The E3 Ubiquitin Ligase RLIM Safeguards Oligodendrocyte Development and Myelination by Targeting SLC7A11 for Polyubiquitination to Regulate Ferroptotic Resistance. [PDF]
RLIM‐mediated SLC7A11 polyubiquitination is required for SPTBN2‐mediated trafficking and membrane localization of SLC7A11, which enables oligodendrocyte precursor cells to be resistant to ferroptosis and safeguards oligodendrocyte lineage progression and thus myelination.
Li Y +8 more
europepmc +2 more sources
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
The linear ubiquitin chain assembly complex (LUBAC) generates heterotypic ubiquitin chains
The linear ubiquitin chain assembly complex (LUBAC) is the only known ubiquitin ligase for linear/Met1-linked ubiquitin chain formation. One of the LUBAC components, heme-oxidized IRP2 ubiquitin ligase 1 (HOIL-1L), was recently shown to catalyse oxyester
Alan Rodriguez Carvajal +14 more
doaj +1 more source
RING Domain E3 Ubiquitin Ligases
E3 ligases confer specificity to ubiquitination by recognizing target substrates and mediating transfer of ubiquitin from an E2 ubiquitin-conjugating enzyme to substrate. The activity of most E3s is specified by a RING domain, which binds to an E2∼ubiquitin thioester and activates discharge of its ubiquitin cargo.
Deshaies, Raymond J. +1 more
openaire +3 more sources
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
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
The E3 ubiquitin ligase RNF135 regulates the tumorigenesis activity of tongue cancer SCC25 cells
Several E3 ubiquitin ligases have been confirmed that they are related to the tumorigenesis. This study aims to find the tongue cancer‐related E3 ubiquitin ligase. The E3 ubiquitin ligase library was screened.
Jian Jin, liya Zhao, Zubing Li
doaj +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
IAPs as E3 ligases of Rac1 : shaping the move [PDF]
Inhibitors of Apoptosis Proteins (IAPs) are well-studied E3 ubiquitin ligases predominantly known for regulation of apoptosis. We uncovered that IAPs can function as a direct E3 ubiquitin ligase of RhoGTPase Rac1.
Oberoi-Khanuja, Tripat Kaur +1 more
core +1 more source
This review summarizes the transcription factors, repressive chromatin‐modifying complexes, and epigenetic mechanisms that control fetal hemoglobin repression. Notably, many regulators of γ‐globin silencing also function in transcriptional and epigenetic networks that drive cancer, highlighting opportunities to translate advances in hemoglobinopathy ...
Meigen Yu +3 more
wiley +1 more source

