Results 121 to 130 of about 45,247 (265)
BACE1 interfering RNA, metallothionein and ruthenium complexes ([Ru(bpy)2dppz]2+) were all loaded in prussian blue nanoparticles (PRM‐siRNA). PRM‐siRNA under near‐infrared light irradiation showed good photothermal effect and triggered instantaneous opening of blood‐brain barrier for enhanced drug delivery.
Xiaoyuan Ding+9 more
wiley +1 more source
Saikosaponin b1 attenuates liver fibrosis by competitively disrupting the interaction between signal transducer and activator of transcription 3 (STAT3) and glioma‐associated oncogene‐1 (Gli1) in the activated hepatic stellate cells (HSCs). The blocked interaction of STAT3 and Gli1 promotes the degradation of Gli1, inhibits Gli1 transcriptional ...
Meiyu Shao+15 more
wiley +1 more source
Functions of BCL-XL at the Interface between Cell Death and Metabolism
The BCL-2 homolog BCL-XL, one of the two protein products of BCL2L1, has originally been characterized for its prominent prosurvival functions. Similar to BCL-2, BCL-XL binds to its multidomain proapoptotic counterparts BAX and BAK, hence preventing the ...
Judith Michels+6 more
doaj +1 more source
Alzheimer-associated presenilin-2 confers increased sensitivity to poptosis in PC12 cells [PDF]
Presenilin-2 is a gene of unknown function recently identified based upon linkage with some forms of familial Alzheimer's disease. To investigate potential effects of PS-2 on cell viability, rat pheochromocytoma (PC12) cells were stably transfected with ...
Cotman, Carl W.+2 more
core +1 more source
Development and crystal structures of a potent second-generation dual degrader of BCL-2 and BCL-xL
Overexpression of BCL-xL and BCL-2 play key roles in tumorigenesis and cancer drug resistance. Advances in PROTAC technology facilitated recent development of the first BCL-xL/BCL-2 dual degrader, 753b, a VHL-based degrader with improved potency and ...
Digant Nayak+12 more
doaj +1 more source
Bcl-xl does not have to bind Bax to protect T cells from death [PDF]
Activated T cells die when antigen disappears from animals. This death is caused by proteins related to Bcl-2. Two hypotheses have been suggested to explain the actions of the different types of Bcl-2 proteins.
Dai, Shaodong+6 more
core +2 more sources
301. Down-Regulation of bcl-xl Gene Expression with bcl-xl siRNA Vectors In Vitro and In Vivo
Introduction: BCL-XL, an anti-apoptotic member of the bcl-2 gene family, is highly expressed in human lung cancer. Over-expression of BCL-XL has been correlated with conventional clinical treatment resistance. We previously demonstrated that down-regulation of BCL-XL expression by antisense will induce apoptosis and sensitize lung cancer cells to ...
Philip A. Rascoe+4 more
openaire +2 more sources
What's New? Poor prognosis in cholangiocarcinoma (CCA) is attributed to late diagnosis and intrinsic chemoresistance. In particular, resistance mechanisms that suppress apoptosis limit the effectiveness of gemcitabine‐based regimens, which remain the standard treatment.
Wunan Mi+7 more
wiley +1 more source
Anti-apoptotic BCL-2 family members bind to BH3-only proteins and multidomain BAX/BAK to preserve mitochondrial integrity and maintain survival. Whereas inhibition of these interactions is the biological basis of BH3-mimetic anti-cancer therapy, the ...
Jessie Pécot+12 more
doaj +1 more source
Insights into p53-Dependent Apoptotic Signaling and Cell Fate vis-a-vis Functional Cooperation among BCL-xL, Cytoplasmic p53, and PUMA [PDF]
Following DNA damage, nuclear p53 induces the expression of PUMA (p53 upregulated modulator of apoptosis), a BH3‑only protein that binds and inhibits the anti‑apoptotic BCL‑2 repertoire, including BCL‑xL.
Fisher, John C.
core +1 more source