EDG-2 Control
- Known as:
- EDG-2 Control
- Catalog number:
- BC-011
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- kamyia
- Gene target:
- EDG-2 Control
Related genes to: EDG-2 Control
- Gene:
- BUD31 NIH gene
- Name:
- BUD31 homolog
- Previous symbol:
- G10
- Synonyms:
- YCR063W, EDG-2, EDG2, fSAP17, Cwc14
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-03-10
- Date modifiied:
- 2017-03-10
- Gene:
- LPAR1 NIH gene
- Name:
- lysophosphatidic acid receptor 1
- Previous symbol:
- EDG2
- Synonyms:
- edg-2, rec.1.3, vzg-1, Gpcr26, Mrec1.3, LPA1, GPR26
- Chromosome:
- 9q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-15
- Date modifiied:
- 2016-10-05
Related products to: EDG-2 Control
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated(DRAAGQPAG)3 (repeat-sequence peptide of the P. vivax circumsporozoite protein, CSP) control blocking peptide(Draxin) C1ORf187 WB control: PC-Drax Host: Rabbit Affinity purifed(Draxin) C1ORf187, WB control(I) LightCycler 1. 0; (Internal Control can't be used for this system) ; (II) LightCycler2. 0; (III) PE5700, MJ_Opticon etc. single color systems; (IV) ABI7000, ABI7300, ABI7500, ABI7900, ABI StepO(NANP)5 peptide (repeat-sequence peptide of the P. falciparum circumsporozoite protein, CSP) control blocking peptide(NVDP)4 peptide (minor repeat-sequence peptide of the P. falciparum circumsporozoite protein, CSP) control blocking peptide(PPPPNAND)3 peptide (repeat-sequence peptide of the P. berghei circumsporozoite protein, CSP) control blocking peptide(WB control) Fel D1 Immunogen: peptide Host: Rabbit(WB control) FelD1 Immunogen: peptide Host: Rabbit, Clone MOPC-21, Isotype IgG1Application FC, IP, WB, IHC(P), IHC(F), negative control Concentration 0.1 mg/ml, Clone MOPC-21, Isotype IgG1Application FC, IP, WB, IHC(P), IHC(F), negative control Concentration 0.1 mg/ml Related articles to: EDG-2 Control
- Sudden Unexpected Death in Epilepsy (SUDEP) refers to the unexplained, sudden death of individuals with epilepsy, and its incidence is closely linked to the severity and duration of seizures. This study aimed to identify plasma biomarkers associated with SUDEP through a combined proteomics and metabolomics approach. - Source: PubMed
Publication date: 2026/03/09
Zheng GaolinYang XinyanChen YinyuZhang PengNie Qianyun - The human gene has been associated with various processes including cancer. To better understand its function, we used genetic methods to study cells lacking the homologous gene () and performed sequence analysis using bioinformatics methods. Mutant cells lacking the gene showed cell size and division defects, altered stress response, rapamycin sensitivity, enhanced chronological aging, and increased sporulation tendency. These processes are known to be regulated by the TOR pathway. The -TOR link was also supported by further experiments. We demonstrated that most protein-coding genes affected by deletion are upregulated, encode hydrolases, oxidoreductases, and are often involved in transport. GO enrichment drew our attention to genes related to nitrogen transport, while additional data pointed to a nutrient/nitrogen (N) sensing problem. Although Cwf14 protein is associated with spliceosome complex, most genes affected by the absence of do not contain introns, suggesting that they are influenced indirectly by the gene. In silico experiments have revealed that orthologous genes are found from yeast to humans, are evolutionarily conserved with a high degree of sequence identity, conserved motifs, and structures. Since the human gene partially complemented the mutant phenotype of cells, indicating functional homology, our data can help better understand pathological mechanisms observed in human cancer cells. - Source: PubMed
Publication date: 2025/11/05
Vig IldikóAcs-Szabo LajosBenkő ZsigmondBagelova Polakova SilviaPapp László AttilaGregan JurajMiklós Ida - Ovarian cancer is the second leading cause of gynecologic cancer death worldwide, with only 20% of cases detected early due to its elusive nature, limiting successful treatment. Most deaths occur from the disease progressing to advanced stages. Despite advances in chemo- and immunotherapy, the 5-year survival remains below 50% due to high recurrence and chemoresistance. Therefore, leveraging new research perspectives to understand molecular signatures and identify novel therapeutic targets is crucial for improving the clinical outcomes of ovarian cancer. Alternative splicing, a fundamental mechanism of post-transcriptional gene regulation, significantly contributes to heightened genomic complexity and protein diversity. Increased awareness has emerged about the multifaceted roles of alternative splicing in ovarian cancer, including cell proliferation, metastasis, apoptosis, immune evasion, and chemoresistance. We begin with an overview of altered splicing machinery, highlighting increased expression of spliceosome components and associated splicing factors like