Results 81 to 90 of about 120,389 (309)
Finding novel vulnerabilities of hypomorphic BRCA1 alleles
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
In vitro Protein Ubiquitination Assays
Ubiquitin can be added to substrate protein as a protein tag by the concerted actions of ubiquitin activating enzyme (E1), ubiquitin conjugating enzyme (E2) and ubiquitin protein ligase (E3).
Qingzhen Zhao, Qi Xie
doaj +1 more source
MITF maintains genome stability in nonmelanocyte lineages
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir +13 more
wiley +1 more source
Data for positive selection test and co-evolutionary analysis on mammalian cereblon
Cereblon (CRBN) is a substrate recognition subunit of the CRL4 E3 ubiquitin ligase complex, directly binding to specific substrates for poly-ubiquitination followed by proteasome-dependent degradation of proteins.
Wataru Onodera +2 more
doaj +1 more source
Ubiquitination relies on a subtle balance between selectivity and promiscuity achieved through specific interactions between ubiquitin-conjugating enzymes (E2s) and ubiquitin ligases (E3s).
Bonvin, Alexandre M. J. J. +14 more
core +1 more source
Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization
In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu +13 more
wiley +1 more source
Characterisation of the Cullin-3 mutation that causes a severe form of familial hypertension and hyperkalaemia [PDF]
Deletion of exon 9 from Cullin-3 (CUL3, residues 403-459: CUL3Δ403-459) causes pseudohypoaldosteronism type IIE (PHA2E), a severe form of familial hyperkalaemia and hypertension (FHHt).
Nichola L Figg +35 more
core +1 more source
IGFBP4 knockdown (KD) impairs preadipocyte proliferation and is associated with IGF1R protein downregulation and attenuated AKT phosphorylation. The mechanisms by which IGFBP4 KD influences the IGF1R/AKT signaling pathway involve newly synthesized proteins and lysosomal degradation pathways. Created in BioRender.
Yujia Guo +6 more
wiley +1 more source
E3 ubiquitin ligases in B-cell malignancies [PDF]
Ubiquitylation is a post-translational modification (PTM) that controls various cellular signaling pathways. It is orchestrated by a three-step enzymatic cascade know as the ubiquitin proteasome system (UPS). E3 ligases dictate the specificity to the substrates, primarily leading to proteasome-dependent degradation.
Jaewoo Choi, Luca Busino
openaire +2 more sources
We present a novel proteolysis‐targeting chimera (PROTAC) system conjugated to lipoic acid gold nanoclusters (PLANC), designed to degrade pTau, regulate inflammatory signaling, and effectively traverse the blood‐brain barrier (BBB). PLANC degraded pTau at various phosphorylation sites, with mechanistic studies confirming proteasome‐mediated degradation
Sarah Nevins +9 more
wiley +1 more source

