Results 51 to 60 of about 105,668 (286)

Inhibiting E3 ligases [PDF]

open access: yesScience-Business eXchange, 2010
Two groups of researchers have identified inhibitors of E3 ubiquitin ligase, which has been considered difficult, if not impossible, to target with small molecules. The findings could lead to compounds that are more specific disrupters of tumor cell proliferation than the proteasome inhibitor Velcade bortezomib.
openaire   +1 more source

Entropy-Driven Mechanism of an E3 Ligase [PDF]

open access: yesBiochemistry, 2011
Ubiquitin-like modifications are macromolecular chemistry for which our understanding of the enzymatic mechanisms is lacking. Most E3 ligases in ubiquitin-like modifications do not directly participate in chemistry but are thought to confer allosteric effects; however, the nature of the allosteric effects has been elusive.
Khue, Truong   +3 more
openaire   +2 more sources

TRIM56 coiled-coil domain structure provides insights into its E3 ligase functions

open access: yesComputational and Structural Biotechnology Journal, 2023
Protein ubiquitination is a post-translation modification mediated by E3 ubiquitin ligases. The RING domain E3 ligases are the largest family of E3 ubiquitin ligases, they act as a scaffold, bringing the E2-ubiquitin complex and its substrate together to
Xiaohua Lou   +7 more
doaj   +1 more source

The E3 Ligases in Cervical Cancer and Endometrial Cancer [PDF]

open access: yes, 2022
Endometrial (EC) and cervical (CC) cancers are the most prevalent malignancies of the female reproductive system. There is a global trend towards increasing incidence and mortality, with a decreasing age trend.
Fengguang Zhai   +9 more
core   +1 more source

TRIM32 is an E3 ubiquitin ligase for dysbindin [PDF]

open access: yesHuman Molecular Genetics, 2009
Mutations in the gene encoding tripartite motif protein 32 (TRIM32) cause two seemingly diverse diseases: limb-girdle muscular dystrophy type 2H (LGMD2H) or sarcotubular myopathy (STM) and Bardet-Biedl syndrome type 11(BBS11). Although TRIM32 is involved in protein ubiquitination, its substrates and the molecular consequences of disease-causing ...
Locke, Matthew   +3 more
openaire   +3 more sources

E3 ubiquitin ligases in bone homeostasis: from regulatory mechanisms to skeletal diseases and therapeutic targeting

open access: yesFrontiers in Cell and Developmental Biology
E3 ubiquitin ligases are key determinants of substrate specificity within the ubiquitin–proteasome system and have emerged as important regulators of skeletal biology.
Yutong Zhao   +4 more
doaj   +1 more source

Small Molecule Modulators of RING-Type E3 Ligases: MDM and Cullin Families as Targets

open access: yesFrontiers in Pharmacology, 2018
Ubiquitin–proteasome system (UPS) is a primary signaling pathway for regulation of intracellular protein levels. E3 ubiquitin ligases, substrate-specific members of the UPS, represent highly attractive protein targets for drug discovery.
Emil Bulatov   +4 more
doaj   +1 more source

A capsid-encoded PPxY-motif facilitates adenovirus entry. [PDF]

open access: yes, 2010
Viruses use cellular machinery to enter and infect cells. In this study we address the cell entry mechanisms of nonenveloped adenoviruses (Ads). We show that protein VI, an internal capsid protein, is rapidly exposed after cell surface attachment and ...
Segura-Morales, Carolina   +28 more
core   +1 more source

MAGE-A cancer/testis antigens inhibit MDM2 ubiquitylation function and promote increased levels of MDM4 [PDF]

open access: yes, 2015
Melanoma antigen A (MAGE-A) proteins comprise a structurally and biochemically similar sub-family of Cancer/Testis antigens that are expressed in many cancer types and are thought to contribute actively to malignancy.
Susan E. Bray (264528)   +41 more
core   +2 more sources

Autophagy and mitophagy in pancreatic β‐cell homeostasis and their involvement in diabetes pathophysiology

open access: yesFEBS Letters, EarlyView.
This review focuses on the role of autophagy and mitophagy in maintaining pancreatic β‐cell function and homeostasis. We discuss how genetic defects affecting these pathways contribute to the development of type 1, type 2, monogenic, and gestational diabetes. We further explore their potential as therapeutic targets. Created in BioRender.
Yunkyeong Lee   +2 more
wiley   +1 more source

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