Ask about this productRelated genes to: HNRNPA2B1 antibody
- Gene:
- HNRNPA2B1 NIH gene
- Name:
- heterogeneous nuclear ribonucleoprotein A2/B1
- Previous symbol:
- HNRPA2B1
- Synonyms:
- -
- Chromosome:
- 7p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-08-29
- Date modifiied:
- 2016-10-05
Related products to: HNRNPA2B1 antibody
Related articles to: HNRNPA2B1 antibody
- Although circRNAs are increasingly implicated in tumor biology, most studies emphasize expression changes while overlooking subcellular distribution. The mechanisms governing circRNA nuclear export in bladder cancer (BCa) and their contribution to progression are poorly defined. - Source: PubMed
Publication date: 2026/07/04
Chen YuhanZhuang JuntaoYu HaoLi KaiZhang YuhengSun HuanyouJiang LinjingYang ZhikaiBai KexinTao YiranFeng TianshuoYang HaiweiYang XiaoLu Qiang - Peripheral arterial disease (PAD) induced by atherosclerosis causes significant health complications and can lead to amputation. Stimulating angiogenesis is a promising therapeutic strategy to treat patients with PAD, but the precise mechanism governing this process in PAD remains unclear. This study aims to uncover the mechanism governing angiogenesis in PAD. We established in vitro and in vivo models of PAD by culturing human umbilical vein endothelial cells (HUVECs) under hypoxic conditions plus serum starvation and femoral artery dissection in mice, respectively. Targeted long non-coding RNA (lncRNA) small nucleolar RNA host gene 3 (SNHG3) methylation was performed by PspCas13b. Our findings indicate that SNHG3 lncRNA in vascular endothelial cells facilitates angiogenesis by inhibiting proteasome 26S subunit ubiquitin receptor, non-ATPase 4 (PSMD4) in PAD in vitro and in vivo. Mechanistically, methylation increases SNHG3 lncRNA levels by improving its stability. Moreover, methylated SNHG3 lncRNA reduces PSMD4 mRNA by decreasing its stability via heterogeneous nuclear ribonucleoprotein A2/B1 (HnRNPA2B1). Furthermore, ubiquitin-conjugating enzyme E2 I (UBE2I)-mediated SUMOylation of HnRNPA2B1 exacerbates PSMD4 mRNA instability by facilitating HnRNPA2B1- PSMD4 mRNA interaction. Additionally, PSMD4 promotes UBE2I degradation to suppress HnRNPA2B1 SUMOylation, suggesting a negative feedback regulatory loop between PSMD4 and HnRNPA2B1. These findings indicate that methylated SNHG3 lncRNA ameliorates PSMD4-inhibited angiogenesis by interactions with SUMOylated HnRNPA2B1 in PAD. - Source: PubMed
Publication date: 2026/07/08
Huang ShuichuanLi HaileiLiu WenjunLiu YifanChen YuanqiLiu HaoQian Kai - MALAT1 has been validated to favor the progression of acute lymphoblastic leukemia (ALL), but its detailed mechanism remains obscure. This study explored the functional roles of ALL cells-derived exosomal MALAT1 in chemoresistance and malignant growth of ALL cells, as well as its underlying mechanisms. - Source: PubMed
Publication date: 2026/07/01
Hong XiaofangYang DaiyanXing JianhaoLi HuihuiZheng Jifu - N6-methyladenosine (m6A) is the most abundant internal RNA modification in eukaryotic transcripts and plays a critical role in RNA metabolism, gene expression, and cellular homeostasis. Dysregulation of m6A regulators, including "writers," "erasers," and "readers", has been increasingly implicated in cancer biology; however, their comprehensive roles in breast cancer remain to be understood. The primary objective of this methods article is to provide bioinformatics beginners with a step-by-step framework for utilizing publicly available cancer datasets to perform mutational analyses, assess gene expression alterations, and examine their associations with patient survival. As a case study, m6A regulators in breast cancer were analyzed using datasets from the Cancer Genome Atlas (TCGA), the Genotype-Tissue Expression (GTEx) project, and microarray platforms. Transcriptomic profiles were systematically analyzed to demonstrate workflows for evaluating the prognostic relevance of m6A regulatory components in breast cancer. Using this analytical framework, distinct patterns of genetic alterations and differential expression among key m6A regulators were identified. Several regulators, including METTL14, CBLL1, YTHDC1, HNRNPC, HNRNPA2B1, and RBMX, were associated with better patient survival, while YWHAG was associated with poor overall survival. This study provides a comprehensive systems genomics overview of m6A regulatory genes in breast cancer while demonstrating a practical and reproducible web-based bioinformatics workflow. These findings advance the understanding of epitranscriptomic regulation in breast cancer and offer a foundation for the development of novel m6A-based diagnostic and therapeutic strategies. - Source: PubMed
Publication date: 2026/06/09
Abdulkarim SarahAkhtar SalwaUr Rehman MatiAbu-Zaid AhmedZhang DingxiaoMehmood Rashid - Lymphovascular invasion (LVI) is a critical early step in metastasis, yet the mechanisms remain elusive. We identify an intragenic antagonistic loop between TNRC6B and circTNRC6B that determines LVI and metastasis in esophageal squamous cell carcinoma. This antagonism is conserved across upper gastrointestinal tumors, where TNRC6B expression correlates positively with LVI and poor prognosis, while circTNRC6B shows the opposite associations. TNRC6B protein degrades circTNRC6B via its middle domain, which otherwise functions as a potent tumor suppressor. Mechanistically, circTNRC6B recruits HNRNPA2B1 in an m6A-dependent manner to orchestrate the nuclear-to-cytoplasmic translocation of KLRC3 mRNA. Concurrently, circTNRC6B acts as a molecular decoy, competing with IGF2BP2 for USP4 binding to impair IGF2BP2 deubiquitination, further destabilizing KLRC3 mRNA. Notably, HNRNPA2B1 mediates the exosomal packaging of m6A-modified circTNRC6B to counteract TNRC6B driven pro-tumorigenic effects. This study highlights the TNRC6B/circTNRC6B axis as a key determinant for LVI, providing potential diagnostic biomarkers and therapeutic targets for upper gastrointestinal tumors. - Source: PubMed
Publication date: 2026/06/25
Meng LingjiaoWu HaotianWu JiaxiangLi TongkunChen ShengLiu YuepingGuo HonghaiDing Ping'anZhao Qun