A1BG antibody - N-terminal region (ARP33810_P050)
- Known as:
- A1BG (anti-) - N-terminal region (ARP33810_P050)
- Catalog number:
- arp33810_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- A1BG antibody - N-terminal region (ARP33810_P050)
Related genes to: A1BG antibody - N-terminal region (ARP33810_P050)
- Gene:
- A1BG NIH gene
- Name:
- alpha-1-B glycoprotein
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.43
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2015-07-13
- Gene:
- A1BG-AS1 NIH gene
- Name:
- A1BG antisense RNA 1
- Previous symbol:
- NCRNA00181, A1BGAS, A1BG-AS
- Synonyms:
- FLJ23569
- Chromosome:
- 19q13.43
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2009-07-20
- Date modifiied:
- 2013-06-27
Related products to: A1BG antibody - N-terminal region (ARP33810_P050)
Related articles to: A1BG antibody - N-terminal region (ARP33810_P050)
- Nerve aberrations and vascular lesions in the distal lower limbs are the etiological factors for diabetic foot ulcers (DFUs). This study aimed to understand the regulatory mechanism of angiogenesis in patients with DFU by examining lncRNA, as well as to explore effective targets for diagnosing and treating DFU. The serum levels of A1BG-AS1 and miR-214-3p and the predictive power of A1BG-AS1 for DFU were determined by quantitative PCR and ROC analysis. The correlation of A1BG-AS1 with clinical characteristics was examined using chi-square tests. The risk factors for DFU in patients with type 2 diabetes mellitus (T2DM) were identified using the logistic regression model. Furthermore, the binding sites of A1BG-AS1 and miR-214-3p were determined. Next, A1BG-AS1 interference plasmid and miR-214-3p inhibitor were co-transfected into high glucose-induced cells to investigate their effects on the expression of angiogenesis-related genes and cell proliferation. The A1BG-AS1 levels were upregulated, whereas the miR-214-3p levels were downregulated in patients with DFU. The upregulation of A1BG-AS1 was significantly associated with both blood glucose levels and ulcer grades. A1BG-AS1 served as a crucial biomarker for diagnosing DFU and evaluating the risk of DFU occurrence in patients with T2DM. Co-transfection experiments revealed that the inhibition of miR-214-3p effectively recovered the suppressive effects of A1BG-AS1 on angiogenesis-related gene expression, endothelial cell differentiation, and proliferation. The sponging effect of A1BG-AS1 on miR-214-3p impaired angiogenesis in patients with DFU. Thus, A1BG-AS1 is a potential therapeutic target for DFU. - Source: PubMed
Publication date: 2025/01/07
Wu FangfangWang LixiaZuo HongjuTian Hanbing - Medullary thyroid carcinoma (MTC) is a rare but aggressive endocrine malignancy that originates from the parafollicular C cells of the thyroid gland. Enhancer RNAs (eRNAs) are non-coding RNAs transcribed from enhancer regions, which are critical regulators of tumorigenesis. However, the roles and regulatory mechanisms of eRNAs in MTC remain poorly understood. This study aims to identify key eRNAs regulating the malignant phenotype of MTC and to uncover transcription factors involved in the regulation of key eRNAs. - Source: PubMed
Liu DaxiangWang WenjingWu YanzhaoQiu YongleZhang Lan - Exosome-derived long non-coding RNAs (lncRNAs) and N6-methyladenosine (mA) modifications of lncRNAs have been shown crucial functions in prostate cancer (PCa). Herein, we aim to investigate the detailed mechanism of exosome-derived lncRNA A1BG-AS1 in PCa process. - Source: PubMed
Publication date: 2024/02/13
Yang ZhiLuo YuZhang FanMa Likun - Adriamycin (ADR) resistance is an obstacle for chemotherapy of breast cancer (BC). ATP binding cassette subfamily B member 1 (ABCB1) expression is indicated to be closely related to the drug resistance of cancer cells. The current work intended to explore the molecular mechanisms to regulate ABCB1 in BC cells with ADR resistance. We found that long noncoding RNA (lncRNA) A1BG antisense RNA 1 (A1BG-AS1) is upregulated in ADR resistant BC cell lines (MCF-7/ADR, MDA-MB-231/ADR). A1BG-AS1 knockdown enhanced the ADR sensitivity by suppressing the viability, proliferation potential and migration ability, and facilitating cell apoptosis in BC. Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) is known to be an m6A reader to modulate the stability of mRNA transcripts in an m6A-dependent manner, which was a shared RNA binding protein (RBP) for A1BG-AS1 and ABCB1. The interaction of IGF2BP2 with A1BG-AS1 or ABCB1 was explored and verified using RNA pulldown and RNA immunoprecipitation (RIP) assays. ABCB1 mRNA and protein expression was positively regulated by A1BG-AS1 and IGF2BP2 in BC cells. ABCB1 mRNA expression was stabilized by A1BG-AS1 via recruiting IGF2BP2 in an m6A-dependent manner. Moreover, rescue assays demonstrated that A1BG-AS1 enhanced BC ADR resistance by positively modulating ABCB1. Xenograft mouse models were used to explore whether A1BG-AS1 affected the ADR resistance in BC in vivo. The findings indicated that A1BG-AS1 silencing inhibited tumor growth and alleviated ADR resistance in vivo. In conclusion, A1BG-AS1 enhances the ADR resistance of BC by recruiting IGF2BP2 to upregulate ABCB1 in an m6A-dependent manner. - Source: PubMed
Publication date: 2023/11/25
Wang JianXu JieZheng Jie - The study aims to explore the role of A1BG antisense RNA 1 (A1BG-AS1), microRNA (miR)-148a-3p and ubiquitin-specific protease 22 (USP22) on osteosarcoma (OS) cell growth. - Source: PubMed
Publication date: 2023/10/30
Han XiuxinYin MengfanGong ChenZhang ChaoZhu GenbaoHu MengxueTan KemengJiang LaWang GuowenLi Lili