Ask about this productRelated genes to: LYPD4 antibody
- Gene:
- LYPD4 NIH gene
- Name:
- LY6/PLAUR domain containing 4
- Previous symbol:
- -
- Synonyms:
- MGC42718
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-08-30
- Date modifiied:
- 2015-07-22
Related products to: LYPD4 antibody
Related articles to: LYPD4 antibody
- Assisted reproductive technologies, such as fertilization, remain inefficient in camelids, largely due to gaps in understanding the molecular interactions that regulate sperm capacitation. Fertilization requires not only viable spermatozoa but also the precise modulation of capacitation by the peri-ovulatory microenvironment, including follicular fluid (FF) and oviductal fluid (OF). In this study, spermatozoa were incubated in Fert-TALP medium supplemented with FF or OF, and both functional outcomes and proteomic remodeling were assessed. Sperm treatments were evaluated in five independent biological replicates per individual (three individuals), with triplicate proteomics performed. FF ( = 20) was collected from pre-ovulatory follicles (7-9 mm) and OF ( = 10) from the corresponding ipsilateral oviducts, thereby reflecting the environment encountered by sperm in the female reproductive tract following mating. Incubation with FF enhanced progressive motility by 72%, rapid progressive motility by 169%, viability by 30%, and acrosome responsiveness by 30%, and was associated with a proteomic shift involving ~12% of proteins ( < 0.05). These included factors implicated in zona pellucida binding (LYPD4, PGK1, ANXA2, and TCP1 complex members) and galactose metabolism (MAOA, AKR1B1, GLA, and HK1). The enriched processes included glycolysis/gluconeogenesis, cytoskeletal reorganization, and protein maturation, all consistent with sperm capacitation. By contrast, sperm incubated with OF showed an underrepresentation of capacitation-related pathways, including the proteasome complex, sperm fibrous sheath, and TCA cycle. Moreover, the OF proteome ( = 2) revealed decapacitation-associated factors such as PEBP1 and PAFAH1B3, which likely stabilize membranes and delay premature capacitation. Together, these findings demonstrate complementary yet contrasting roles of FF and OF in modulating sperm physiology: FF acting as a capacitating medium, and OF providing a stabilizing environment. This study presents the first partial proteome of capacitated alpaca sperm together with matched reproductive fluids, providing mechanistic insights with direct implications for improving assisted reproduction in camelids. - Source: PubMed
Publication date: 2025/11/06
Torres Hualla Edith AMartiarena AlbaBuglio Ballesteros María GabrielaMedina Rojas Maribel FortunataRivera Chino CristianGandarillas Espezua DanielArgañaraz Martin E - More than 20 genes expressed in the male reproductive tract have been identified as essential factors for sperm migration to and through the utero-tubal junction (UTJ), and they are divided into ADAM3-dependent and ADAM3-independent pathways. In parallel, sperm having UTJ migration defects also show impaired binding to the zona pellucida (ZP). Herein, we demonstrate that knockout of Galntl5, encoding a sperm surface protein, causes impaired sperm binding with the UTJ and ZP, and null males have severe infertility. GALNTL5 appreciably disappears in sperm lacking Adam3 or Lypd4, required for ADAM3-dependent and ADAM3-independent pathways, and GALNTL5 binds to N-acetylgalactosamine (GalNAc) distributed on the UTJ and ZP. Blockage of GalNAc decreases the number of sperm binding to the UTJ and ZP. Thus, we unveil that GALNTL5 is a responsible factor for UTJ migration and sperm-ZP binding, and that sperm bind to the UTJ and ZP through interaction of GALNTL5 and GalNAc. - Source: PubMed
Publication date: 2025/09/17
Noda TaichiUriu ReikaMashiko DaisukeShinohara HinaQu YongcunTaira AyumuMatzuk Ryan MTahala DuriNakano MotochikaAraki KimiYu ZhifengZhang YingMatzuk Martin MIkawa Masahito - Background: Critical illness stemming from severe traumatic injury is a leading cause of morbidity and mortality worldwide and involves the dysfunction of multiple organ systems, driven, at least in part, by dysregulated inflammation. We and others have shown a key role for genetic predisposition to dysregulated inflammation and downstream adverse critical illness outcomes. Recently, we demonstrated an association among genotypes at the single-nucleotide polymorphism (SNP) rs10404939 in LYPD4 , dysregulated systemic inflammation, and adverse clinical outcomes in a broad sample of ~1,000 critically ill patients. Methods: We sought to gain mechanistic insights into the role of LYPD4 in critical illness by bioinformatically analyzing potential interactions among rs10404939 and other SNPs. We analyzed a