Results 71 to 80 of about 153,102 (279)

RBM10 Deficiency Promotes Anti‐PD‐1 Resistance in LUAD via STING Alternative Splicing‐Driven CCL7 Signaling and Macrophage Polarization

open access: yesAdvanced Science, EarlyView.
RBM10 deficiency promotes anti‐PD‐1 resistance in lung adenocarcinoma by altering STING alternative splicing, which enhances CCL7 secretion and CCR2‐dependent M2 macrophage polarization. A positive feedback loop via mitochondrial transfer sustains this immunosuppression.
Weitong Gao   +14 more
wiley   +1 more source

Bcl-XL is qualitatively different from and ten times more effective than Bcl-2 when expressed in a breast cancer cell line

open access: yesBMC Cancer, 2006
Background Bcl-2 and Bcl-XL are anti-apoptotic paralogues that inhibit apoptosis elicited by a wide variety of stimuli, and play critical roles in cancer development and resistance to treatment.
Leber Brian   +4 more
doaj   +1 more source

Bcl-xL DNAzymes promote radiosensitivity and chemosensitivity in colorectal cancer cells via enhancing apoptosis

open access: yesBMC Pharmacology and Toxicology, 2022
Background RNA-cleaving deoxyribozymes (DNAzymes) are catalytic deoxyribonucleic acid molecules that have become a promising new class of gene suppressors by binding and cleaving target mRNA.
Zhen Yu   +6 more
doaj   +1 more source

Multi‐Omics Profiling Reveals Immunomodulatory and Pro‐Regenerative Effects of a Graphene Oxide–Collagen Scaffold in Massive Rotator Cuff Tears

open access: yesAdvanced Science, EarlyView.
A graphene oxide/collagen scaffold is developed for chronic massive rotator cuff tear repair. The scaffold improves compressive stability, supports reparative mesenchymal differentiation, and modulates the immune microenvironment. In chronic MRCT models, it reduces muscle degeneration, enhances tendon–bone regeneration, and improves functional recovery,
Renwen Wan   +24 more
wiley   +1 more source

Targeting Bcl-xL enhances the cytotoxicity of chemotherapeutics [PDF]

open access: yesCancer Biology & Therapy, 2008
Commentary to:Synergistic cytotoxicity of Bcl-xL inhibitor, gossypol and chemotherapeutic agents in non-Hodgkin’s lymphoma cellsZhi-Ming Li, Wen-Qi Jiang, Zhen-Yu Zhu, Xiao-Feng Zhu, Jun-Min Zhou, Zong-Chao Liu, Da-Jun Yang and Zhong-Zhen ...
openaire   +2 more sources

BM-1197: a novel and specific Bcl-2/Bcl-xL inhibitor inducing complete and long-lasting tumor regression in vivo. [PDF]

open access: yesPLoS ONE, 2014
Bcl-2 and Bcl-xL are critical regulators of apoptosis that are overexpressed in a variety of human cancers and pharmacological inhibition of Bcl-2 and Bcl-xL represents a promising strategy for cancer treatment.
Longchuan Bai   +6 more
doaj   +1 more source

T Cell‐Independent Role of PD‐L1 in Kidney Repair: Mitigation of Tubular DNA Damage via PD‐L1/BRCA1 Interaction Following AKI

open access: yesAdvanced Science, EarlyView.
PD‐L1 is primarily expressed in renal tubules and upregulated in both murine models of AKI and renal biopsy samples from patients with AKI. PD‐L1 can promote adaptive TECs repair through interacting with BRCA1, independent of its canonical immunomodulatory function of T cells, and PD‐L1 supplementation may represent a promising therapeutic strategy for
Wei Jiang   +17 more
wiley   +1 more source

BCL-XL overexpression promotes tumor progression-associated properties article [PDF]

open access: yes, 2017
By using human melanoma and glioblastoma cell lines and their derivative BCL-XL overexpressing clones, we investigated the role of BCL-XL in aggressive features of these two tumor histotypes.
Gabellini C.   +9 more
core   +2 more sources

CK2α Deficiency Drives Myocardial Fibrosis via Desmin‐Induced Mitochondrial Dysfunction

open access: yesAdvanced Science, EarlyView.
CK2α preserves mitochondrial homeostasis by phosphorylating Desmin to recruit Cryab, ensuring proper filament assembly. CK2α deficiency disrupts this interaction, causing mitochondrial dysfunction, metabolic shifts, bioenergetic failure, and oxidative stress—ultimately establishing a pro‐fibrotic environment that drives cardiac fibrosis.
Canjie Ma   +12 more
wiley   +1 more source

Bcl-xL is a key mediator of apoptosis following KRASG12C inhibition in KRASG12C-mutant colorectal cancer

open access: yes, 2023
Novel covalent inhibitors of KRASG12C have shown limited response rates in patients with KRASG12C-mutant (MT) colorectal cancer. Thus, novel KRASG12C inhibitor combination strategies that can achieve deep and durable responses are needed.
Alberto Bardelli (163979)   +18 more
core   +1 more source

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