oncogenic transformation of respiratory cells and its inhibition potentiates molecular therapy targeting mutant EGFR, BRAF and PI3K

Maintaining protein stability of ∆Np63 via USP28 is required by squamous cancer cells