Results 151 to 160 of about 989,774 (270)
A CASE OF ABDOMINAL AORTIC ANEURYSM WITH CONGENITAL FACTOR X DEFICIENCY
Sayaka Uchida +5 more
openalex +2 more sources
Survivin and Aurora Kinase A control cell fate decisions during mitosis
Aurora A interacts with survivin during mitosis and regulates its centromeric role. Loss of Aurora A activity mislocalises survivin, the CPC and BubR1, leading to disruption of the spindle checkpoint and triggering premature mitotic exit, which we refer to as ‘mitotic slippage’.
Hana Abdelkabir +2 more
wiley +1 more source
CDK11 inhibition stabilises the tumour suppressor p53 and triggers the production of an alternative p21WAF1 splice variant p21L, through the inactivation of the spliceosomal protein SF3B1. Unlike the canonical p21WAF1 protein, p21L is localised in the cytoplasm and has reduced cell cycle‐blocking activity.
Radovan Krejcir +12 more
wiley +1 more source
A mouse model for vascular normalization and a human breast cancer cohort were studied to understand the relationship between vascular leakage and tumor immune suppression. For this, endothelial and immune cell RNAseq, staining for vascular function, and immune cell profiling were employed.
Liqun He +8 more
wiley +1 more source
Pediatric split liver transplantation for congenital factor X deficiency: first 10-year follow-up of a case with portal vein stenting. [PDF]
Namgoong JM +7 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
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

