Cacng4 polyclonal antibody
- Known as:
- Cacng4 pab (anti-)
- Catalog number:
- PAB9886
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- Cacng4 polyclonal antibody
Related genes to: Cacng4 polyclonal antibody
- Gene:
- CACNG4 NIH gene
- Name:
- calcium voltage-gated channel auxiliary subunit gamma 4
- Previous symbol:
- -
- Synonyms:
- MGC11138, MGC24983
- Chromosome:
- 17q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-20
- Date modifiied:
- 2016-10-05
Related products to: Cacng4 polyclonal antibody
Related articles to: Cacng4 polyclonal antibody
- Graves' orbitopathy (GO) is an autoimmune disorder characterized by orbital inflammation, fibrosis, and adipogenesis. circulating exosomesomes, critical mediators of intercellular communication, are implicated in autoimmune pathologies through miRNA cargo delivery. However, their direct role in GO pathogenesis and mechanisms driving systemic-to-local disease progression remain unexplored. - Source: PubMed
Publication date: 2026/05/26
Xu ZhihuiBao XiaoliWang XiChen CongyingXiao WeiZhang TeSha XiaotongSun AnqiGuan JiaqiYe HuijingYang Huasheng - The selection of high feed efficiency (FE) animals impacts sustainability and profitability of beef and dairy cattle production systems. An approach to investigate the mechanisms of FE involves analyzing gene expression profile in liver. This study used residual feed intake as a metric of FE to select 10 Gir x Holstein crossbred cows (Girolando F1) divided into high (HE) and low (LE) FE groups. Hepatic biopsies were used for differential gene expression investigation using RNA-seq analyses which revealed 20,787 known genes mapped accordingly to the bovine reference genome. The comparison of HE and LE revealed 149 significantly differentially expressed genes (DEG), 41 up-regulated, and 108 down-regulated in the LE group. Among DEG, some stood out as potential candidate genes, including DLK1, CACNG4, SLC2A12, SLC26A4, DUOX2, and DUOXA2. Functional enrichment analyses showed pathways that potentially influence FE, such as the negative regulation of leukocyte migration, regulation of calcium channel activity, negative regulation of cell migration and adhesion, extracellular matrix (ECM) organization, and thyroid hormone synthesis. ECM composition and immune system roles were also highlighted. These results could help understanding the mechanisms related to FE in dairy cattle and the development of selection strategies to improve this trait. - Source: PubMed
Publication date: 2026/01/19
Faza Daniele Ribeiro de Lima ReisCampos Mariana MagalhãesTomich Thierry RibeiroMachado Fernanda SamariniPereira Luiz Gustavo RibeiroDomingues RobertFranco Ana LuizaMartins Marta FonsecaPanetto João Cláudio do CarmoSilva Marcos Vinicius Gualberto Barbosa daCarvalho Wanessa AraújoMachado Marco Antonio - BACKGROUND: The reprogramming of energy metabolism, particularly glycolysis, upholds the malignancy of tumors. The relationship between CUE domain-containing protein-1 (CUEDC1) and glycolysis, along with its influence on the development of estrogen receptor-positive breast cancer (ER+ BRCA), is not well defined. This investigation explores the functional involvement of CUEDC1 in glycolysis regulation and uncovers a previously unidentified pathway contributing to the progression of ER+ BRCA. METHODS: Immunohistochemistry, western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were used to detect the expression of CUEDC1 in ER+ BRCA tissues and cell lines. A series of molecular analyses, including dual-luciferase reporter assays, RNA-seq, and chromatin immunoprecipitation (ChIP), were performed to elucidate the potential mechanisms underlying CUEDC1’s involvement in ER+ BRCA progression. Metabolic assays focusing on glycolysis were employed to investigate the functional roles of CUEDC1 and calcium voltage-gated channel auxiliary subunit gamma 4 (CACNG4). The Connectivity Map (CMap) database was utilized to screen CUEDC1 inhibitors. RESULTS: CUEDC1 is aberrantly upregulated in ER+ BRCA tissues and cells. Increased CUEDC1 can promote enhanced tumor growth and lead to poor clinical outcomes in patients with ER+ BRCA. The MYC associated zinc finger protein (MAZ) can upregulate CUEDC1 gene transcription in ER+ BRCA cells by directly binding to its promoter. We determined that CUEDC1 directly modulated CACNG4 to enhance phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway activation, thereby facilitating tumor growth of ER+ BRCA. Clinical observations also revealed a positive correlation between CACNG4 expression and CUEDC1, with both factors being strongly associated with poor prognosis in patients with ER+ BRCA. Mechanistically, The CUEDC1/CACNG4/PI3K signal axis enhanced glycolysis through upregulating glucose transporter 1 (GLUT1), a crucial protein in glucose metabolism, thereby supporting tumor growth of ER+ BRCA. Furthermore, methotrexate was identified as a potential inhibitor of CUEDC1. Importantly, the combination of ipatasertib (a PI3K/AKT pathway inhibitor), with methotrexate effectively suppressed growth of ER+ BRCA in a mouse model. CONCLUSIONS: Our research reveals that enhanced CUEDC1 plays an essential role to ER+ BRCA cell proliferation and tumor growth via the CACNG4/PI3K axis. CUEDC1 is a promising prognostic factor of ER+ BRCA, and the CUEDC1/CACNG4/PI3K axis can serve as a potential therapeutic target for ER+ BRCA treatment. - Source: PubMed
Publication date: 2025/11/28
Lu ZexiuLei MingChen JianDeng AoChang ChaoChen JingMeng DieWang RuiWan XueyingTu GangLiu ManranTang Lingfeng - Cancer-related fatigue (CRF) is a prominent cancer-related complication occurring in Prostate cancer (PCa) patients, profoundly affecting prognosis. The lack of diagnostic criteria and biomarkers hampers the management of CRF. - Source: PubMed
Publication date: 2024/12/15
Chen MingZhou SiqiHe XiongweiWen Haiyan - Miller-Dieker syndrome (MDS) is a rare neurogenetic disorder resulting from a heterozygous deletion of 26 genes in the MDS locus on human chromosome 17. MDS patients often die in utero and only 10% of those who are born reach 10 years of age. Current treatments mostly prevent complications and control seizures. A detailed understanding of the pathogenesis of MDS through gene expression studies would be useful in developing precise medical approaches toward MDS. To better understand MDS at the molecular level, we performed RNA sequencing on RNA and mass spectrometry on total protein isolated from BJ (non-MDS) cells and GM06097 (MDS) cells, which were derived from a healthy individual and an MDS patient, respectively. Differentially expressed genes (DEGs) at the RNA and protein levels involved genes associated with phenotypic features reported in MDS patients (CACNG4, ADD2, SPTAN1, SHANK2), signaling pathways (GABBR2, CAMK2B, TRAM-1), and nervous system development (CAMK2B, BEX1, ARSA). Functional assays validated enhanced calcium signaling, downregulated protein translation, and cell migration defects in MDS. Interestingly, overexpression of methyltransferase-like protein 16 (METTL16), a protein encoded in the MDS locus, restored defects in protein translation, phosphor states of mTOR (mammalian target of rapamycin) pathway regulators, and cell migration in MDS cells. Although DNA- and RNA-modifying enzymes were among the DEGs and the intracellular SAM/SAH ratio was eightfold lower in MDS cells, global nucleoside modifications remained unchanged. Thus, this study identified specific genes and pathways responsible for the gene expression changes, which could lead to better therapeutics for MDS patients. - Source: PubMed
Publication date: 2024/11/07
Mahendran GowthamiBreger KurtisMcCown Phillip JHulewicz Jacob PBhandari TulsiAddepalli BalasubrahmanyamBrown Jessica A