OCT

Last update 08 May 2025

Basic Info

Synonyms

FLJ11751, FLJ30634, KIAA0463

+ [6]

Introduction

Coreceptor for SEMA3A and SEMA6A. Necessary for signaling by SEMA6A and class 3 semaphorins and subsequent remodeling of the cytoskeleton. Plays a role in axon guidance, invasive growth and cell migration. Class 3 semaphorins bind to a complex composed of a neuropilin and a plexin. The plexin modulates the affinity of the complex for specific semaphorins, and its cytoplasmic domain is required for the activation of down-stream signaling events in the cytoplasm (By similarity).

100 Clinical Results associated with OCT

100 Translational Medicine associated with OCT

0 Patents (Medical) associated with OCT

1,061

Literatures (Medical) associated with OCT

13 Feb 2025·Journal of Medicinal Chemistry

Kidney Targeting Smart Antibiotic Discovery: Multimechanism Pleuromutilins for Pyelonephritis Therapy

Article

Author: Tian, Lei ; Wang, Yongbo ; Xia, Juan ; Lu, Qi ; Zhang, Boxin ; Yang, Xiuding ; Hu, Jinrong ; Zhang, Dezhu ; Liu, Yuting ; Zhang, Jiayun ; Liang, Chengyuan ; Qiang, Taotao ; Kang, Kairui ; Li, Jialin ; Gao, Hong

Multidrug-resistant (MDR) bacteria pose a global health threat, underscoring the need for new antibiotics. Lefamulin, the first novel-mechanism antibiotic approved by the FDA in decades, showcases pleuromutilins' promise due to low mutation frequency. However, their clinical use is limited by poor pharmacokinetics and organ toxicity. To overcome these limitations, we modified lefamulin's C14 side chain via quaternization and incorporated rigid molecular fragments to enhance pharmacological properties. Introducing a quaternary ammonium group improved liver and kidney targeting via organic cation transporters (OCTs). Candidate 8i, a quaternized imidazo[4,5-c]pyridine pleuromutilin, demonstrated broad-spectrum activity against MDR bacteria, Mycoplasma and Chlamydophila at low doses. 8i targeted transport to infected kidneys, disrupted biofilms, damaged membranes, and inhibited protein synthesis by targeting 50S ribosomal subunit. It cleared rapidly, reducing long-term toxicity. Daily injections were an effective short-course treatment for systemic infections and pyelonephritis. This research presents a novel OCT-mediated, organ-targeted antibiotic design strategy to manage antibiotic-resistant infections.

01 Feb 2025·Journal of Hazardous Materials

Influence of atomic coordination on the activity of lattice oxygen and catalytic oxidation of toluene over regular Cu2O crystalline

Article

Author: Zhao, Zitong ; Bin, Feng ; Gao, Xin ; Dou, Baojuan ; Yi, Xiaokun ; Deng, Linlin ; Li, Mingtai ; Zhao, Yang ; Yang, Yulong ; Chen, Jiarui

VOCs oxidation over transition metal catalyst is commonly understood via the Mars-van Krevelen mechanism involving the crucial role of lattice oxygen (O_L) activity, however, how it is influenced by atomic coordination is still unclear. Herein, we use model catalysts of Cu₂O-cub, Cu₂O-oct and Cu₂O-dod with crystal planes of (100), (111) and (110), respectively, to investigate the O_L activity and catalytic oxidation of toluene. The activity of Cu₂O-oct is found to be the highest, followed by Cu₂O-cub and Cu₂O-dod. Experiments results combined with density functional theory show that, although low di-coordinated O atoms leads to the lowest surface oxygen vacancy formation energy (2.47 eV) and the highest surface O_L activity of Cu₂O-cub, it cannot determine the activity. The lowest bulk oxygen vacancy formation energy (3.16 eV) in Cu₂O-oct terminated with tri-coordinated O atoms and open surface can accelerate the migration and replenishment of O_L, thereby promoting the catalytic activity.

28 Jan 2025·Investigative Ophthalmology & Visual Science

CAMK2D and Complement Factor I–Involved Calcium/Calmodulin Signaling Modulates Sodium Iodate-Induced Mouse Retinal Degeneration

Article

Author: Liu, Hua ; Xu, Weixing ; Cao, Liu

PurposeTo investigate the effect of Ca2+/calmodulin-dependent protein kinase II (CAMKII) δ subtypes (CAMK2D) on sodium iodate (NaIO3)-induced retinal degeneration in mice.MethodsBioinformatics analysis and Western blot experiments were used to screen the significantly differentially expressed genes in age-related macular degeneration (AMD) disease. CAMK2D knockdown and overexpression models were constructed by lentivirus (LV) infection of adult retinal pigment epithelial cell line-19 (ARPE-19) cells in vitro. Flow cytometry was used to detect ARPE-19 cell apoptosis induced by NaIO3. In vivo, CAMK2D knockdown and overexpression mouse models were generated by infecting mouse retinal pigment epithelium (RPE) with adeno-associated virus (AAV). Retinography, optical coherence tomography (OCT), and histological analysis (hematoxylin and eosin staining) were used to detect NaIO3-induced retinal structural changes in mice. Electroretinography (ERG) was used to detect NaIO3-induced retinal function changes in mice. TdT-mediated dUTP nick-end labeling (TUNEL) staining was used to detect the apoptosis of retinal cells induced by NaIO3. RNA sequencing (RNA-Seq) and bioinformatics analysis were used to screen for target genes affected by CAMK2D in CAMK2D-overexpressing ARPE-19 cells. And flow cytometry, OCT, and ERG were used to evaluate the regulatory effect of CAMK2D on target genes.ResultsBioinformatics analysis found the expression of genes related to Ca2+ signal was significantly reduced in AMD patients. Western blot showed that in a mouse model of dry AMD induced by NaIO3, CAMK2D expression in RPE-Choroid tissue significantly lower than normal mice. In vitro, our results showed that overexpression of CAMK2D in ARPE-19 cells decreased apoptosis induced by NaIO3 and knockdown increased apoptosis. In vivo, CAMK2D overexpression in RPE cells can attenuate the retina degeneration induced by NaIO3 and CAMK2D knockdown aggravated degeneration. The bioinformatics analysis indicated that CAMK2D might affect AMD pathology through complement factor I (CFI). In vitro, knockdown of CFI in ARPE-19 cells increased apoptosis induced by NaIO3. In knockdown CFI ARPE-19 cells, overexpression of CAMK2D reduced the above apoptosis. In mice retina, CFI knockdown can aggravate the retina degeneration induced by NaIO3. In knockdown CFI mice, overexpression of CAMK2D in RPE can attenuate the above retina degeneration. Western blot confirmed that CAMK2D regulated the expression of CFI in mice.ConclusionsCAMK2D can attenuate the retinal degeneration induced by NaIO3, which was achieved by regulating the CFI.

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