Mouse CCNB1 Antibody (N-term S35)
- Known as:
- Mouse CCNB1 Antibody (N-terminus S35)
- Catalog number:
- AP20010a
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- Mouse CCNB1 Antibody (N-term S35)
Related genes to: Mouse CCNB1 Antibody (N-term S35)
- Gene:
- CCNB1 NIH gene
- Name:
- cyclin B1
- Previous symbol:
- CCNB
- Synonyms:
- -
- Chromosome:
- 5q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-12-10
- Date modifiied:
- 2016-10-05
- Gene:
- MRPS28 NIH gene
- Name:
- mitochondrial ribosomal protein S28
- Previous symbol:
- -
- Synonyms:
- MRP-S28, HSPC007, MRPS35
- Chromosome:
- 8q21.13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-26
- Date modifiied:
- 2016-10-05
- Gene:
- RNA5SP35 NIH gene
- Name:
- RNA, 5S ribosomal pseudogene 35
- Previous symbol:
- RN5S35
- Synonyms:
- -
- Chromosome:
- 13q31.3
- Locus Type:
- pseudogene
- Date approved:
- 2011-08-08
- Date modifiied:
- 2012-08-07
- Gene:
- RNA5SP350 NIH gene
- Name:
- RNA, 5S ribosomal pseudogene 350
- Previous symbol:
- RN5S350
- Synonyms:
- -
- Chromosome:
- 11q23.1
- Locus Type:
- pseudogene
- Date approved:
- 2012-01-30
- Date modifiied:
- 2014-11-19
- Gene:
- RNA5SP351 NIH gene
- Name:
- RNA, 5S ribosomal pseudogene 351
- Previous symbol:
- RN5S351
- Synonyms:
- -
- Chromosome:
- 11q23.1
- Locus Type:
- pseudogene
- Date approved:
- 2012-01-30
- Date modifiied:
- 2014-11-19
Related products to: Mouse CCNB1 Antibody (N-term S35)
Related articles to: Mouse CCNB1 Antibody (N-term S35)
- Palladium nanoparticles (Pd NPs), extensively used in automobile catalytic converters, are increasingly released into the environment and represent an emerging nanopollution concern for aquatic ecosystems. This study examined the chronic effects of environmentally relevant Pd NP exposure on the freshwater vertebrate model , integrating bioaccumulation analysis, oxidative stress profiling, histopathology, and bulk RNA-seq transcriptomics with computational cell-type inference analyses. Adult zebrafish were exposed for 42 days to low (0.4 ng/L) and high (22 ng/L) Pd NP concentrations. Inductively coupled plasma-mass spectrometry confirmed dose-dependent Pd bioaccumulation in whole-body tissues. Biochemical analyses indicated a disruption of gonadal redox homeostasis, characterized by altered activities of superoxide dismutase, catalase, glutathione S-transferase, glutathione reductase, and lipid peroxidation, indicating sustained oxidative stress. Histological examination of ovaries and testes demonstrated progressive structural damage, including follicular atresia, delayed oocyte maturation, and impaired spermatogenesis, highlighting reproductive vulnerability. Transcriptomic profiling showed concentration-dependent transcriptional changes under Pd NP exposure, including reduced expression of mitochondrial energy metabolism genes and increased expression of DNA repair, cell cycle regulation, steroid biosynthesis, and stress-response pathways. High-dose Pd exposure strongly increased the expression of cell cycle and stress-response genes, including ccnb1 (41 to 8296 TPM), cdc25b (41 to 1937 TPM), and tp53 (110 to 604 TPM), while mitochondrial energy metabolism genes were consistently suppressed. Notably, --, , and cell cycle signaling axes exhibited biphasic regulation, reflecting compensatory and maladaptive stress responses. This study identifies potential ecological and human health risks associated with palladium nanoparticle dispersal and emphasizes the need for safer catalyst design and stricter environmental management of platinum group nanoparticles. - Source: PubMed
Publication date: 2026/07/16
Pottanthara Ashokan AnilaEswaran MurugeshGovindhan ThiruppathiMathan Ramesh - Sepsis is a systemic inflammatory response caused by a variety of causes, which is characterized by high morbidity and mortality. Our work aimed to screen the candidate genes of sepsis and evaluate their diagnostic value using bioinformatics tools. - Source: PubMed
Publication date: 2026/06/29
