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gene knockdown

Multi-Omic Analysis Reveals Divergent Molecular Events in Scarring and Regenerative Wound Healing

[Cell Stem Cell] Scientists profiled scarring versus YAP-inhibition-induced wound regeneration at the transcriptional, protein, and tissue levels, and showed that disrupting YAP mechanotransduction yielded regenerative repair by fibroblasts with activated Trps1 and Wnt signaling.

Knockdown of Salusin-β Improves Cardiovascular Function in Myocardial Infarction-Induced Chronic Heart Failure Rats

[Oxidative Medicine and Cellular Longevity] The authors investigated the effects of silencing salusin-β on endothelial function, cardiac function, vascular and myocardial remodeling, and its underlying signaling pathways in chronic heart failure rats induced by coronary artery ligation.

Ribosomal L1 Domain-Containing Protein 1 Coordinates with HDM2 to Negatively Regulate p53 in Human Colorectal Cancer Cells

[Journal of Experimental & Clinical Cancer Research] RSL1D1 distributed throughout the nucleus in human colorectal cancer cells. Silencing of RSL1D1 gene induced cell cycle arrest at G1/S and cell apoptosis in a p53-dependent manner.

NDUFA4L2 Promotes Glioblastoma Progression, Is Associated with Poor Survival, and Can Be Effectively Targeted by Apatinib

[Cell Death & Disease] Gene knockdown of NADH dehydrogenase [ubiquinone] 1 alpha subcomplex, 4-like 2 (NDUFA4L2) inhibited tumor cell proliferation and enhanced apoptosis, while tumor cells initiated protective mitophagy in vitro and in vivo.

Protocol to Profile the Bioenergetics of Organoids Using Seahorse

[STAR Protocols] Scientists shared their in-house optimized protocols to examine organoid bioenergetics in response to drugs, gene knockdown, or to characterize the metabolism of specific cell types.

Synaptotagmin-1 Interacts with PI(4,5)P2 to Initiate Synaptic Vesicle Docking in Hippocampal Neurons

[Cell Reports] Scientists showed that in mouse hippocampal synapses, synaptic vesicle (SV) docking initiates at ∼12 nm to the active zone (AZ) by Synaptotagmin-1 (Syt1). They also demonstrated that PI(4,5)P2 was the membrane partner of Syt1 to initiate SV docking, and disrupting their interaction could abolish the docking initiation.

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