KCNMB4 antibody - middle region (ARP35241_P050)
- Known as:
- KCNMB4 (anti-) - middle region (ARP35241_P050)
- Catalog number:
- arp35241_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- KCNMB4 antibody - middle region (ARP35241_P050)
Related genes to: KCNMB4 antibody - middle region (ARP35241_P050)
- Gene:
- KCNMB4 NIH gene
- Name:
- potassium calcium-activated channel subfamily M regulatory beta subunit 4
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 12q15
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-02
- Date modifiied:
- 2016-02-04
Related products to: KCNMB4 antibody - middle region (ARP35241_P050)
Related articles to: KCNMB4 antibody - middle region (ARP35241_P050)
- Concurrent chemotherapy is the standard treatment strategy for advanced-stage nasopharyngeal carcinoma (NPC). However, chemoresistance inevitable develops and the underlying mechanism remains poorly understood. In this study, we identify the arginine methyltransferase PRMT5 as a key gene associated with chemoresistance to paclitaxel in NPC. We demonstrate that PRMT5 facilitated paclitaxel resistance by inducing KCNMB4 expression in nasopharyngeal carcinoma cells. Mechanistically, PRMT5 is recruited to the promoter region of KCNMB4, where it catalyzes H3R2me2s and enhances KCNMB4 expression. Furthermore, elevated levels of PRMT5 or KCNMB4 correlated with poorer survival and higher recurrence rates in NPC patients. Notably, genetic or pharmacological inhibition of PRMT5 significantly sensitized NPC cells to paclitaxel, both in vitro and in vivo. Collectively, these results suggest that the PRMT5-KCNMB4 axis plays a crucial role in mediating chemoresistance in NPC and targeting this axis may provide a promising therapeutic strategy for late-stage NPC patients. - Source: PubMed
Publication date: 2026/01/09
Liu LizhenLiu SailanWang YaliWang PeiliZhong GuixiangHong Jing HanXiao RongGuo YaoyuZhu FangHao JingChen JianFengMai Hai-QiangTan Jing - Decreased nitric oxide (NO) production from the vascular endothelium is a major factor for vascular aging. Because vascular aging has few specific subjective symptoms, assessing the susceptibility to vascular aging is beneficial for its early detection and improvement. Therefore, this study evaluated the associations between single nucleotide polymorphisms (SNPs) on L-citrulline (Cit) pathways essential for NO production and the health characteristics involved in vascular aging using a candidate gene approach. Associations with a significance level included those between the KCNMB4 rs17108108 C allele and tendency to gain weight, the ADCY8 rs6470860 G allele and numbness of limbs, the NOS1 rs2271987 T allele and lower back pain, and the PDE9A rs2284972 G allele and body pain with negative mood states. A genome-wide association study was also conducted to analyze SNPs more extensively across genes related to Cit and NO metabolism, which revealed genome-wide significant associations between the PRMT6 rs12028323 C allele and mood disturbance. These significant associations could be explained by the change in downstream NO signaling, supporting the relationship between the investigated traits and vascular function. These traits can be manifested as subjective symptoms of vascular aging. Therefore, the identified SNPs could predict susceptibility to the subjective symptoms of vascular aging, which could lead to genotype-based personalized interventions of Cit for an efficient improvement of vascular health. - Source: PubMed
Publication date: 2025/05/29
Nogimura DaiMoriyasu KazukiIshida SachikoKohda MasakazuYazawa TakayukiMorita Masahiko - Patent foramen ovale (PFO) is a congenital defect between the atria, resulting in abnormal hemodynamics. We conducted a genome-wide association study (GWAS) to identify common genetic variants associated with PFO. - Source: PubMed
Publication date: 2025/01/13
Dong BosiLi YajiaoAi FandiGeng JiaTang TingPeng WanTang YushaWang HuiTian ZixuanBu FengxiaoChen Lei - Alzheimer's disease (AD) plays a prominent role as the most common form of dementia. Moreover, the traditional mechanism of AD does not explain the microvascular damage observed in about 25-30 years between the onset of AD, which results in late application treatment that inhibits or delays neurodegeneration. - Source: PubMed
Jara-Medina KevinsLillo LuisLagunas ConstanzaCabello-Guzmán GerardoValenzuela-Melgarejo Francisco J - Significant progress has been made in elucidating the basic principles that govern neuronal specification in the developing central nervous system. In contrast, much less is known about the origin of astrocytic diversity. Here, we demonstrate that a restricted pool of progenitors in the mouse spinal cord, expressing the transcription factor Dbx1, produces a subset of astrocytes, in addition to interneurons. Ventral p0-derived astrocytes (vA0 cells) exclusively populate intermediate regions of spinal cord with extraordinary precision. The postnatal vA0 population comprises gray matter protoplasmic and white matter fibrous astrocytes and a group of cells with strict radial morphology contacting the pia. We identified that vA0 cells in the lateral funiculus are distinguished by the expression of reelin and Kcnmb4. We show that Dbx1 mutants have an increased number of vA0 cells at the expense of p0-derived interneurons. Manipulation of the Notch pathway, together with the alteration in their ligands seen in Dbx1 knockouts, suggest that Dbx1 controls neuron-glial balance by modulating Notch-dependent cell interactions. In summary, this study highlights that restricted progenitors in the dorsal-ventral neural tube produce region-specific astrocytic subgroups and that progenitor transcriptional programs highly influence glial fate and are instrumental in creating astrocyte diversity. - Source: PubMed
Publication date: 2022/08/02
Sartoretti Maria MicaelaCampetella Carla ALanuza Guillermo M