OPN1SW

Last update 08 May 2025

Basic Info

Synonyms

BCP, blue cone photoreceptor pigment, blue-sensitive opsin

+ [7]

Introduction

Visual pigments are the light-absorbing molecules that mediate vision. They consist of an apoprotein, opsin, covalently linked to cis-retinal (Probable). Required for the maintenance of cone outer segment organization in the ventral retina, but not essential for the maintenance of functioning cone photoreceptors (By similarity). Involved in ensuring correct abundance and localization of retinal membrane proteins (By similarity). May increase spectral sensitivity in dim light (By similarity).

100 Clinical Results associated with OPN1SW

100 Translational Medicine associated with OPN1SW

0 Patents (Medical) associated with OPN1SW

676

Literatures (Medical) associated with OPN1SW

31 Dec 2025·Emerging Microbes & Infections

Mechanisms underlying delayed loss of HBeAg and HBV DNA following HBsAg seroclearance in PEG-IFNα treated patients of chronic hepatitis B

Article

Author: Jiang, Bei ; Li, Minghui ; Cao, Zhenhuan ; Chen, Xiangmei ; Guan, Guiwen ; Zhao, Kaitao ; Lu, Fengmin ; Guo, Yifei ; Gu, Zhiqiang ; Xia, Yuchen ; Zhang, Jiming ; Wang, Lin ; Gu, Weilin ; Yuen, Man-fung

BACKGROUND & AIMSA notable proportion of CHB patients undergoing PEG-IFNα based therapy experience lagged serum HBeAg and/or HBV DNA disappearance in patients achieving HBsAg loss. In this study, we explored the molecular mechanisms behind this clinical phenomenon, offering novel insights into the sustainability of chronic HBV infection.METHODSTwo independent clinical cohorts were enrolled to validate this phenomenon. Then comprehensive analysis was performed using public datasets, coupled with a series of molecular biology experiments.RESULTSApproximately 17-20% CHB patients underwent PEG-IFNα based therapy experienced seroclearance of HBsAg, while serum HBeAg and/or HBV DNA remained positive. These patients are more prone to serum HBsAg reappearance compared to those achieving complete virological response. Analysis of public datasets revealed that compared to the PC/BCP, the SP1/SP2 promoter displayed more pronounced inhibitory epigenetic modifications in HBeAg-negative patients and SP1/SP2 in-frame mutation peaked in immune active patients. In vitro experiments demonstrated that introduced SP1/SP2 inactive mutations would enhance PC/BCP transcriptional activity by a mechanism known as adjacent transcriptional interference. Furthermore, the deletion of L-HBsAg facilitated intracellular cccDNA replenishment.CONCLUSIONThis study elucidates that under IFNα treatment and low viral load, transcriptional suppression of SP1/SP2 promoters through mutations and/or epigenetic changes would favour the maintenance of sustain chronic HBV infection, via enhancing the transcription activity of BCP to promote cccDNA replenishment.IMPACT AND IMPLICATIONSIn clinical practice with IFNα antiviral treatment for CHB patients, a "paradoxical" phenomenon is observed where serum HBsAg disappears while HBV DNA or/and HBeAg remains at low positive levels, with delayed disappearance. Our study confirms this clinical phenomenon using two independent clinical cohorts and explores the potential mechanisms behind the persistence of chronic HBV infection under IFNα treatment and low viral load. Transcriptional suppression of SP1/SP2 promoters through mutations and/or epigenetic changes supports the maintenance of chronic HBV infection by enhancing the transcriptional activity of the BCP, which in turn promotes cccDNA replenishment.HighlightsApproximately 20% of patients with CHB who have just achieved HBsAg loss under IFNα treatment show positive serum HBV DNA and/or HBeAg.During disease progression, in frame indel mutations accumulate in the HBV genome's SP1 and SP2 promoters, with epigenetic modifications contributing to their suppression.In frame indel mutations in the HBV genome's SP1 and SP2 promoters inhibit the transcription of HBV S mRNA and promote the transcription of 3.5 kb HBV RNA.The loss of L-HBs and envelop proteins leads to an increase in intracellular cccDNA, promoting the maintenance of chronic infection.

