GANP antibody Polyclonal Antibodies Primary antibodies
- Known as:
- GANP (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100622
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- GANP antibody Polyclonal Antibodies Primary antibodies
Related genes to: GANP antibody Polyclonal Antibodies Primary antibodies
- Gene:
- MCM3AP NIH gene
- Name:
- minichromosome maintenance complex component 3 associated protein
- Previous symbol:
- -
- Synonyms:
- Map80, KIAA0572, GANP, SAC3
- Chromosome:
- 21q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-03-04
- Date modifiied:
- 2014-11-19
Related products to: GANP antibody Polyclonal Antibodies Primary antibodies
Related articles to: GANP antibody Polyclonal Antibodies Primary antibodies
- Hepatocellular carcinoma (HCC) poses a significant threat to human health. Tumor microenvironment alterations, particularly immune-related changes, play a pivotal role in HCC progression, with high-throughput technologies facilitating the exploration of these dynamics. This study aimed to investigate the role of long non-coding RNA (lncRNA) AC019080.1 in HCC cells. A total of 24 circadian rhythm-related (CRR) messenger RNAs (mRNAs) and 433 CRR-lncRNAs were identified. Among them, 46 prognostically relevant circadian rhythm-related lncRNAs (PCRR-lncRNAs) were found to be upregulated in the HCC group. Molecular clustering analysis of 370 HCC samples revealed expression differences of PCRR-lncRNAs across three subtypes. Immune cell infiltration levels and tumor microenvironment analysis revealed significant subtype-specific differences. AC019080.1 and MCM3AP-AS1 were identified as core PCRR-lncRNAs in HCC, with elevated expression in both HCC tissues and cell lines. Through suppression of the Wnt/β-catenin signaling pathway, knockdown of lncRNA AC019080.1 significantly inhibited the proliferation, colony formation, migration, and invasion of HCC cells, while promoting apoptosis. This study suggests that circadian rhythm-related genes can predict immune infiltration and the molecular subtypes of HCC, providing valuable insights for diagnosis and treatment. lncRNA AC019080.1 holds potential as a therapeutic target for HCC. - Source: PubMed
Publication date: 2026/01/01
Wang JinhaiMa LiWang JinjuanMa ZheWang WeiweiYu Songning - Biallelic pathogenic variants in MCM3AP, encoding the germinal center-associated nuclear protein (GANP), have been linked to autosomal recessive peripheral neuropathies variably accompanied by cognitive impairment and multisystem involvement. To date, anterior horn cell involvement has not been documented in association with MCM3AP-related disorders. - Source: PubMed
Lemos Ana Flávia AndradeFrezatti Rodrigo Siqueira SoaresDos Santos Antônio CarlosTomaselli Pedro JoséMarques Wilson - Forkhead box K2 (FOXK2) is over-expressed in several human malignancies, yet how it is regulated triple-negative breast cancer (TNBC) remained unclear. We aimed to clarify whether FOXK2 drives TNBC progression, and elucidate the upstream molecular circuitry that controls FOXK2 abundance. FOXK2 mRNA and protein were quantified by qPCR and Western blot in 30 paired TNBC and adjacent tissues. Some assays assessed proliferation, migration and invasion after FOXK2 knockdown or overexpression. Bioinformatics predicted miR-211-5p targeting FOXK2 and lncRNA MCM3AP-AS1 (MCAS1) targeting miR-211-5p. RNA immunoprecipitation (RIP) and dual-luciferase assays validated these interactions. RNA pulldown, mass spectrometry and ChIP identified p53 binding to the MCAS1 promoter. FOXK2 was upregulated in TNBC tissues as opposed to the para-carcinoma tissues. FOXK2 silencing significantly reduced proliferation, migration and invasion, whereas overexpression accelerated these phenotypes. Mechanistically, MCAS1 acts as a sponge for miR-211-5p, ultimately protecting its target gene FOXK2 from degradation. Furthermore, employing RNA pulldown, mass spectrometry, ChIP, and luciferase reporter assays, our studies revealed a direct interaction between P53 and the promoter of MCAS1. This interaction resulted in the suppression of MCAS1 transcription. Clinical samples from TNBC patients further confirmed a correlation between FOXK2 expression and tumor size, lymphatic involvement, as well as the expression level of Ki-67. Our findings unveil a novel P53/MCAS1/miR-211-5p/FOXK2 regulatory axis that dictates TNBC aggressiveness. FOXK2 may sever as both a prognostic biomarker and a therapeutic target in TNBC. - Source: PubMed
Publication date: 2025/09/13
Wu ZankaiZhang YantingXiang DandanLi TianGong YipingSong QibinHu Jin - Long non-coding RNAs (lncRNAs) have emerged as promising cancer biomarkers due to their stability and detectability. This study aimed to investigate the clinical significance and molecular mechanisms of lncRNA MCA3AP-AS1 in glioma. This study collected the clinical data from 177 glioma patients, and the expression of MCM3AP-AS1 was measured in glioma tissues and cell lines. Kaplan-Meier and COX regression analyses were employed to assess its prognostic value in glioma. In the mechanism study, bioinformatics prediction, correlation analysis, and dual-luciferase assays were conducted to validate the regulatory network involving MCM3AP-AS1, miR-23c, and PIK3R3. Functional experiments (CCK-8, Transwell assays, and Western blot) further determined the impact of MCM3AP-AS1 on glioma cell functions and confirmed the potential regulatory mechanism. Upregulation of MCM3AP-AS1 in glioma was related to the WHO grade, KFS scores, and glioma poor prognosis. Correlation analysis, binding site prediction, and the dual-luciferase reporter assay confirmed the interaction relationship among MCM3AP-AS1, miR-23c, and PIK3R3. In mechanism, MCM3AP-AS1 knockdown suppressed the glioma cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). This attenuated effect of downregulated MCM3AP-AS1 expression in glioma cell proliferation, migration, and invasion could be further reversed by miR-23c inhibition. Upregulated MCM3AP-AS1 expression in glioma was associated with the poor prognosis of glioma. MCM3AP-AS1 may promote glioma progression by enhancing cell proliferation, migration, and invasion through the miR-23c/PIK3R3 axis. - Source: PubMed
Publication date: 2025/09/04
Gao KangSong LinaNiu Deying - Lung cancer remains the leading cause of cancer-related mortality worldwide, largely due to the development of resistance to standard chemotherapeutic agents such as cisplatin. Recent evidence has highlighted the regulatory role of long non-coding RNAs (lncRNAs) in mediating drug resistance mechanisms. In this study, we aimed to reveal the role of MCM3AP-AS1 in cisplatin-induced cell death in lung cancer cells. - Source: PubMed
Publication date: 2025/07/14
Bozgeyik IbrahimTasdemir DemetBozgeyik EsraBagis HaydarOztuzcu SerdarIsik Ahmet Ferudun