Fu XueYang JianLv QinZhang XiaotianWang SenCai ShangkunZhang Meng - Polypropylene nanoplastics (PP-NPs) are emerging environmental contaminants, but their gestational toxicity and underlying mechanisms remain poorly understood. In this study, we integrated maternal exposure mouse models, HTR8/SVneo trophoblast assays, quantitative proteomics, and phosphoproteomics to delineate the pathogenic basis of PP-NP-induced placental injury. PP-NPs accumulated prominently in the placenta, eliciting placental structural disruption, reduced placental efficiency, impaired fetal growth, and increased embryo loss. In trophoblasts, PP-NPs were readily internalized and impaired viability, proliferation, migration, invasion, and tube formation, accompanied by mitochondrial damage. To decipher the underlying molecular mechanisms, we performed integrated quantitative proteomic and phosphoproteomic analyses. These multi-omics landscapes revealed that cellular senescence is the dominant pathogenic program triggered by PP-NPs, accompanied by extensive phosphorylation remodeling. CDK1 emerged as the top predicted upstream kinase within this senescence-associated network. Notably, although CDK1 abundance was increased after PP-NPs exposure, its canonical cell-cycle-driving activity was not effectively engaged, as evidenced by reduced Thr161 phosphorylation, weakened CDK1-CCNB1 complex formation, and G1-phase arrest. Instead, PP-NPs were associated with increased phosphorylation of senescence-related substrates linked to CDK1-predicted signaling, including RBL2 at Thr, SQSTM1 at Ser, and FOXO3 at Ser, together with activation of DNA damage signaling, the P53-P21/P16 axis, and a SASP-like inflammatory response. Pharmacological inhibition of CDK1 with Ro-3306 attenuated trophoblast senescence, restored trophoblast function, alleviated placental injury, and improved fetal outcomes in vivo, while siRNA-mediated CDK1 knockdown similarly suppressed CDK1-linked phosphorylation and rescued senescence-associated functional defects in trophoblasts. In conclusion, our study demonstrates that PP-NPs drive premature placental ageing through global proteomic and phosphoproteomic reprogramming, providing a new theoretical basis and potential therapeutic targets for environmental pollutant-induced adverse pregnancy outcomes. - Source: PubMed
Publication date: 2026/07/10
Li ShuxianWang KaiLi LingbingLi ZihanZhou MeijuanGuo JunjunGong PihaiZhang Meihua - To identify baseline gene expression programs associated with recurrence timing in estrogen receptorpositive (ER+) breast cancer (BC) using a multi-state modeling framework. - Source: PubMed
Publication date: 2026/06/30
Wang YongzheQuinones ChristineKang IreneRugo HopeMartinez ErnestSeewaldt VictoriaMortimer JoanneNath AritroJones Veronica - Maintenance of genome integrity is essential for cellular homeostasis, and its perturbation leads to tumorigenesis. Here, we uncover an unanticipated somatic role for the synaptonemal complex protein SYCP1, previously regarded as strictly meiosis specific, in a broad spectrum of human cancers including breast cancer. Through integrative genomic, proteomic, and functional analyses, we demonstrate that SYCP1 is aberrantly reexpressed in tumor cells, where it actively promotes DNA damage repair, cell cycle progression, and malignant growth. SYCP1 binds chromatin at regulatory elements and directly controls transcriptional programs governing genome maintenance, including key effectors such as , , , and . Loss of SYCP1 impairs DNA repair kinetics, attenuates tumor cell proliferation and migration, and increases sensitivity to chemotherapeutics cisplatin and gemcitabine. Mechanistically, SYCP1 coimmunoprecipitates with chromatin remodeling complexes and transcription factors SP1 and SP2 and modulates their genomic occupancy and oncogenic transcriptional outputs. Clinically, high SYCP1 expression stratifies patients with poor prognosis and therapy resistance across multiple cancer types. Our findings illuminate a previously unrecognized moonlighting function of SYCP1 in somatic cancer cells and position it as a critical chromatin-associated regulator of genome stability, with implications for biomarker development and therapeutic targeting. - Source: PubMed
Publication date: 2026/07/08
Brennan Louise CGrinchuk Oleg VPachon-Penalba MiguelSou Ieng FFawcett Conor JNogueira Claudia GGuthrie MeganBates Andrew DHine MeganThomaz AmandaFielding Andew BDavies Owen RTee Wee-WeiMcClurg Urszula L