Results 91 to 100 of about 208,982 (285)

Sacrificial Biofabrication for Vascularization: Concept, Materials, Technologies, and Applications

open access: yesAdvanced Materials, EarlyView.
Vasculature is indispensable for tissue viability in regenerative medicine. The sacrificial biofabrication enables precise fabrication of vascular channels by using temporary templates that are subsequently removed. This review defines the concept and delves into sacrificial materials, surrounding materials, fabrication technologies, and biomedical ...
Jiezhong Shi   +7 more
wiley   +1 more source

The Human Adenovirus Type 5 E4orf6/E1B55K E3 Ubiquitin Ligase Complex Can Mimic E1A Effects on E2F

open access: yesmSphere, 2016
The human adenovirus E4orf6/E1B55K E3 ubiquitin ligase is well known to promote viral replication by degrading an increasing number of cellular proteins that inhibit the efficient production of viral progeny.
Frédéric Dallaire   +5 more
doaj   +1 more source

Sealing of gaps in duplex DNA by T4 DNA ligase

open access: yesNucleic Acids Research, 1982
Single-strand gaps in DNA molecules were found to be a substrate for T4 DNA ligase. Sealing of the gaps was optimal at the same conditions as ligation of blunt-ended DNA molecules. Spermidine at a concentration of 2 mM stimulated the ligation of gaps, as well as the joining of DNA molecules with cohesive and blunt ends.
Göran Magnusson, Stefan Nilsson
openaire   +4 more sources

Excessive DNA Double‐Strand Breaks–Associated 3D Genome Reorganization Contributes to Neural Tube Defects with Folate Deficiency

open access: yesAdvanced Science, EarlyView.
Neural tube defects (NTDs) are among the most common congenital malformations. However, the underlying etiology and mechanism remain elusive. Here, the role of DNA double‐strand breaks (DSBs) in 3D genome organization within the NTDs with folate deficiency is reported.
Ting Zhang   +12 more
wiley   +1 more source

TRIM30α Is a Negative-Feedback Regulator of the Intracellular DNA and DNA Virus-Triggered Response by Targeting STING.

open access: yesPLoS Pathogens, 2015
Uncontrolled immune responses to intracellular DNA have been shown to induce autoimmune diseases. Homeostasis regulation of immune responses to cytosolic DNA is critical for limiting the risk of autoimmunity and survival of the host. Here, we report that
Yanming Wang   +9 more
doaj   +1 more source

FBXO44 Regulates FOXP1 Degradation Through AURKA‐Dependent Phosphorylation to Promote Colorectal Cancer Progression

open access: yesAdvanced Science, EarlyView.
FBXO44 promotes colorectal cancer progression by targeting FOXP1 for ubiquitin‐mediated degradation. This study reveals a phosphorylation‐dependent mechanism involving AURKA and highlights the FBXO44/FOXP1/Cyclin E2 axis as a potential therapeutic target in colorectal cancer.
Hongxu Nie   +10 more
wiley   +1 more source

5’‐Methylthioadenosine Metabolic Reprogramming Drives H3K79 Monomethylation‐Mediated PAK2 Upregulation to Promote Cadmium‐Induced Breast Cancer Progression by Impairing Autophagic Flux

open access: yesAdvanced Science, EarlyView.
Cadmium, a carcinogenic heavy metal, drives breast cancer progression via metabolic reprogramming and autophagic flux disruption. Multi‐omics revealed cadmium‐induced 5'‐methylthioadenosine depletion activates DOT1L‐mediated H3K79me1 at PAK2 promoter, upregulating PAK2 to block autophagy and driving malignancy. Clinically, 5'‐methylthioadenosine levels
Jingdian Li   +24 more
wiley   +1 more source

MicroRNA-300 Regulates the Ubiquitination of PTEN through the CRL4BDCAF13 E3 Ligase in Osteosarcoma Cells

open access: yesMolecular Therapy: Nucleic Acids, 2018
Cullins, critical members of the cullin-RING ubiquitin ligases (CRLs), are often aberrantly expressed in different cancers. However, the underlying mechanisms regarding aberrant expression of these cullins and the specific substrates of CRLs in different
Zhi Chen   +9 more
doaj   +1 more source

PRDM16 Reduces Cellular Senescence by Upregulating GSTM1

open access: yesAdvanced Science, EarlyView.
Cellular senescence drives aging and aging‐related organ disorders, yet PRDM16's role remains unexplored. This work uncovers that PRDM16 decreases significantly in aged organs, while its loss accelerates cellular senescence and aging‐related organ injury.
Qian Yuan   +7 more
wiley   +1 more source

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