Human Polyclonal CUL1 Ab
- Known as:
- Human Polyclonal CUL1 Antibody
- Catalog number:
- a0545
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal CUL1
Related genes to: Human Polyclonal CUL1 Ab
- Gene:
- CUL1 NIH gene
- Name:
- cullin 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 7q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-29
- Date modifiied:
- 2014-11-19
Related products to: Human Polyclonal CUL1 Ab
Related articles to: Human Polyclonal CUL1 Ab
- Replication fork reversal is a DNA damage tolerance mechanism important for genome stability that entails annealing of parental DNA to push the fork backwards. F-box helicase 1 (FBH1) is a 3'-5' ssDNA translocase and SCF (SKP-CUL1-F box) E3 ubiquitin ligase that catalyzes fork reversal and limits aberrant recombination, yet how its helicase activity drives strand annealing is unknown. Here, using single-molecule and biochemical assays, we show that SCF reverses forks through a two-stage reaction in which translocation on the lagging strand template while remaining affixed at the junction destabilizes the leading strand duplex to ultimately displace the nascent leading strand. Reversal is force-sensitive and does not generate a four-way junction, revealing an annealing-independent mechanism distinct from those of SMARCAL1, HLTF, and ZRANB3. These results establish the importance of nascent strand unwinding to fork reversal and suggest the existence of distinct pathways that produce unique DNA structures, which has implications for fork restart and its measurement in cells. - Source: PubMed
Publication date: 2026/06/07
Mendia-García JavierPeacock Emma MAicart-Ramos ClaraEichman Brandt FMoreno-Herrero Fernando - The Arabidopsis MAX2 gene encodes an F-box protein containing a leucine-rich repeat (LRR) domain, which plays a pivotal role in regulating plant development and stress responses. Although MAX2 has been extensively characterized in these processes, its specific function in post-fertilization ovule development remains elusive. Our previous work identified XsMAX2, a MAX2 homolog in Xanthoceras sorbifolium, as highly expressed in fertilized ovules. Here, we demonstrate that XsMAX2 is a nuclear-localized protein that interacts with SKP1, a core component of the SCF (SKP1-CUL1-F-box) ubiquitin ligase complex. Furthermore, we show that the auxin-responsive transcription factor ARF2 directly binds to the XsMAX2 promoter, regulating its expression in fertilized ovules. Functional studies reveal that upregulation of XsMAX2 leads to increased fruit and ovule abortion, whereas its downregulation enhances their growth and development. Notably, XsMAX2 expression is precisely modulated by nutrient availability (e.g., phosphate and sugars) and the phytohormone pathways (e.g. strigolactone and abscisic acid). Mechanistically, XsMAX2 may suppress cell cycle-related genes and induce aberrant programmed cell death (PCD) in post-fertilization ovules, thereby impairing early seed development. Collectively, our findings establish XsMAX2 as a critical negative regulator of post-fertilization ovule development in X. sorbifolium, integrating environmental and endogenous signals to control reproductive success. - Source: PubMed
Publication date: 2026/06/08
Zhou QingyuanCai QingZhou LinyiLiu Jing - Post-translational modifications (PTMs) play a crucial role in the regulation of protein function. Protein O-linked -acetylglucosamine (O-GlcNAc) is a type of nutrient-sensitive PTM that occurs on serine or threonine residues of substrates, catalysed by a single pairs of enzymes, O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA). In the present study, we have observed that serum deprivation decreased OGT levels without affecting its transcription. Instead, we found that serum deprivation activated AMP-activated protein kinase (AMPK) and induced the phosphorylation of OGT at threonine 444, resulting in the proteolysis of OGT by the CUL1/SKP1/SKP2 E3 ubiquitin ligase. Knocking down significantly impaired 3T3-L1 cell differentiation in the presence of serum. Likewise, treatment with AICAR, an AMPK activator, or OSMI-1, an OGT small molecule inhibitor, attenuated serum-induced 3T3-L1 differentiation. Together, our results demonstrate that OGT is essential for 3T3 cell differentiation in which serum starvation activates AMPK to phosphorylate OGT at Thr444, triggering the proteolysis of OGT by the CUL1/SKP1/SKP2 E3 ligase. - Source: PubMed
Publication date: 2026/06/05
Ngo Hoang HaiLe Dang QuynhNam Le BaKeum Young-Sam - Mammalian Atg8-family (ATG8) proteins are crucial for macroautophagic/autophagic degradation in the lysosome and facilitate non-degradative processes including multiple distinct forms of unconventional protein secretion. These secretion pathways, collectively termed secretory autophagy, depend upon ATG8 conjugated to membranes to both specify and traffic molecules for extracellular release. Here, we review the current understanding of how membrane ATG8ylation supports secretory autophagy, and propose a cell biological framework for classifying the growing repertoire of secretory autophagy pathways based on membrane ATG8ylation at discrete intracellular vesicular intermediates. Finally, we detail the emerging roles of these pathways in physiology and disease.: Aβ, amyloid-β; Acb1, acyl-coA-binding 1; ALS, amyotrophic lateral sclerosis; APP, amyloid beta precursor protein; APEX2, ascorbate peroxidase; ATG, autophagy related; AWOL, autophagosome-mediated exit without lysis; BafA1, bafilomycin A; BirA*, mutant BirA biotin ligase; BMI, body-mass index; CASM, ATG8 conjugation at single membranes; DAMPs, danger/damage-associated molecular patterns; DBI, diazepam binding inhibitor, acyl-CoA binding protein; DSS, dextran sodium sulfate; ER, endoplasmic reticulum; ERGIC, endoplasmic reticulum intermediate compartment; ESCRT, endosomal complexes required for transport; EVs, extracellular vesicles; EVPs, extracellular vesicles and particles; HMGB1, high mobility group box 1; IDE, insulin degrading enzyme; IFNB, interferon beta; ILV, intralumenal vesicles; LANDO, LC3-associated endocytosis; LAP, LC3-associated phagocytosis; LIR, LC3 interacting region; LDELS, LC3-dependent EV loading and secretion; LLOMe, L-leucyl-L-leucine methyl ester hydrobromide; M2, influenza A virus matrix 2, MAD, migratory autolysosome disposal; miRNAs, microRNAs; M-MDSC, monocytic myeloid derived suppressor cells; MVEs, multivesicular endosomes; PAMPs, pathogen-associated molecular patterns; P-bodies, processing bodies; PE, phosphatidylethanolamine; PD, Parkinson disease; PS, phosphatidylserine; RBPs, RNA binding proteins; R-EV, RAB22A-induced extracellular vesicle; SLC2A1, solute carrier family 2 member 1; TFRC, transferrin receptor; TGN, trans-Golgi network; TMED10, transmembrane p24 trafficking protein 10; THU, TMED10-channeled unconventional secretion; SALI, secretory autophagy during lysosome inhibition; SCF, SKP1-CUL1-F-box; SNAREs, soluble NSF attachment protein receptors. - Source: PubMed
Publication date: 2026/05/24
Debnath JayantaLeidal Andrew M - Glioblastoma (GBM) is a treatment-challenging disease with a poor prognosis and few treatment options available. Patients with GBM with BRAF gene mutations are expected to benefit from targeted therapy with BRAF inhibitors. - Source: PubMed
Publication date: 2026/05/18
Da RongWang MaodeJiang HaitaoWang Wei