dataset of common (i.e., not rare) SNPs previously defined to be associated with genotype-specific, significantly dysregulated systemic inflammation trajectories in trauma patients, in comparison to a control dataset of common SNPs determined to exhibit an absence of genotype-specific inflammatory responses. Results: In the control dataset, this analysis implicated SNPs associated with phosphatidylinositol and various membrane transport proteins, but not LYPD4. In the patient subset with genotypically dysregulated inflammation, our analysis suggested the co-localization to lipid rafts of LYPD4 and the complement receptor CD55, as well as the neurally related CNTNAP2 and RIMS4. Segregation of trauma patients based on genotype of the CD55 SNP rs11117564 showed distinct trajectories of organ dysfunction and systemic inflammation despite similar demographics and injury characteristics. Conclusion: These analyses define novel interactions among SNPs that could enhance our understanding of the response to traumatic injury and critical illness. - Source: PubMed
Publication date: 2024/08/12
El-Dehaibi FaytenZamora RubenYin JinlingNamas Rami ABilliar Timothy RVodovotz Yoram - Resilience is the capacity to adapt to stressful life events. As such, this trait is associated with physical and mental functions and conditions. Here, we aimed to identify the genetic factors contributing to shape resilience. We performed variant- and gene-based meta-analyses of genome-wide association studies from six German cohorts (N = 15822) using the 11-item version of the Resilience Scale (RS-11) as outcome measure. Variant- and gene-level results were combined to explore the biological context using network analysis. In addition, we conducted tests of correlation between RS-11 and the polygenic scores (PGSs) for 12 personality and mental health traits in one of these cohorts (PROCAM-2, N = 3879). The variant-based analysis found no signals associated with resilience at the genome-wide level (p < 5 × 10), but suggested five genomic loci (p < 1 × 10). The gene-based analysis identified three genes (ROBO1, CIB3 and LYPD4) associated with resilience at genome-wide level (p < 2.48 × 10) and 32 potential candidates (p < 1 × 10). Network analysis revealed enrichment of biological pathways related to neuronal proliferation and differentiation, synaptic organization, immune responses and vascular homeostasis. We also found significant correlations (FDR < 0.05) between RS-11 and the PGSs for neuroticism and general happiness. Overall, our observations suggest low heritability of resilience. Large, international efforts will be required to uncover the genetic factors that contribute to shape trait resilience. Nevertheless, as the largest investigation of the genetics of resilience in general population to date, our study already offers valuable insights into the biology potentially underlying resilience and resilience's relationship with other personality traits and mental health. - Source: PubMed
Publication date: 2024/08/08
Herrera-Rivero MarisolGarvert LindaHorn KatrinLöbner MargritWeitzel Elena CarolineStoll MonikaLichtner PeterTeismann HenningTeumer AlexanderVan der Auwera SandraVölzke HenryVölker UweAndlauer Till F MMeinert SusanneHeilmann-Heimbach StefanieForstner Andreas JStreit FabianWitt Stephanie HKircher TiloDannlowski UdoScholz MarkusRiedel-Heller Steffi GGrabe Hans JBaune Bernhard TBerger Klaus - Acute inflammation is heterogeneous in critical illness and predictive of outcome. We hypothesized that genetic variability in novel, yet common, gene variants contributes to this heterogeneity and could stratify patient outcomes. We searched algorithmically for significant differences in systemic inflammatory mediators associated with any of 551,839 SNPs in one derivation (n = 380 patients with blunt trauma) and two validation (n = 75 trauma and n = 537 non-trauma patients) cohorts. This analysis identified rs10404939 in the gene. Trauma patients homozygous for the A allele (rs10404939AA; 27%) had different trajectories of systemic inflammation along with persistently elevated multiple organ dysfunction (MOD) indices vs. patients homozygous for the G allele (rs10404939GG; 26%). rs10404939AA homozygotes in the trauma validation cohort had elevated MOD indices, and non-trauma patients displayed more complex inflammatory networks and worse 90-day survival compared to rs10404939GG homozygotes. Thus, rs10404939 emerged as a common, broadly prognostic SNP in critical illness. - Source: PubMed
Publication date: 2023/10/28
El-Dehaibi FaytenZamora RubenRadder JosiahYin JinlingShah Ashti MNamas Rami ASitu MichelleZhao YanwuBain WilliamMorris AlisonMcVerry Bryan JBarclay Derek ABilliar Timothy RZhang YingzeKitsios Georgios DVodovotz Yoram