Mouse Anti Human Geminin GMNN
- Known as:
- Mouse Anti Human Geminin GMNN
- Catalog number:
- ant-319
- Product Quantity:
- 5
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- Mouse Anti Human Geminin GMNN
Related genes to: Mouse Anti Human Geminin GMNN
- Gene:
- GMNN NIH gene
- Name:
- geminin DNA replication inhibitor
- Previous symbol:
- -
- Synonyms:
- Gem
- Chromosome:
- 6p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-19
- Date modifiied:
- 2019-01-21
Related products to: Mouse Anti Human Geminin GMNN
Related articles to: Mouse Anti Human Geminin GMNN
- Esophageal squamous cell carcinoma (ESCA) is one of the most common cancers worldwide. PANoptosis is an inflammatory programmed cell death pathway event regulated by the PANoptosome complex. Currently, there is limited research on the PANoptosis-related genes (PORGs) in ESCA. We aim to explore the prognostic biomarkers of PANoptosis in ESCA and their underlying mechanisms through comprehensive bioinformatics analysis. - Source: PubMed
Publication date: 2026/03/18
Jie RundaLiu YiningWang TianbiaoWusiman ShabahaitiRen HongdaTuoheniyazi WugelinisanLiu Ling - Primary Sjögren's disease (SjD) is a systemic autoimmune disorder where diagnosis relies on the presence of Ro/SS-A and La/SS-B autoantibodies. However, approximately one-third of SjD patients are seronegative, often requiring an invasive minor salivary gland biopsy, which can lead to significant diagnostic delays. This review comprehensively evaluates a wide array of novel autoantibodies to determine their potential as diagnostic biomarkers for Ro/SS-A-negative SjD patients. While many newly identified autoantibodies, such as those targeting ASCA, TRIM38, and PUF60, were found to be strongly associated with Ro/SS-A positivity and thus offer limited utility for seronegative diagnosis, several others show significant promise. Notably, autoantibodies targeting functional proteins like the muscarinic M3 receptor (anti-M3R) have demonstrated high diagnostic sensitivity and specificity. Furthermore, systematic screenings have uncovered highly specific markers. One panel of 12 autoantigens (including GMNN, GRAMD1A, and NUP50) identified by human proteome arrays exhibited 54% sensitivity with 100% specificity for Ro/SS-A-negative SjD. Another validated panel combining immunoglobulin G autoantibodies against FNBP4, SNRPC, CCL4, M3R, and KDM6B achieved 46% sensitivity with 95% specificity. Other individual markers, such as anti-NA14 and anti-calponin-3, also show potential for identifying seronegative SjD subsets. In conclusion, a growing body of evidence supports the clinical utility of several novel autoantibodies in diagnosing Ro/SS-A-negative SjD. The integration of these biomarkers into clinical practice could significantly improve early and accurate diagnosis, reduce the reliance on invasive procedures, and potentially aid in patient stratification for targeted therapies. Further validation of these markers in large cohorts is warranted. - Source: PubMed
Publication date: 2026/01/14
Elsaghir AlaaWitte Torsten - α-synucleinopathies are clinically and biologically heterogeneous disorders lacking reliable biomarkers to assist with early diagnosis, disease progression, patient stratification, and therapeutic targeting. Genetic variation is known to impact biomarker levels, influencing their utility and interpretation in research and clinical settings. We aimed to identify common genetic modulators of biomarker levels implicated in α-synucleinopathy pathogenesis. - Source: PubMed
Publication date: 2025/12/30
