Ask about this productRelated genes to: LDLRAD3 Blocking Peptide
- Gene:
- LDLRAD3 NIH gene
- Name:
- low density lipoprotein receptor class A domain containing 3
- Previous symbol:
- -
- Synonyms:
- LRAD3
- Chromosome:
- 11p13
- Locus Type:
- gene with protein product
- Date approved:
- 2005-10-07
- Date modifiied:
- 2014-11-18
Related products to: LDLRAD3 Blocking Peptide
Related articles to: LDLRAD3 Blocking Peptide
- Gastrointestinal (GI) cancers remain a leading cause of cancer-related mortality worldwide, underscoring the urgent need for reliable, non-invasive diagnostic biomarkers. Circular RNAs (circRNAs), characterized by high stability and tissue specificity, have emerged as promising molecular indicators for early cancer detection. This study aimed to evaluate the diagnostic accuracy of circular RNAs (circRNAs) for detecting gastrointestinal (GI) cancers, including gastric cancer (GC), hepatocellular carcinoma (HCC), esophageal cancer (EC), colorectal cancer (CRC), and pancreatic cancer (PC). - Source: PubMed
Publication date: 2025/12/18
Bahramirad JilaMoradi YousefMoradi GhobadDehghanbanadaki HojatAbdi MohammadNasseri Sherko - Venezuelan (VEEV), eastern (EEEV), and western (WEEV) equine encephalitis viruses are alphaviruses from different serocomplexes that cause neurological disease in humans. Given their antigenic distance, it has been challenging to isolate cross-reactive antibodies that neutralize infection by multiple medically relevant encephalitic alphaviruses. Recently, distinct entry receptors were identified for these encephalitic alphaviruses: LDLRAD3 for VEEV, VLDLR for EEEV and some strains of WEEV, and PCDH10 for WEEV. Here, using structure-guided mutagenesis, we generated a soluble chimeric protein derived from the LA1 domain of LDLRAD3 and the LA2 domain of VLDLR, termed LDLRAD3-vLA1-VLDLR-LA2, which neutralized infection by VEEV, EEEV, and some WEEV strains in cell culture and protected mice from infection. Structural analysis of this engineered decoy revealed binding to distinct sites on each virus, which corresponded to those engaged by their endogenous entry receptors. We extended the neutralizing and protective capacity to contemporary WEEV strains by adding a single extracellular cadherin domain from sparrow PCDH10 through a stabilized symmetric bispecific decoy scaffold. Our designed receptor decoy serves as a possible countermeasure against multiple encephalitic alphaviruses, and this design platform could be harnessed to develop therapeutic agents against viruses from other families. - Source: PubMed
Publication date: 2026/04/08
Palakurty SathvikRaju SaravananSariol AlanWagoner NganGilliland Theron CKlimstra William BDiamond Michael S - Variants linked to the risk of ischemic stroke have been discovered through genome-wide association studies (GWASs). These variations frequently have little consequences that lack apparent biological significance. Hence, these findings demonstrate that exome sequencing can be highly relevant to stroke, even though stroke is a complex phenotype with various diseases and risk factors. - Source: PubMed
Publication date: 2026/01/27
Hamadi AbdullahMir RashidAl-Amer Osama MAlasseiri MohammedAlZamzami WaseemAlatawi SaelAlanazi Mohammad AMoawadh Mamdoh SOyouni Atif Abdulwahab AAl Tuwaijri AbeerAlthenayyan SalehMadkhali Hassan AAlserihi Raed - Venezuelan equine encephalitis virus (VEEV) poses a significant public health and biodefense threat due to periodic epidemics of severe neurological disease in the Americas, yet no licensed human vaccines or specific antiviral therapies exist. - Source: PubMed
Publication date: 2025/12/24
Tang RuiWang DaojingChen GuojiangLiu ChenghuaZhang LiangPeng FenghaoYu JijunLi XinyingLuo HengWen YanQiao Chunxia - Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), remains a major public health threat, particularly in vulnerable populations. SARS-CoV-2 spike proteins interact with the human angiotensin-converting enzyme 2 (ACE2) receptor, together with accessory molecules that facilitate viral entry, through its spike receptor-binding domain (RBD). Although ACE2 is the primary receptor required for viral replication, its expression patterns do not fully correlate with viral distribution or tissue pathology. Moreover, SARS-CoV-2 has been shown to infect cells and tissues lacking detectable ACE2 expression. Viral entry via ACE2-independent pathways may also confer resistance to some monoclonal antibodies (Abs) targeting the spike RBD that block ACE2-mediated binding. These observations highlight the potential significance of ACE2-independent entry factors in SARS-CoV-2 infection, particularly in vaccinated individuals with Abs directed against ACE2-dependent viral entry. In this review, we discuss the emerging roles of ACE2-independent entry factors in SARS-CoV-2 infection and the immune responses. These factors include CD147, AXL, CD169/Siglec-1, CD209L, CD209, CLEC4G, ASGR1, LDLRAD3, TMEM30A, TMEM106B, transferrin receptor 1, GPR78, integrin α5β1, KREMEN1, LFA-1, and CD4. While ACE2 remains central to viral replication, ACE2-independent entry appears sufficient to elicit immune responses. Therefore, future investigations are warranted to elucidate the roles of ACE2-independent mechanisms in immune-mediated pathology and viral evolution, independent of immune pressure targeting ACE2-mediated entry in previously infected or vaccinated individuals. - Source: PubMed
Publication date: 2025/12/22
Sun YiyuWong Lok-Yin RoyChang Theresa L