OCRL Mouse Monoclonal Antibody
- Known as:
- OCRL Mouse Monoclonal Antibody
- Catalog number:
- BIN-004952-M02
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- OCRL Mouse Monoclonal Antibody
Related genes to: OCRL Mouse Monoclonal Antibody
- Gene:
- OCRL NIH gene
- Name:
- OCRL inositol polyphosphate-5-phosphatase
- Previous symbol:
- -
- Synonyms:
- OCRL1
- Chromosome:
- Xq26.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-01-22
Related products to: OCRL Mouse Monoclonal Antibody
Related articles to: OCRL Mouse Monoclonal Antibody
- The emergence of resistance against first-generation non-nucleoside reverse transcriptase inhibitors (NNRTIs) necessitates the development of novel scaffolds with improved antiviral efficacy. In this study, a series of pyridinone derivatives were designed and synthesized as potential NNRTIs. The antiviral evaluation against wild-type HIV-1 in MT-4 cells revealed that most of the compounds displayed limited or no activity, often accompanied by cytotoxic effects. However, two derivatives, 4e and 4i, demonstrated remarkable inhibition of HIV-1 replication, with 4i exhibiting low-nanomolar potency against HIV-1 (EC = 5.3 nM), having almost one half of the Rilpivirine activity. Molecular docking confirmed critical hydrogen bonding interactions with Lys103 and π-π stacking with Trp229 and Tyr181, while 300 ns molecular dynamics simulations verified the stability of the compound-enzyme complexes. Collectively, these findings highlight the pyridinone scaffold, particularly compound 4i, as a promising lead for further optimization toward next-generation NNRTIs. - Source: PubMed
Publication date: 2026/05/23
Movahednia NiloofarRamazani AliFassihi AfshinShirvani PouriaSchols Dominique - Genetic variants are the leading cause of congenital cataract (CC). To date, numerous genes have been implicated in the development of CC. The objective of the present study was to report two previously unrecognized gene variants associated with CC in two unrelated Chinese families, identified through whole exome sequencing (WES). - Source: PubMed
Publication date: 2026/05/08
Zhuang JianlongHuang NanChen Yu ELou HaijuanWang JunyuFu WanyuChen Chunnuan - Dent disease is a hereditary kidney tubular disorder caused by pathogenic variants in either the CLCN5 (Dent disease 1) or OCRL1 (Dent disease 2) genes. As a rare genetic disorder, Dent disease often presents with variable clinical manifestations, leading to frequent misdiagnosis or underdiagnosis, especially in milder cases. Consequently, limited research has addressed the long-term clinical outcomes of Dent disease. - Source: PubMed
Publication date: 2026/04/18
Yang Eun MiAhn Yo HanKim Ji HyunSong Ji YeonCho Min HyunHan Kyoung HeePark Se JinKang Hee GyungCho HeeyeonCheong Hae Il - Our research showed that the nanoparticles incorporated within the Metal-Organic Framework (MOF) substrate can facilitate self-driven electron transfer without the need for external stimulation to produce reactive oxygen species (ROS). The potential difference between bismuth nanoparticles and the central metal in the MOF is recognized as a key factor in the process of autonomous electron transfer. This study investigates the impact of central metal on electrochemical performance of bismuth nanoparticles and the production of active radical species. In this work, the MOF-303 with aluminum central metal was chosen to reduce the potential difference compared to previous our research focused on zirconium metal. The results indicate that the reduction in potential difference leads to a decrease in impedance and an increase in semiconductor capability. These changes improve the performance of bismuth nanoparticles in electron transfer, resulting in increased production of reactive oxygen species (ROS) under physiological conditions. Concurrently, this system depletes intracellular glutathione (GSH), converting it to oxidized glutathione (GSSG), and thereby disrupts redox homeostasis in tumor microenvironments. The acidic pH further enhances GSH oxidation, demonstrating the potential of Bi@MOF-303 as a pH-responsive, self-driven ROS amplifier. Live/dead cell staining assay validated the findings, revealing that Bi@MOF-303 had the highest percentage of cell death. This was due to significant oxidative stress caused by its self-driven electron transfer and depletion of GSH. Our innovative protocol, which emphasizes the accumulation of ROS in cancer cells through self-driven electron transfer, highlights the importance of central metal selection and its impact on electrical behavior and active species production for the first time. - Source: PubMed
Publication date: 2026/04/11
Miri Omid FeghheRamazani AliMorsali AliTarasi Somayeh - Muscle biopsy has long been regarded as the cornerstone for diagnosing pediatric muscular disorders; however, it is invasive and may be limited by sampling error and inconclusive histopathological findings. This study aimed to evaluate whether whole-exome sequencing (WES) can effectively replace muscle biopsy as a first-line diagnostic approach in children with suspected neuromuscular disorders. Between January 2018 and December 2025, we prospectively enrolled 47 pediatric patients presenting with clinical features suggestive of muscular disorders at a tertiary medical center in Taiwan. The cohort included patients with suspected muscular dystrophies ( = 21), congenital myopathies ( = 23), and multiplex ligation-dependent probe amplification (MLPA)-negative Duchenne muscular dystrophy (DMD; = 3). All patients underwent WES as the initial diagnostic test without prior muscle biopsy. Trio-based analysis using parental samples was performed in 29.8% of cases. Variant interpretation followed the American College of Medical Genetics and Genomics (ACMG) guidelines. WES identified a definitive molecular diagnosis in 72.3% of patients (34/47). Diagnostic yields varied by subgroup: 100% (3/3) in MLPA-negative DMD, 71.4% (15/21) in muscular dystrophies, and 69.6% (16/23) in congenital myopathies. Pathogenic or likely pathogenic variants were detected in 31 distinct genes, including COL6A1 and COL6A3, which are associated with Ullrich congenital muscular dystrophy. Notably, 58.8% of diagnosed patients (20/34) received molecular diagnoses that differed from their initial clinical impression, encompassing conditions such as ZSWIM6-associated neurodevelopmental disorders, GJB2-related hearing loss, OCRL-associated Lowe syndrome, and various metabolic or syndromic disorders. In all three MLPA-negative DMD cases, WES identified point mutations amenable to mutation-specific therapies. No patient required a muscle biopsy for diagnostic confirmation during the study period. First-tier WES demonstrates high diagnostic utility in pediatric muscular disorders while avoiding invasive muscle biopsy. The high rate of diagnostic reclassification underscores the substantial phenotypic overlap between primary neuromuscular diseases and other neurological or systemic conditions. These findings support the early implementation of genetic testing to enable accurate diagnosis and timely initiation of targeted therapies. - Source: PubMed
Publication date: 2026/03/06
Lee Chung-LinChang Ya-HuiChuang Chih-KuangChiu Huei-ChingTu Yuan-RongLo Yun-TingWu Jun-YiLin Hsiang-YuLin Shuan-Pei