Somerville Emma NLiu LangTa MichaelIwaki HirotakaSenkevich KonstantinAlcalay Roy NGan-Or Ziv - DNA replication is tightly regulated to occur once per cell cycle, with the MCM2-7 helicase loaded onto replication origins only during G1-phase. In higher eukaryotes, geminin negatively regulates this process during S-, G2- and M-phases by binding the essential licensing factor CDT1. Although geminin's function is crucial for genomic stability, its inhibitory mechanism remains elusive. Here, we utilise a fully reconstituted human DNA replication licensing assay to dissect geminin's role. AlphaFold modelling provides structural insights into an N-terminal CDT1-binding helix of geminin, which proves essential for inhibition. Structural docking of the CDT1-geminin complex into the ORC-CDC6-CDT1-MCM2-7 (OCCM) assembly shows that geminin's long coiled-coil domain sterically clashes with the MCM2 C-terminus, rather than directly blocking CDT1 binding to ORC-CDC6-MCM2-7. Shortening the coiled-coil preserves geminin dimerisation and CDT1 binding but abolishes inhibition, confirming its mechanistic role. Surprisingly, geminin is not able to fully inhibit DNA licensing. However, CDK1/2-cyclin A can partially inhibit DNA licensing and, in conjunction with geminin, result in a complete block. These findings uncover geminin's steric inhibitory mechanism and suggest that a dual CDK-geminin axis controls human DNA replication. - Source: PubMed
Publication date: 2025/12/09
Tomkins JoshuaEdwardes Lucy VFaull Sarah VPeach MatthewGillespie Peter JLeber VeraSchmidt AnnaBounoua HalilSim NicholasCamarillo RosaBlow J JulianBarr Alexis RBarnard AnnaSpeck Christian - Lymphoma remains a significant global health burden, necessitating innovative, targeted therapeutic strategies. Nisin (N), a bacteriocin produced by , has demonstrated antimicrobial and anticancer properties through membrane disruption and apoptotic induction. Urolithin B (UB), a gut microbiota-derived metabolite of ellagitannins, has shown anti-inflammatory and antiproliferative activities in various cancer models. Vincristine (Vinc), a common anti-lymphoma drug, disrupts microtubule formation, leading to cell cycle arrest and apoptosis in cancer cells. This study explored the antiproliferative and pro-apoptotic effects of a triple combination therapy comprising N, UB, and Vinc against human lymphoma cell lines (HKB-11 and Hs 313.T). This study systematically evaluated the synergistic efficacy of both monotherapy and dual and triple combinations and molecular mechanisms using Alamar Blue viability assays, combination index (CI) modelling, reactive oxygen species (ROS) quantification, annexin V/7-AAD flow cytometry, and bottom-up label-free proteomics. The potential cytotoxicity of the combination on normal stromal HS-5 cells was also assessed using the Alamar Blue assay. The N: UB: Vinc combination at 2240: 210: 0.94 µM demonstrated potent synergy (CI values 0.31-0.50 at IC - IC) and induced near-complete growth inhibition (> 99%) in both lymphoma cell lines with reduced toxicity (42.09 ± 1.21% viability) toward normal stromal HS-5 cells. ROS analysis revealed significant oxidative stress, while flow cytometry confirmed enhanced apoptosis (p < 0.0001) in the combination groups. Proteomic profiling of the combination N: UB: Vinc at 2450.94 µM uncovered distinct molecular responses, including upregulation of MAP1LC3B2 (LogFC = 1.4), GMNN (LogFC = 1.3), and SLC38A2 (LogFC = 1.5), promoting apoptosis, cell cycle regulation, and mTOR signaling inhibition. Concurrently, key oncogenic and metabolic proteins were downregulated, including NNMT (LogFC = -2.9), PLTP (LogFC = -2.5), and CYP4X1 (LogFC = -2.0), which implicated the suppression of MAPK-Akt signaling, ferroptosis activation, and lipid metabolism disruption. These results established a mechanistic rationale for combining postbiotics such as N and UB with standard chemotherapy, highlighting a promising avenue for safer and more effective lymphoma management in the future. - Source: PubMed
Publication date: 2025/09/23
Al-Khazaleh Ahmad KAlsherbiny Muhammad AChang DennisMünch GeraldBhuyan Deep Jyoti