Polyclonal Rabbit BORG4 Antibody
- Known as:
- Polyclonal Rabbit BORG4 Antibody
- Catalog number:
- KA0430
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit BORG4 Antibody
Related genes to: Polyclonal Rabbit BORG4 Antibody
- Gene:
- CDC42EP4 NIH gene
- Name:
- CDC42 effector protein 4
- Previous symbol:
- -
- Synonyms:
- CEP4, KAIA1777, BORG4, MGC3740, MGC17125
- Chromosome:
- 17q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-27
- Date modifiied:
- 2016-01-15
Related products to: Polyclonal Rabbit BORG4 Antibody
Related articles to: Polyclonal Rabbit BORG4 Antibody
- Hidden cardiotoxicity is defined as cardiotoxicity of a drug that manifests only in the diseased heart. We have previously shown that the proarrhythmic hidden cardiotoxic properties of a model drug, the selective cyclooxygenase-2 inhibitor rofecoxib, can be revealed in preclinical models of ischemia/reperfusion injury. As metabolic comorbidities, such as hypercholesterolemia (HC), may exacerbate hidden cardiotoxicity, we aimed to investigate the hidden cardiotoxic effects of the model drug, rofecoxib, in the presence of hypercholesterolemia. Rats were fed a high-cholesterol diet for 12 weeks and treated with 5.12 mg/kg rofecoxib. Four weeks of rofecoxib treatment surprisingly improved HC-induced mild cardiac dysfunction by restoring end-diastolic pressure, stroke work, and mechanical efficiency. Then, RNA sequencing revealed that the expression of 28 miRNAs and 300 genes was significantly altered in the HC-fed group. The HC-induced expression changes of miR-27a-5p and miR-30d-5p were reversed by rofecoxib treatment. Cdc42ep4, Cox5, and Cxcl9 genes were also counter-regulated following rofecoxib treatment compared to HC-induced changes. This is the first demonstration that rofecoxib improves HC-induced cardiac dysfunction, with the mechanism involving changes in the gene expression profile, including some key regulators of rofecoxib action. - Source: PubMed
Publication date: 2025/11/29
Kiss BernadettNagy Regina NBrenner Gábor BVáradi BarnabásBihary DóraÁgg BenceMakkos AndrásKovácsházi CsengerSayour Nabil VGergely Tamás GHusti ZoltánBaczkó IstvánReé DóraApáti ÁgotaRuppert MihályRadovits TamásMerkely BélaPoggi PaolaChatgilialoglu AlexandrosVarga Zoltán VGiricz ZoltánFerdinandy PéterGörbe Anikó - Prostate cancer (PCa) is the most common malignancy among men worldwide. The cell division cycle 42 effector protein 4 (CDC42EP4) functions downstream of CDC42, yet its role and molecular mechanisms in PCa remain unexplored. This study aimed to elucidate the role of CDC42EP4 in the progression of PCa and its underlying mechanisms. Bioinformatical analysis indicated that CDC42EP4 expression was significantly lower in PCa tissue compared to normal prostate tissue. Cellular phenotyping analysis suggested that CDC42EP4 markedly inhibited the proliferation, migration, and invasion of PCa cells. Xenograft tumor assays further demonstrated that CDC42EP4 suppressed the growth of PCa cells in vivo. Mechanistically, the study established that CDC42EP4 inhibited the ERK pathway in PCa cells. Additionally, the ERK pathway inhibitor PD0325901 was employed, revealing that PD0325901 significantly nullified the effects of CDC42EP4 on PCa cell proliferation, migration, and invasion. Collectively, our findings demonstrate that CDC42EP4 acts as a critical tumor suppressor gene, inhibiting PCa cell proliferation, migration, and invasion through the ERK pathway, thereby presenting potential targets for PCa therapy. - Source: PubMed
Publication date: 2023/12/27
Zhang XiaowenYu TaoGao GuojunXu JunbaoLin RuihuiPan ZhifangLiu JianyingFeng Weiguo - Hypertrophic cardiomyopathy (HCM), a leading cause of heart failure and sudden death, requires early diagnosis and treatment. This study investigated the underlying pathogenesis and explored potential diagnostic gene biomarkers for HCM. - Source: PubMed
You HongjunDong Mengya - This study aimed to identify differentially methylated genes (DMGs) and differentially expressed genes (DEGs) to investigate new biomarkers for the diagnosis and treatment of polycystic ovary syndrome (PCOS). - Source: PubMed
Publication date: 2023/09/11
Zhang FeiDing YicenZhang BohanHe MengjuWang ZhijiangLu ChunboKang Yani - Incomplete recovery of blood-brain barrier (BBB) function contributes to stroke outcomes. How the BBB recovers after stroke remains largely unknown. Emerging evidence suggests that epigenetic factors play a significant role in regulating post-stroke BBB recovery. This study aimed to evaluate the epigenetic and transcriptional profile of cerebral microvessels after thromboembolic (TE) stroke to define potential causes of limited BBB recovery. RNA-sequencing and reduced representation bisulfite sequencing (RRBS) analyses were performed using microvessels isolated from young (6 months) and old (18 months) mice seven days poststroke compared to age-matched sham controls. DNA methylation profiling of poststroke brain microvessels revealed 11,287 differentially methylated regions (DMR) in old and 9818 DMR in young mice, corresponding to annotated genes. These DMR were enriched in genes encoding cell structural proteins (e.g., cell junction, and cell polarity, actin cytoskeleton, extracellular matrix), transporters and channels (e.g., potassium transmembrane transporter, organic anion and inorganic cation transporters, calcium ion transport), and proteins involved in endothelial cell processes (e.g., angiogenesis/vasculogenesis, cell signaling and transcription regulation). Integrated analysis of methylation and RNA sequencing identified changes in cell junctions (occludin), actin remodeling (ezrin) as well as signaling pathways like Rho GTPase (RhoA and Cdc42ep4). Aging as a hub of aberrant methylation affected BBB recovery processes by profound alterations (hypermethylation and repression) in structural protein expression (e.g., claudin-5) as well as activation of a set of genes involved in endothelial to mesenchymal transformation (e.g., Sox9, Snai1), repression of angiogenesis and epigenetic regulation. These findings revealed that DNA methylation plays an important role in regulating BBB repair after stroke, through regulating processes associated with BBB restoration and prevalently with processes enhancing BBB injury. - Source: PubMed
Publication date: 2023/02/28
Phillips Chelsea MStamatovic Svetlana MKeep Richard FAndjelkovic Anuska V