Results 191 to 200 of about 7,204,743 (394)
Liquid biopsy epigenetics: establishing a molecular profile based on cell‐free DNA
Cell‐free DNA (cfDNA) fragments in plasma from cancer patients carry epigenetic signatures reflecting their cells of origin. These epigenetic features include DNA methylation, nucleosome modifications, and variations in fragmentation. This review describes the biological properties of each feature and explores optimal strategies for harnessing cfDNA ...
Christoffer Trier Maansson +2 more
wiley +1 more source
Gene targeting as a therapeutic avenue in diseases mediated by the complement alternative pathway. [PDF]
Dreismann AK +6 more
europepmc +1 more source
Intein‐based modular chimeric antigen receptor platform for specific CD19/CD20 co‐targeting
CARtein is a modular CAR platform that uses split inteins to splice antigen‐recognition modules onto a universal signaling backbone, enabling precise, scarless assembly without re‐engineering signaling domains. Deployed here against CD19 and CD20 in B‐cell malignancies, the design supports flexible multi‐antigen targeting to boost T‐cell activation and
Pablo Gonzalez‐Garcia +9 more
wiley +1 more source
Minimal role for the alternative pathway in complement activation by HIT immune complexes. [PDF]
Barnes AP +11 more
europepmc +1 more source
Insulin Regulates Alternative Splicing of Protein Kinase C βII through a Phosphatidylinositol 3-Kinase-dependent Pathway Involving the Nuclear Serine/Arginine-rich Splicing Factor, SRp40, in Skeletal Muscle Cells [PDF]
Niketa Patel +6 more
openalex +1 more source
Cytoplasmic p21 promotes stemness of colon cancer cells via activation of the NFκB pathway
Cytoplasmic p21 promotes colorectal cancer stem cell (CSC) features by destabilizing the NFκB–IκB complex, activating NFκB signaling, and upregulating BCL‐xL and COX2. In contrast to nuclear p21, cytoplasmic p21 enhances spheroid formation and stemness transcription factor CD133.
Arnatchai Maiuthed +10 more
wiley +1 more source
C. Hawkes +5 more
semanticscholar +1 more source
HDAC4 is degraded by the E3 ligase FBXW7. In colorectal cancer, FBXW7 mutations prevent HDAC4 degradation, leading to oxaliplatin resistance. Forced degradation of HDAC4 using a PROTAC compound restores drug sensitivity by resetting the super‐enhancer landscape, reprogramming the epigenetic state of FBXW7‐mutated cells to resemble oxaliplatin ...
Vanessa Tolotto +13 more
wiley +1 more source

