ZEB2 antibody - N-terminal region (ARP33695_P050)
- Known as:
- ZEB2 (anti-) - N-terminal region (ARP33695_P050)
- Catalog number:
- arp33695_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZEB2 antibody - N-terminal region (ARP33695_P050)
Related genes to: ZEB2 antibody - N-terminal region (ARP33695_P050)
- Gene:
- ZEB2 NIH gene
- Name:
- zinc finger E-box binding homeobox 2
- Previous symbol:
- ZFHX1B
- Synonyms:
- KIAA0569, SIP-1, SIP1
- Chromosome:
- 2q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-14
- Date modifiied:
- 2015-07-31
- Gene:
- ZEB2-AS1 NIH gene
- Name:
- ZEB2 antisense RNA 1
- Previous symbol:
- ZEB2AS, ZEB2-AS
- Synonyms:
- ZEB2NAT
- Chromosome:
- 2q22.3
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2009-08-30
- Date modifiied:
- 2016-12-16
Related products to: ZEB2 antibody - N-terminal region (ARP33695_P050)
Related articles to: ZEB2 antibody - N-terminal region (ARP33695_P050)
- Endothelial dysfunction is a fundamental pathological process in atherosclerosis (AS), a leading cause of cardiovascular disease worldwide. The present study aimed to explore lncRNA ZEB2-AS1's expression, diagnostic value in AS, and its function on proliferation, inflammation, and potential mechanism in AS-related endothelial dysfunction. ZEB2-AS1 was detected in the specimens of 120 patients with AS and 115 control subjects, and the findings were validated using the GSE120521 dataset. An in vitro model of AS was established by inducing HUVECs with ox-LDL. In this model, ZEB2-AS1 expression was silenced. Assessment of cell viability was carried out with a CCK-8 kit. The secretion profiles of key inflammatory factors (TNF-α, IL-6, IL-1β), along with the chemokine MCP-1 and adhesion molecules (VCAM-1, ICAM-1), were analyzed by ELISA. Potential target miRNAs were predicted through LncRNASNP2 and miEAA databases, and miR-149-5p was verified using rescue experiments. Upregulation of ZEB2-AS1 was observed in the blood and tissues of individuals with AS, consistent with the data on unstable plaques from GSE120521. ZEB2-AS1 knockdown intensified the viability inhibition triggered by ox-LDL and decreased the secretion of inflammatory factors and adhesion molecules. miR-149-5p, a target molecule of ZEB2-AS1, exerted a reversing influence on these alterations. In conclusion, ZEB2-AS1 upregulation in AS promotes ox-LDL-induced endothelial dysfunction via miR-149-5p, acting as a potential AS biomarker/therapeutic target. - Source: PubMed
Zhang KunSong WeiLiu BingXiao ShunGuo Mingjin - Antisense genes (usually suffixed by -AS) represent a class of long non-coding RNAs (lncRNAs) transcribed from the opposite strand of annotated human genes or exon(s). A total of ~2236 human antisense genes exist in the human genome. Their genomic locations with respect to the corresponding sense genes, their dysregulated expression patterns in cancer specimens, and clinical associations with patient outcomes reveal their potential importance in clinical settings. As of today, there lacks a comprehensive review of HNC-associated antisense genes/transcripts to help move forward the antisense field for genetic biomarker development or future drug research. In total, 2.3% (52/2236 antisense genes) of all known human antisense genes have been investigated in head and neck cancer (HNC). Thus, we perform a comprehensive review of the genomic aberrations (mutations, copy number changes, RNA-expression dysregulation, and single nucleotide polymorphisms) associated with HNC patient prognosis, disease progression, cancer cell signaling, drug sensitivity, and radio-resistance. Four antisense genes, namely , , , and , have been clinically cross-validated and have consistently demonstrated to be associated with patient outcomes in multiple independent cohorts by different research teams, with clear evidence for the prioritization of clinical biomarker development in HNC. Single nucleotide polymorphisms (SNPs) of antisense genes with evidence for HNC risk or outcomes should be further validated in different ethnic groups, for potential global HNC applications. - Source: PubMed
Publication date: 2025/12/19
Ye JishiAbbang Stacy MagdaleneNg Yuen-KengLui Vivian Wai Yan - Noncoding RNAs (ncRNAs), including microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs), play critical epigenetic roles in regulating gene expression and cancer development. Dysregulation of these molecules is closely associated with breast cancer initiation, progression, metastasis, and therapeutic resistance. Another major epigenetic mechanism, DNA methylation, also contributes to cancer susceptibility. - Source: PubMed
Publication date: 2025/12/20
Mashayekh ZeynabFard Rasool FatehiVallian Sadeq - In recent years, immunogenic cell death (ICD) and long non-coding RNAs (lncRNAs) have been implicated in tumor invasion and growth. However, the role of ICD-associated lncRNAs in pancreatic adenocarcinoma (PAAD) remains unclear. Therefore, this study aimed to develop and validate a prognostic signature based on ICD-associated lncRNAs for PAAD patients and to explore its potential associations with immune processes. - Source: PubMed
Publication date: 2025/10/29
Zhu HaoGan XiaojieShen DanyangSun Ding - Uterine fibroids (leiomyomas) are benign tumors whose growth is influenced by estrogen and progesterone. This study aimed to compare the profiles of differentially expressed long non-coding RNAs (lncRNAs) in fibroids from postmenopausal and premenopausal women to identify hormone-responsive lncRNAs. RNA sequencing was performed on six pairs of fibroid (Fib) and adjacent myometrium (Myo) tissues from postmenopausal women. Out of 7876 normalized lncRNAs, 3684 were differentially expressed (≥1.5-fold), with 1702 upregulated and 1982 downregulated in Fib. Comparative analysis with a previously published premenopausal dataset identified 741 lncRNAs that were altered based on their menopausal status, including 62 lncRNAs that were uniquely dysregulated in postmenopausal samples. Overall, 9 lncRNAs were selected for validation by PCR in an expanded cohort of 31 postmenopausal and 84 premenopausal paired samples. Several lncRNAs, including , , , , and , were upregulated in premenopausal Fib but not in postmenopausal ones, while displayed the opposite pattern. and were elevated in Fib from both groups, although the increase was less pronounced in the postmenopausal group. was significantly downregulated in postmenopausal Fib, with no change observed in premenopausal samples. Additionally, analysis based on MED12 mutation status revealed that lncRNAs such as , , and showed limited or reduced differential expression (mutation-positive vs. mutation-negative) in postmenopausal patients compared to the premenopausal group. These findings indicate that lncRNA expression in fibroids is modulated by menopausal status, likely reflecting hormonal influence. Hormone-responsive lncRNAs may play key roles in fibroid pathogenesis and represent potential targets for therapeutic intervention. - Source: PubMed
Publication date: 2025/07/16
Chuang Tsai-DerRysling ShawnTon NhuBaghdasarian DanielKhorram Omid