CCND1 polyclonal antibody
- Known as:
- CCND1 pab (anti-)
- Catalog number:
- PAB9944
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- CCND1 polyclonal antibody
Related genes to: CCND1 polyclonal antibody
- Gene:
- CCND1 NIH gene
- Name:
- cyclin D1
- Previous symbol:
- BCL1, D11S287E, PRAD1
- Synonyms:
- U21B31
- Chromosome:
- 11q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-06
- Date modifiied:
- 2019-04-23
Related products to: CCND1 polyclonal antibody
Related articles to: CCND1 polyclonal antibody
- Anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase (anti-HMGCR) immune-mediated necrotizing myopathy (IMNM) is a subtype of autoimmune necrotizing myopathy that presents with progressive proximal weakness and persistent creatine kinase (CK) elevation, which may continue despite statin discontinuation. Its relationship with hematologic malignancy is not well established. A 67-year-old woman developed markedly elevated CK levels after starting high-intensity statin. Despite statin withdrawal, CK levels remain persistently elevated, accompanied by progressive symmetrical proximal weakness. Anti-HMGCR IgG was strongly positive, while other autoimmune serologies were unrevealing. A diagnosis of statin-associated anti-HMGCR IMNM was established, and treatment with mycophenolate mofetil and intravenous immunoglobulin resulted in partial biochemical improvement. Five weeks after initiation of immunosuppressive therapy, routine laboratory testing showed rapidly rising leukocytosis. Further evaluation revealed mantle cell lymphoma with bone marrow involvement, IGH::CCND1 rearrangement, and deletion, consistent with high-risk disease. In this context, continued clinical and laboratory monitoring is appropriate in inflammatory myopathy, and new hematologic abnormalities warrant further evaluation. - Source: PubMed
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Publication date: 2025/09/01
Mansouri VahidArjmand BabakAsri NastaranRazzaghi ZahraRezaei-Tavirani MostafaRazi FaridehBandarian FatemehRobati Reza MRezaei Mitra - Microplastics (MPs), as environmental pollutants, have garnered widespread attention. Growing evidence suggests a close association between MP exposure and lung diseases. However, the molecular mechanisms through which MP exposure influences the onset and progression of lung diseases remain unclear. This study positions MP exposure as a cross-disease driving risk factor and employs integrated computational toxicology and bioinformatics approaches to explore potential key targets underlying the impact of MP exposure on the development of lung diseases (COPD, IPF, and LUAD). Common differentially expressed genes (cDEGs) and shared common DEGs (scDEGs) associated with MP exposure and COPD, IPF, and LUAD were identified through database screening and intersection analysis. A protein-protein interaction (PPI) network was constructed using the STRING database, followed by enrichment analysis. The expression patterns and cellular localization of key targets among the shared common differentially expressed genes were validated using single-cell datasets of COPD, IPF, and LUAD. Finally, experimental validation was conducted based on the cell types identified through analysis. MP exposure may influence the occurrence and progression of COPD, IPF, and LUAD through mechanisms involving the cell cycle, mitosis, and DNA repair. Potential key targets identified include CDK1, BRCA1, and CCND1. Validation via database and single-cell analyses suggests that MP exposure may increase the risk of COPD, IPF, and LUAD by upregulating CDK1 expression in pulmonary fibroblasts. Experimental validation in human pulmonary fibroblasts demonstrated that PS-NPs significantly upregulated CDK1 mRNA and protein levels in a dose-dependent manner. CDK1 inhibition experiments confirmed that PS-NP exposure promotes fibrosis in human pulmonary fibroblasts by upregulating CDK1. This study defines MP exposure as a cross-disease driving risk factor and identifies CDK1 as a potential key target mediating the development of MPs-driven lung diseases. This finding offers a new perspective for understanding MPs-related lung diseases and establishes a novel paradigm for exploring the intrinsic connections between pollutant exposure and disease pathogenesis. - Source: PubMed
Publication date: 2026/05/31
Ruan HaonanZhang BufanXu QiqiLiu YifengZhang Dan - Calf diarrhea represents a prevalent and serious challenge in dairy farming. While medicinal plants demonstrate considerable potential for preventing calf diarrhea within antibiotic-free farming systems, their active components and mechanisms remain poorly characterized. The objective of this study was to investigate a polyherbal mixture (PM; including Crataegus pinnatifida, Callicarpa nudiflora Hook. & Arn., Mallotus apelta (Lour.) Müll.Arg., Amomum villosum Lour., Centella asiatica (L.) Urban, and Alpinia oxyphylla Miq.) supplemented to preweaning calves from d 4 to 60, utilizing an integrated approach combining network pharmacology, metabolomics, and microbiomics. - Source: PubMed
Publication date: 2026/05/31
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Publication date: 2026/05/27
El-Hema Hagar SEl-Ghorab Rasha A-SHawata Mohamed ANossier Eman SHussein Modather FElhendawy Ahmed THamza Mohammed FAbdel-Rahman Adel A-H