Results 131 to 140 of about 185,904 (310)
Mixed Lineage Kinase Domain‐Like Protein (MLKL): From Mechanisms to Therapeutic Opportunities
The mixed lineage kinase domain‐like protein (MLKL) acts as the executioner in the necroptosis pathway, transitioning from an inactive to active state through phosphorylation, oligomerization, membrane recruitment, and membrane insertion, ultimately forming membrane hotpots.
Lijuan Xu, Chunlin Zhuang
wiley +1 more source
Treatment strategies in acute myeloid leukemia (AML) [PDF]
Thomas Buechner, Wolfgang Hiddemann
openalex +1 more source
In this study, ASH2L‐K312‐lac is identified as a critical driver that promotes the malignant progression of hepatocellular carcinoma (HCC). Furthermore, through a comprehensive series of cell biological and molecular biological experiments, integrated with diverse animal models and systematic application of high‐throughput sequencing technologies, it ...
Hexu Han+14 more
wiley +1 more source
KAT7‐acetylated and cytoplasm‐translocated G‐protein GαS enhances IL‐6 effect and drives HCC progenitor cell progression. Abstract Background and Aims Hepatocarcinogenesis goes through HCC progenitor cells (HcPCs) to fully established HCC, and the mechanisms driving the development of HcPCs are still largely unknown.
Ye Zhou+15 more
wiley +1 more source
Expression of isoforms of the human receptor tyrosine kinase c-kit in leukemic cell lines and acute myeloid leukemia [PDF]
PS Crosier+5 more
openalex +1 more source
In superficial second‐degree burn wounds, Gb3 turns on genes related to papillary cells through the FGF2 signaling pathway. This increases the ability of cells to break down fibrin and decreases fibrosis, which ultimately prevents scar formation in burn injuries.
Sujie Xie+13 more
wiley +1 more source
Analysis of proto-oncogenes in acute myeloid leukemia: loss of heterozygosity for the Ha-ras gene [PDF]
HG Ahuja, A Foti, DJ Zhou, MJ Cline
openalex +1 more source
This study demonstrated that ATG4B translocates from the cytoplasm to the nucleus during energy deficiency. Nuclear ATG4B inhibits DNA repair by interacting with PRMT1. The nuclear ATG4B‐mediated DNA repair defect is significantly exacerbated within acute myeloid leukemia (AML) cells, promoting leukemia progression in an AML mouse model.
Zhenkun Wang+20 more
wiley +1 more source