Additional reflections seemingly leading to a tetragonal fivefold supercell have been observed in a number of melilites. A careful examination of the collected intensity data reveals that this feature is due to the coexistence of two twin domains related by a (120) twin plane. Reflections of the first domain (I) with h(b)(2) + k(b)(2) = 5n overlap those of the second domain (II) when both the following additional conditions are verified: -h(b) + 2k(b) = 5n and 2h(b) + k(b) = 5n. Indices of the superimposed reflections are h(b,I) k(b,I) l(b,I) for the first domain, and h(b,II) = 3/5h(b,I) + 4/5k(b,I), k(b,II) = 4/5h(b,I) - 3/5k(b,I), l(b,II) = l(b,I) for the second domain. The non-crystallographic pseudosymmetry in the melilite structure is discussed.
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http://dx.doi.org/10.1107/s0108768103000041 | DOI Listing |
Nat Chem Biol
January 2025
Department of Gynecology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
The regressed arms of reversed replication forks exhibit structural similarities to one-ended double-stranded breaks and need to be protected against uncontrolled nucleolytic degradation. Here, we identify MSANTD4 (Myb/SANT-like DNA-binding domain-containing protein 4), a functionally uncharacterized protein that uniquely counters the replication protein A (RPA)-Bloom (BLM)/Werner syndrome helicase (WRN)-DNA replication helicase/nuclease 2 (DNA2) complex to safeguard reversed replication forks from detrimental degradation, independently of the breast cancer susceptibility proteins (BRCA1/2)-DNA repair protein RAD51 pathway. MSANTD4 specifically interacts with the junctions between single-stranded DNA (ssDNA) and double-stranded DNA (dsDNA) in DNA substrates harboring a 3' overhang, which resemble the structural features of regressed arms processed by WRN-DNA2.
View Article and Find Full Text PDFNat Commun
January 2025
Department of Life Sciences, Imperial College London, London, SW7 2AZ, UK.
Conjugation plays a major role in dissemination of antimicrobial resistance genes. Following transfer of IncF-like plasmids, recipients become refractory to a second wave of conjugation with the same plasmid via entry (TraS) and surface (TraT) exclusion mechanisms. Here, we show that TraT from the pKpQIL and F plasmids (TraT and TraT) exhibits plasmid surface exclusion specificity.
View Article and Find Full Text PDFEcotoxicol Environ Saf
January 2025
Department of Occupational and Environmental Health, School of Public Health, Dalian Medical University, No. 9 West Section Lvshun South Road, Dalian 116044, PR China; Global Health Research Center, Dalian Medical University, No. 9 West Section Lvshun South Road, Dalian 116044, PR China. Electronic address:
Arsenic in the environment, such as sodium arsenic (NaAsO), is a frequently occurring hazard that has been linked to nonalcoholic steatohepatitis (NASH). Our prior research established the involvement of ferroptosis in arsenic-induced NASH, but the precise underlying mechanisms remain elusive. Here, we found that exposure to NaAsO had a suppressive effect on the expression of CDGSH iron-sulfur domain-containing protein 2 (CISD2) at the protein and gene levels, and overexpression of CISD2 inhibited NaAsO-induced ferroptosis and NASH.
View Article and Find Full Text PDFTransl Oncol
January 2025
Department of Surgery, The Second Affiliated Hospital of Jiaxing University, No. 397, Huangcheng North Road, Jiaxing, Zhejiang, 314000, China. Electronic address:
Epidermal growth factor receptor (EGFR) plays an important role in the regulation of cell proliferation and migration [1]. It forms a homodimer or heterodimer with other ErbB receptor family members to activate downstream signaling. Emerging evidence indicates that the EGFR activity and downstream signaling are regulated by other proteins except its family members during tumorigenesis.
View Article and Find Full Text PDFAnticancer Drugs
January 2025
Department of Urology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou City, Zhejiang Province, China.
Chemotherapy resistance has long stood in the way of therapeutic advancement for lung cancer patients, the malignant tumor with the highest incidence and fatality rate in the world. Patients with lung adenocarcinoma (LUAD) now have a dismal prognosis due to the development of cisplatin (DDP) resistance, forcing them to use more costly second-line therapies. Therefore, overcoming resistance and enhancing patient outcomes can be achieved by comprehending the regulatory mechanisms of DDP resistance in LUAD.
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