Polyclonal Rabbit ARSK Antibody
- Known as:
- Polyclonal Rabbit ARSK Antibody
- Catalog number:
- KA0304
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit ARSK Antibody
Related genes to: Polyclonal Rabbit ARSK Antibody
- Gene:
- ARSK NIH gene
- Name:
- arylsulfatase family member K
- Previous symbol:
- -
- Synonyms:
- DKFZp313G1735, TSULF
- Chromosome:
- 5q15
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-09
- Date modifiied:
- 2016-06-28
Related products to: Polyclonal Rabbit ARSK Antibody
Related articles to: Polyclonal Rabbit ARSK Antibody
- In this study, we used single-cell sequencing data analysis to explore differentially expressed genes in the polarization process of macrophages in hepatocellular carcinoma. We then integrated these genes with cuproptosis-related genes (CRGs) to identify potential biomarkers. Through a rigorous screening process, including univariate Cox regression analysis and machine learning algorithms, we identified six key risk genes: GLIPR2, ANP32E, LIPT1, ALAD, ARSK, and PGAM1. These genes form the foundation of our prognostic risk prediction model. ROC curve analysis showed that these models had high specificity and accuracy in predicting prognostic characteristics, and Kaplan-Meier curve analysis showed that the survival rate of the low-risk group was significantly higher than that of the high-risk group. In addition, patients stratified by our model showed differences in tumor microenvironment, sensitivity to immunotherapy, and response to chemotherapy. After incorporating patient clinical data, we constructed a nomogram that further improved the accuracy of predicting patient survival. We further analyzed the expression characteristics and spatial distribution of these six risk genes in hepatocellular carcinoma through bulk transcriptomics, single-cell, and spatial transcriptomics data, and validated the expression of risk genes using qPCR. The construction of predictive models in this study helps clinicians to predict the overall survival of patients with hepatocellular carcinoma, which enables patient stratification and has the potential to help personalize patient treatment. The discovery of candidate tumor markers helps to identify potential targeted therapeutic options, which will play a key role in the diagnosis and treatment of hepatocellular carcinoma in the future. - Source: PubMed
Publication date: 2025/12/30
Deng XinCao JinyingLiang YingyingLyu BoTong Ling - - Source: PubMed
Publication date: 2025/12/25
- Chronic obstructive pulmonary disease (COPD) is a heterogeneous lung condition characterized by irreversible airflow limitation, primarily due to cigarette smoke (CS) exposure. Emerging research underscores the pivotal role of cellular senescence in the pathogenesis of COPD. The arylsulfatase family, known for its involvement in various age-related diseases, has yet to be investigated in the context of COPD. This study investigated the role of the arylsulfatase family, particularly ARSK, in COPD pathogenesis. Bioinformatics analysis and clinical validation revealed significantly reduced ARSK expression in COPD patients' lungs, especially in airway epithelium. ARSK overexpression alleviated CS-induced epithelial cellular senescence and improved mitophagy and mitochondrial function, while ARSK knockdown had an opposite effect. In vivo, Arsk-AAV administration relieved lung senescence and impaired lung function upon CS exposure, whereas airway-specific Arsk knockout aggravated these effects. Mechanistically, ARSK interacted with Parkin (PRKN) to regulate the phosphorylation of PRKN at serine 65 and subsequent mitophagy, thus attenuating cellular senescence. Additionally, the androgen receptor (AR) was identified as a transcription factor binding to the ARSK promoter, modulating its expression. These findings highlight the protective role of ARSK against epithelial cellular senescence, offering a potential therapeutic target for COPD. - Source: PubMed
Publication date: 2025/07/31
Yang RuonanZhan YuanDeng ZhesongZhang JiahengChen ShanshanZhang YatingFu HaoMeng XianglingWu JixingGu YiyaHuang QianWang CongyiXie Jungang - Mucopolysaccharidosis type 10 (MPS10) is a recently discovered lysosomal storage disorder caused by biallelic loss of function variants in ARSK. To date, 10 ARSK-related MPS10 patients from six families have been reported, with a median age at presentation of 9.5 years. The affected individuals usually present with progressive hip joint abnormalities. Coarse facial features, genu valgum, and joint abnormalities are variable. None demonstrated hepatosplenomegaly, neurological deficits, or cognitive impairment. Radiographically, platyspondyly, inferior tapering of the ilea with acetabular hypoplasia, irregularity of the central part of the femoral head, and metaphyseal striation of the long bones characterize this condition. Biochemical analyses reveal variable dermatan sulfate (DS) excretion in urine, with some patients showing increased DS, while others had normal urinary glycosaminoglycans (GAGs), suggesting that a normal GAG profile does not exclude this condition. This report provides a comprehensive review of existing knowledge on ARSK-related mucopolysaccharidosis. - Source: PubMed
Publication date: 2025/07/31
Al Fahdi IntisarSingh SwatiYadavalli KrishnaveniChatti KiranamBhavani Gandham SriLakshmiGirisha Katta M - One of the most remarkable adaptations to survive attacks from predators is to detach an appendage-a process known as autotomy. This occurs in a variety of animals, including lizards (tail), crabs (legs), and starfish (arms). There has been extensive investigation of the evolution, ecology, and biomechanical impact of autotomy, but little is known about neural mechanisms controlling autotomy in animals. However, evidence for the existence of a peptide that acts as an autotomy-promoting factor in starfish has been reported. While investigating in vivo effects of a sulfakinin/cholecystokinin-type neuropeptide (ArSK/CCK1) in the starfish Asterias rubens, we observed that this peptide triggered arm autotomy in some animals. Furthermore, when injection of ArSK/CCK1 was combined with mechanical clamping of an arm, autotomy of the clamped arm occurred in 85% of animals tested, with 46% also autotomizing one or more other arms. In contrast, no autotomy was observed in clamped animals that were injected with water (control). To examine the physiological relevance of these findings, we analyzed expression of ArSK/CCK1 in the autotomy plane, a specialized region at the base of the arms in A. rubens. In accordance with its in vivo effects, nerve fibers expressing ArSK/CCK1 were revealed in the tourniquet muscle, a band of muscle that mediates constriction of the arm during and after autotomy. We conclude that ArSK/CCK1 acts as an autotomy-promoting factor in starfish and as such it is the first neuropeptide to be identified as a regulator of autotomy in animals. - Source: PubMed
Publication date: 2024/08/29
Tinoco Ana BKirupakaran VyshnavieCapatina DeliaEgertová MichaelaElphick Maurice R