Results 111 to 120 of about 24,258,002 (357)

Caspase-9 swings both ways in the apoptosome

open access: yesMolecular & Cellular Oncology, 2017
For nearly 2 decades, investigators have debated whether cysteinyl-aspartate-specific protease 9 (caspase-9) is activated within the apoptotic protease-activating factor 1 (Apaf-1) apoptosome through proximity-induced homodimerization or through ...
Chu-Chiao Wu, Shawn B. Bratton
doaj   +1 more source

Intestinal restriction of Salmonella Typhimurium requires caspase-1 and caspase-11 epithelial intrinsic inflammasomes.

open access: yesPLoS Pathogens, 2020
We investigated the role of the inflammasome effector caspases-1 and -11 during Salmonella enterica serovar Typhimurium infection of murine intestinal epithelial cells (IECs).
Shauna M Crowley   +6 more
doaj   +1 more source

A bioinformatics screen identifies TCF19 as an aggressiveness‐sustaining gene in prostate cancer

open access: yesMolecular Oncology, EarlyView.
Gene expression meta‐analysis in multiple prostate cancer patient cohorts identifies Transcription factor 19 (TCF19) as an aggressiveness‐sustaining gene with prognostic potential. TCF19 is a gene repressed by androgen signaling that sustains core cancer‐related processes such as vascular permeability or tumor growth and metastasis.
Amaia Ercilla   +15 more
wiley   +1 more source

A Signal for the Caspase-1 Inflammasome Free of TLR [PDF]

open access: yesImmunity, 2007
Secretion of the proinflammatory cytokine IL-1beta requires caspase-1 and Toll-like receptor (TLR) signaling. However, Kanneganti et al. (2007) find that bacteria can use pore-forming mechanisms to activate caspase-1 for the production of IL-1beta precursor independently of TLRs.
openaire   +3 more sources

Modeling hepatic fibrosis in TP53 knockout iPSC‐derived human liver organoids

open access: yesMolecular Oncology, EarlyView.
This study developed iPSC‐derived human liver organoids with TP53 gene knockout to model human liver fibrosis. These organoids showed elevated myofibroblast activation, early disease markers, and advanced fibrotic hallmarks. The use of profibrotic differentiation medium further amplified the fibrotic signature seen in the organoids.
Mustafa Karabicici   +8 more
wiley   +1 more source

PYCR1 inhibition in bone marrow stromal cells enhances bortezomib sensitivity in multiple myeloma cells by altering their metabolism

open access: yesMolecular Oncology, EarlyView.
This study investigated how PYCR1 inhibition in bone marrow stromal cells (BMSCs) indirectly affects multiple myeloma (MM) cell metabolism and viability. Culturing MM cells in conditioned medium from PYCR1‐silenced BMSCs impaired oxidative phosphorylation and increased sensitivity to bortezomib.
Inge Oudaert   +13 more
wiley   +1 more source

Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine

open access: yesMolecular Oncology, EarlyView.
The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu   +18 more
wiley   +1 more source

A synthetic benzoxazine dimer derivative targets c‐Myc to inhibit colorectal cancer progression

open access: yesMolecular Oncology, EarlyView.
Benzoxazine dimer derivatives bind to the bHLH‐LZ region of c‐Myc, disrupting c‐Myc/MAX complexes, which are evaluated from SAR analysis. This increases ubiquitination and reduces cellular c‐Myc. Impairing DNA repair mechanisms is shown through proteomic analysis.
Nicharat Sriratanasak   +8 more
wiley   +1 more source

Growth inhibition of cytosolic Salmonella by caspase-1 and caspase-11 precedes host cell death

open access: yesNature Communications, 2016
Sensing bacterial products in the cytosol of mammalian cells by NOD-like receptors leads to the activation of caspase-1 inflammasomes, and the production of the pro-inflammatory cytokines interleukin (IL)-18 and IL-1β.
Teresa L. M. Thurston   +7 more
semanticscholar   +1 more source

Survivin and Aurora Kinase A control cell fate decisions during mitosis

open access: yesMolecular Oncology, EarlyView.
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

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