BUD31, SF3B4, and CTNNBL1, and their relationships to ovarian cancer. Next, we summarize the impact of specific variants of CD44, ECM1, and KAI1 on tumorigenesis and drug resistance through diverse mechanisms. Recent genomic and bioinformatics advances have enhanced our understanding. By incorporating data from The Cancer Genome Atlas RNA-seq, along with clinical information, a series of prognostic models have been developed, which provided deeper insights into how the splicing influences prognosis, overall survival, the immune microenvironment, and drug sensitivity and resistance in ovarian cancer patients. Notably, novel splicing events, such as PIGV|1299|AP and FLT3LG|50,941|AP, have been identified in multiple prognostic models and are associated with poorer and improved prognosis, respectively. These novel splicing variants warrant further functional characterization to unlock the underlying molecular mechanisms. Additionally, experimental evidence has underscored the potential therapeutic utility of targeting alternative splicing events, exemplified by the observation that knockdown of splicing factor BUD31 or antisense oligonucleotide-induced BCL2L12 exon skipping promotes apoptosis of ovarian cancer cells. In clinical settings, bevacizumab, a humanized monoclonal antibody that specifically targets the VEGF-A isoform, has demonstrated beneficial effects in the treatment of patients with advanced epithelial ovarian cancer. In conclusion, this review constitutes the first comprehensive and detailed exposition of the intricate interplay between alternative splicing and ovarian cancer, underscoring the significance of alternative splicing events as pivotal determinants in cancer biology and as promising avenues for future diagnostic and therapeutic intervention. - Source: PubMed
Publication date: 2024/10/18
Wei LiweiLi YishengChen JiawangWang YuanmeiWu JianminYang HuanmingZhang Yi - BUD31, a splicing factor, is linked to various cancers. This study examines BUD31's expression, prognostic value, mutation profile, genomic instability, tumor immune environment, and role in clear cell renal cell carcinoma (ccRCC), focusing on cell cycle regulation via alternative splicing. BUD31 expression was analyzed using TCGA and GTEx databases across 33 cancers. Techniques included IHC staining, survival analysis, Cox regression, and nomogram construction. Mutation landscape, genomic instability, and tumor immune microenvironment were evaluated. Functional assays on ccRCC cell lines involved BUD31 knockdown, RNA sequencing, and alternative splicing analysis. BUD31 was upregulated in multiple tumors, including ccRCC. High BUD31 expression correlated with worse survival outcomes and was identified as an independent predictor of poor prognosis in ccRCC. High BUD31 expression also correlated with increased genomic instability and a less active immune microenvironment. BUD31 knockdown inhibited cell proliferation, migration, and invasion in vitro and reduced tumor growth in vivo. RNA sequencing identified 390 alternative splicing events regulated by BUD31, including 17 cell cycle-related genes. KEGG analysis highlighted pathways involved in cell cycle regulation, indicating BUD31's role in promoting cell cycle progression through alternative splicing. BUD31 is upregulated in various tumors and is associated with poor outcomes, increased genomic instability, and a suppressed immune microenvironment in ccRCC. BUD31 promotes cell cycle progression via alternative splicing, suggesting it as a prognostic biomarker and potential therapeutic target in ccRCC. - Source: PubMed
Publication date: 2024/08/13
Wu XiaoliangFan RuixinZhang YangjunDuan ChenYao XiangyangLiu KaiLin DongxuChen Zhong - The testicular stem cell niche is the central regulator of spermatogenesis in Drosophila melanogaster. However, the underlying regulatory mechanisms are unclear. This study demonstrated the crucial role of lethal (1) 10Bb [l(1)10Bb] in regulating the testicular stem cell niche. Dysfunction of l(1)10Bb in early-stage cyst cells led to male fertility disorders and compromised cyst stem cell maintenance. Moreover, the dysfunction of l(1)10Bb in early-stage cyst cells exerted non-autonomous effects on germline stem cell differentiation, independently of hub signals. Notably, our study highlights the rescue of testicular defects through ectopic expression of L(1)10Bb and the human homologous protein BUD31 homolog (BUD31). In addition, l(1)10Bb dysfunction in early-stage cyst cells downregulated the expression of spliceosome subunits in the Sm and the precursor RNA processing complexes. Collectively, our findings established l(1)10Bb as a pivotal factor in the modulation of Drosophila soma-germline communications within the testicular stem cell niche. - Source: PubMed
Publication date: 2024/05/23
He LeiSun FeitengWu YunhaoLi ZhiranFu YangboHuang QiuruLi JiaxinWang ZihanCai JiayingFeng ChenruiDeng XiaonanGu HanHe XuxinYu JunSun Fei