LRRC33 Blocking Peptide
- Known as:
- LRRC33 Blocking Peptide
- Catalog number:
- 33r-3389
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- LRRC33 Blocking Peptide
Related genes to: LRRC33 Blocking Peptide
- Gene:
- NRROS NIH gene
- Name:
- negative regulator of reactive oxygen species
- Previous symbol:
- LRRC33
- Synonyms:
- UNQ3030, ELLP3030, MGC50789, GARPL1
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-25
- Date modifiied:
- 2014-11-18
Related products to: LRRC33 Blocking Peptide
Related articles to: LRRC33 Blocking Peptide
- Traumatic brain injury (TBI) elicits robust neuroinflammation and oxidative stress, coupled with an acute inhibition of macro-autophagy (autophagy) in neurons and microglia. Rubicon (), a Beclin1 interacting protein that suppresses autophagy and mediates LC3-associated phagocytosis and endocytosis (LAP/LANDO), influences inflammatory signaling in metabolic, neurodegenerative, and inflammaging diseases; yet its role in acquired brain injury has not been defined. Using a controlled cortical impact model, we investigated the role of Rubicon in acute neuroinflammatory responses following injury by comparing wild-type and -mutant mice. Bulk-RNA sequencing of injured cortex revealed attenuated induction of inflammatory pathways and reduced activation of pro-inflammatory microglial/macrophage phenotype in injured -mutant mice. -mutant mice demonstrated less pronounced inhibition of autophagy during the acute phase of injury. Although the inflammatory differences were transient, Rubicon mutant mice exhibited improved motor coordination and gait stability during recovery. Proteomic analyses revealed the presence of a truncated Rubicon protein in the mutant mice and identified the negative regulator of reactive oxygen species (NRROS) as a novel interactor of Rubicon. Consistent with this interaction, -mutant mice displayed markedly reduced oxidative damage, indicated by decreased lipid peroxidation after injury. Together, these findings indicate that Rubicon promotes acute neuroinflammatory and oxidative stress responses following TBI by modulating autophagy and ROS production. Rubicon mediated pathways may serve as therapeutic targets that offer a neuroprotective strategy to improve outcomes after TBI. - Source: PubMed
Publication date: 2026/03/06
Thapa SagarinaMehrabani-Tabari AmirPettyjohn-Robin OliviaNguyen Dexter PhWeldemariam Mehari MSarkar ChinmoyKhan MaryamKane Maureen ALipinski Marta M - Bone defects, caused by diseases or trauma, significantly impact patients' quality of life. While porous Tantalum (pTa) scaffolds have shown promise in bone defect repair due to their excellent properties, their bioinert nature cannot meet the bioactive stimulation required for bone regeneration. To address these challenges, this study designed a composite scaffold composed of a 3D-printed pTa scaffold and a silk fibroin-crosslinked polyvinyl alcohol (SP) hydrogel loaded with whitlockite (WH). WH, a secondary inorganic component of bone tissue, was incorporated into the hydrogel to enhance its osteogenic, angiogenic and anti-inflammatory properties. The optimal proportions of PVA and WH were determined through extensive experiments. The resulting scaffold, designated as SP-pTa@WH, demonstrated remarkable biocompatibility and effectively promoted bone tissue repair in vitro and in vivo. Mechanistic studies revealed that SP-pTa@WH significantly modulated macrophage polarization towards the M2 phenotype and upregulated the expression of key osteogenic genes. High-throughput gene sequencing analysis further identified the TGF-β signaling pathway, particularly the NRROS gene, as critical in mediating the anti-inflammatory effects of SP-pTa@WH. Overall, this study provides a novel composite scaffold with enhanced osteogenic and immunomodulatory capabilities, offering broad prospects for clinical applications in bone defect repair. - Source: PubMed
Publication date: 2025/11/07
Ge BingJiao HaolinXu JianfengWu DiXie QinwenZheng GuoshuangCao FangYin GuangxiaoZhao DeweiLi Junlei - The central nervous system (CNS) represents a uniquely immune-privileged environment, with inflammatory responses involving several resident CNS-specific cell types. While stereotyped cellular and transcriptional responses recur across varied diseases, relevant signaling pathways and regulatory networks are not fully understood. Here, we investigate multi-modal inflammatory gene networks at large scale by developing a high-throughput RNA-seq screening and analysis workflow. As proof-of-concept, we investigate genetically heterogeneous mice from a large-scale chemical mutagenesis screen to identify novel functionally relevant variants in six genes previously linked to human CNS disorders: Nrros, Ctsd, Smpd1, Idua, Nlrp1a, and Inpp5d. We leverage the readily interpretable data from our large-scale study to demarcate distinct inflammatory states arising from each mutation. In all, our work provides a validated analysis framework for identifying discrete gene expression modules that are engaged divergently across disease contexts, which can be used to discover novel regulators of CNS neuroimmune homeostasis. - Source: PubMed
Publication date: 2025/09/29
Xiong MonicaMiosge Lisa ACorrea-Ospina CarolinaYan Claudia M YCripps TiffanyBauernfried StefanWang YuanyuanCrow MaggieMorris Lucy XAndrews T DanielTrujillo AndrewRezzonico Mitchell GLiang YuxinBei QixinModrusan ZoraStark Kimberly LYuen Tracy JFriedman Brad AHanson Jesse EBertram Edward MBohlen Christopher J - Negative regulator of reactive oxygen species ()-related microgliopathy (MIM# 618875) is a rare autosomal recessive neurodegenerative disorder. This case report describes a Saudi Arabian child with a novel homozygous variant, NM_198565.2: c.257T>C (p.Leu86Pro) presenting with drug-resistant epilepsy, rapid developmental regression, microcephaly, dystonia, and intracranial calcifications. Neuroimaging revealed bilateral intracranial calcifications, generalized brain volume loss, and connatal cysts; EEG showed a slow, suppressed background with multifocal epileptiform discharges. The variant is predicted to be deleterious by multiple in silico tools, suggesting a pathogenic effect on microglial function. This case underscores the importance of considering -related microgliopathy in children with early-onset neurodegeneration, drug-resistant epilepsy, and intracranial calcifications, enabling targeted genetic testing, diagnosis, and counseling. - Source: PubMed
Publication date: 2025/05/30
Al-Omari Mohammed A - Biallelic variants in NRROS are associated with the rare entity of seizures, early-onset, with neurodegeneration and brain calcification (SENEBAC). Here, we report a novel loss of function variant c.720G>A, p.(Trp240*) in a patient with the clinical presentation of developmental regression, refractory seizures, and intracranial calcification. The notable clinical features included normal early development followed by regression of milestones, dysmorphism, microcephaly, refractory seizures, absent deep tendon reflexes, and hypotonia. Neuroimaging features included cerebral atrophy, thin corpus callosum, and white matter calcifications. The phenotype observed in the current report overlaps strongly with the reported phenotype in literature; however, areflexia and dysmorphic features have not been reported before with this entity. A total of 11 individuals have been reported to date. Here, we present a detailed description of the phenotype in an Indian child, expanding the clinical and molecular spectrum of NRROS-related syndrome. - Source: PubMed
Publication date: 2024/10/18
Srinivasan Varunvenkat MGowda Vykuntaraju KMarkose Annsmol PKinhal Uddhava VPandey Himani