09 Apr 2025·mBio

Defense arsenal of the strict anaerobe Clostridioides difficile against reactive oxygen species encountered during its infection cycle

Article

Author: Morvan, Claire ; Alves Feliciano, Carolina ; Martin-Verstraete, Isabelle ; Martins Alves, Catarina ; Caulat, Léo ; Folgosa, Filipe ; Lotoux, Aurélie

ABSTRACTClostridioides difficile , a strict anaerobe, is the major cause of antibiotic-associated diarrhea. This enteropathogen must adapt to oxidative stress mediated by reactive oxygen species (ROS), notably those released by the neutrophils and macrophages recruited to the site of infection or those endogenously produced upon high oxygen (O 2 ) exposure. C. difficile uses a superoxide reductase, Sor, and several peroxidases to detoxify ROS. We showed that Sor has a superoxide reductase activity in vitro and protects the bacterium from exposure to menadione, a superoxide donor. After confirming the peroxidase activity of the rubrerythrin, Rbr, we showed that this enzyme together with the peroxiredoxin, Bcp, plays a central role in the detoxification of H 2 O 2 and promotes the survival of C. difficile in the presence of not only H 2 O 2 but also air or 4% O 2 . Under high O 2 concentrations encountered in the gastrointestinal tract, the bacterium generated endogenous H 2 O 2 . The two O 2 reductases, RevRbr2 and FdpF, have also a peroxidase activity and participate in H 2 O 2 resistance. The CD0828 gene, which also contributes to H 2 O 2 protection, forms an operon with rbr , sor , and perR encoding a H 2 O 2 -sensing repressor. The expression of the genes encoding the ROS reductases and the CD0828 protein was induced upon exposure to either H 2 O 2 or air. We showed that the induction of the rbr operon is mediated not only by PerR but also by OseR, a recently identified O 2 -responsive regulator of C. difficile , and indirectly by σ B , the sigma factor of the stress response, whereas the expression of bcp is only controlled by σ B . IMPORTANCE ROS plays a fundamental role in intestinal homeostasis, limiting the proliferation of pathogenic bacteria. Clostridioides difficile is an important enteropathogen that induces an intense immune response, characterized by the massive recruitment of immune cells responsible for secreting ROS, mainly H 2 O 2 and superoxide. We showed in this work that ROS exposure leads to the production of an armada of enzymes involved in ROS detoxification. This includes a superoxide reductase and four peroxidases, Rbr, Bcp, revRbr2, and FdpF. These enzymes likely contribute to the survival of vegetative cells of C. difficile in the colon during the host immune response. Distinct regulations are also observed for the genes encoding the ROS detoxification enzymes allowing a fine tuning of the adaptive response to ROS exposure. Understanding the mechanisms of ROS protection during infection could shed light on how C. difficile survives under conditions of an exacerbated inflammatory response.

26 Mar 2025·Neuro-oncology

Co-occurrence of congenital anomalies and childhood brain tumors in 22 million live births.

Article

Author: Yazdy, Mahsa ; Plon, Sharon E ; Nestoridi, Eirini ; Janitz, Amanda E ; Huff, Chad D ; Scheurer, Michael E ; Shumate, Charles ; Tanner, J P ; Salemi, Jason L ; Schraw, Jeremy M ; Taylor, Michael D ; Chambers, Tiffany M ; Desrosiers, Tania A ; Hoang, Thanh T ; Kirby, Russell S ; Lupo, Philip J ; Nembhard, Wendy N

BACKGROUNDChildren born with a congenital anomaly have a higher risk of developing a brain tumor during childhood or adolescence, but the co-occurrence between specific types of congenital anomalies and specific types of childhood brain tumors (CBTs) is not well described. This study characterized the associations between specific congenital anomalies and CBTs.METHODSWe leveraged a population-based registry linkage study of births (1990-2018), congenital anomalies, and cancer from nine states (n=22,599,099 births). Congenital anomalies were classified as major structural without a known chromosomal or genetic syndrome, chromosomal, neurofibromatosis, and/or tuberous sclerosis complex. CBT classification was based on the International Classification of Childhood Cancer for children diagnosed <20 years. Cox regression analyses were conducted separately by congenital anomaly for anomaly-CBT combinations with at least 5 co-occurring cases. We conducted analyses for any CBT and separately for astrocytoma, atypical teratoid/rhabdoid tumor, ependymoma, medulloblastoma, mixed and unspecified gliomas, and primitive neuroectodermal tumors.RESULTSThere were 6,247 children diagnosed with a CBT. Having any major structural anomaly was associated with risk of any CBT and across all subgroups (aHR range: 1.48-3.69) except ependymoma, particularly among children diagnosed with a tumor by 1 year of age. Of the 66 anomaly-CBT combinations analyzed, 42 were significant (p<0.05), including 25 in an earlier version of this study and 16 novel associations (aHR range: 1.46-525). Anomaly-CBT associations also differed by astrocytoma histology.CONCLUSIONSWe observed consistent evidence that having a structural congenital anomaly increases risk of developing a CBT, particularly in infancy, which may provide insights into etiology.

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