Results 61 to 70 of about 109,331 (244)

Erioflorin stabilizes the tumor suppressor Pdcd4 by inhibiting its interaction with the E3-ligase β-TrCP1 [PDF]

open access: yes, 2012
Loss of the tumor suppressor Pdcd4 was reported for various tumor entities and proposed as a prognostic marker in tumorigenesis. We previously characterized decreased Pdcd4 protein stability in response to mitogenic stimuli, which resulted from p70S6K1 ...
Bernhard Brüne   +35 more
core   +1 more source

The ubiquitin system in normal and infected germinal center B cells

open access: yesFEBS Letters, EarlyView.
The ubiquitin system plays a central role in germinal center (GC) B cells, influencing differentiation to long‐lived memory B cells. Oncogenic gammaherpesviruses gain access to memory B cells by establishing latency in GC B cells. Mapping ubiquitin mechanisms in normal and infected GC B cells will define specific molecular circuits in B cells germane ...
Destiny Davis   +2 more
wiley   +1 more source

The role of NEDD4 related HECT-type E3 ubiquitin ligases in defective autophagy in cancer cells: molecular mechanisms and therapeutic perspectives

open access: yesMolecular Medicine, 2023
The homologous to the E6-AP carboxyl terminus (HECT)-type E3 ubiquitin ligases are the selective executers in the protein ubiquitination, playing a vital role in modulation of the protein function and stability. Evidence shows the regulatory role of HECT-
Rui Zhang, Shaoqing Shi
doaj   +1 more source

Table_1_How to Inactivate Human Ubiquitin E3 Ligases by Mutation.DOCX

open access: yes, 2020
E3 ubiquitin ligases are the ultimate enzymes involved in the transfer of ubiquitin to substrate proteins, a process that determines the fate of the modified protein.
Ugo Mayor (404331)   +3 more
core   +1 more source

Inhibition of dipeptidyl peptidase 7 impairs lysophagy in LLOMe‐treated HepG2 cells

open access: yesFEBS Letters, EarlyView.
DPP7 inhibition delays ubiquitin‐dependent lysophagy by attenuating ubiquitin accumulation and the recruitment of SQSTM1 and LC3 to damaged lysosomes, resulting in delayed clearance of damaged lysosomes and impaired restoration of lysosomal homeostasis. Created using FigureLabs (Certificate ID: FL‐PUB‐20260922‐Z99XNX).
Na Yeon Park   +8 more
wiley   +1 more source

Going viral − Virus‐targeting nanobodies for research, diagnostics and therapy

open access: yesFEBS Letters, EarlyView.
The increasing prevalence of viral diseases represents a major threat for global human health. Nanobodies, small binding fragments derived from camelid heavy‐chain antibodies, offer versatile tools for viral research, diagnostics, and antiviral therapy.
Domenic Ebert, Ulrich Rothbauer
wiley   +1 more source

Tumour–host interactions in Drosophila: mechanisms in the tumour micro‐ and macroenvironment

open access: yesMolecular Oncology, EarlyView.
This review examines how tumour–host crosstalk takes place at multiple levels of biological organisation, from local cell competition and immune crosstalk to organism‐wide metabolic and physiological collapse. Here, we integrate findings from Drosophila melanogaster studies that reveal conserved mechanisms through which tumours hijack host systems to ...
José Teles‐Reis, Tor Erik Rusten
wiley   +1 more source

NEDD8 and ubiquitin ligation by cullin-RING E3 ligases [PDF]

open access: yes, 2021
RING E3s comprise the largest family of ubiquitin (UB) and ubiquitin-like protein (UBL) ligases. RING E3s typically promote UB or UBL transfer from the active site of an associated E2 enzyme to a distally-recruited substrate.
Baek, K.   +5 more
core   +1 more source

USP29‐regulated noncanonical stabilization of the hypoxia‐inducible factor‐α in aggressive prostate cancer

open access: yesMolecular Oncology, EarlyView.
We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober   +16 more
wiley   +1 more source

Finding novel vulnerabilities of hypomorphic BRCA1 alleles

open access: yesMolecular Oncology, EarlyView.
Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder   +10 more
wiley   +1 more source

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