Ask about this productRelated genes to: IL1RAPL1 antibody
- Gene:
- IL1RAPL1 NIH gene
- Name:
- interleukin 1 receptor accessory protein like 1
- Previous symbol:
- IL1RAPL, MRX34, MRX21, MRX10
- Synonyms:
- OPHN4, TIGIRR-2, IL1R8
- Chromosome:
- Xp21.3-p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-07
- Date modifiied:
- 2018-02-13
Related products to: IL1RAPL1 antibody
Related articles to: IL1RAPL1 antibody
- In livestock, understanding the genetic basis of adaptation to the environment is essential for enhancing resilience to climate change and sustaining productivity in diverse environments. Indigenous Ethiopian cattle represent an ideal model for such studies, as they have evolved across a wide range of environments from the cool, oxygen-limited highlands to the hot, pathogen-rich lowlands. These environmental gradients imposed intense selective pressures, shaping their genomic landscape. In this study, we performed the first comprehensive analysis of X-linked adaptive signatures in Ethiopian indigenous cattle using whole-genome sequencing data. - Source: PubMed
Publication date: 2026/04/10
Ayalew WondossenTarekegn Getinet MXiaoyun WuChu MinNaboulsi RakanTessema Tesfaye SBongcam-Rudloff ErikNegussie EnyewPing YanZhang Zhe - Alleviating hepatic lipid deposition in aging laying hens is critical for maintaining liver health and extending their productive lifespan. This study aimed to identify potential indicators and elucidate the underlying mechanisms associated with liver fat accumulation. Hepatic lipid ratio is a key indicator of the lipid deposition in the liver. A total of 509 healthy G1 line hens at 66 weeks of age were assessed for hepatic lipid ratio and stratified into three groups: low (L, <5%), medium (M, 5-10%), and high (H, >10%). The results revealed that the correlation coefficients of liver triglyceride (TG) and total cholesterol (TC) with the hepatic lipid ratio were 0.907 and 0.870, respectively, indicating a strong and highly significant association. All three metrics differed significantly among the three groups (P < 0.01), validating the grouping approach. Compared with the L group, the M and H groups showed significantly higher body weight, abdominal fat weight, abdominal fat index, plasma TG, TC, and LDL-c (P < 0.05), while plasma HDL-C was significantly lower in group H compared with groups L and M (P < 0.05). Abdominal skinfold thickness differed significantly across all groups (P < 0.05). Transcriptomic analysis revealed 115 up-regulated and 50 down-regulated genes in the H group compared with the L group. We identified: four genes (PCSK9, ABCG8, G6PC2, FOLH1) were associated with lipid metabolism; three (IL1RAPL1, TNIP2, HPSE2) with inflammatory response; five (CCL3, CCL17, CCL20, SAMSN1, ICOS) with immune response; and six (HBA1, HBAD, HBBA, CHAC1, CREG1, DDIT4) with antioxidant function. KEGG pathway analysis highlighted enrichments in lipid metabolism-related pathways such as "ABC transporters" and "Insulin secretion," as well as in the inflammatory response-related pathway "Cytokine-cytokine receptor interaction." In conclusion, body weight, abdominal skinfold thickness, plasma TG, TC, LDL-c, and HDL-c may serve as practical indicators for evaluating hepatic lipid deposition in laying hens. Excessive lipid accumulation perturbs hepatic metabolic homeostasis, triggering transcriptional reprogramming associated with both inflammatory and oxidative stress responses, alongside adaptive antioxidant defense and anti-inflammatory responses. However, further studies are required to determine whether these changes reflect a bona fide compensatory protective mechanism in the liver. - Source: PubMed
Publication date: 2026/03/13
Li YongfengWang XingguoTong HaibingQu LiangShao DanWang QiangGuo WeiGuo JunDou TaocunHu YupingLu JianMa MengFeng Chungang - Danzhou chicken (DZC) is a native chicken breed endemic to Hainan Island, which is renowned for its superior meat quality and strong disease resistance. Prolonged geographical isolation, coupled with natural and artificial selection events in response to the tropical environment, has significantly transformed the behavior, appearance, and economically important traits of DZC. However, the relatively small size of its conservation population has impeded research on the genetic mechanisms of specific traits and population genetics, exerting an adverse influence on resource conservation and commercial development. This study aims to investigate the formation mechanisms of environmental adaptability through a scanning analysis of population selection in DZC. - Source: PubMed
Publication date: 2026/02/02
Xie X FFan J WWang Z YZhong Z QPan D YShi L GXiao QHou G Y - X-linked adrenal hypoplasia congenita (AHC) is a rare, life-threatening disorder caused by pathogenic variants in NR0B1 (DAX1), leading to adrenal insufficiency and hypogonadotropic hypogonadism. AHC is often associated with Xp21 contiguous gene deletion syndrome, which involves the deletion of multiple genes, including NR0B1, GK, DMD, and IL1RAPL1, resulting in a spectrum of phenotypic manifestations, such as glycerol kinase deficiency (GKD), Duchenne muscular dystrophy (DMD), and neurodevelopmental disorders. We report two cases of AHC with neurodevelopmental delays due to contiguous Xp21 deletions involving NR0B1 and IL1RAPL1, each diagnosed through distinct clinical pathways. Case 1 involved a neonate with adrenal insufficiency, persistent hyperCKemia, and excessive urinary glycerol excretion, leading to a diagnosis of Xp21 deletion syndrome with DMD and GKD. The patient's sister, an asymptomatic carrier, exhibited elevated CK levels and mild developmental delays. Array comparative genomic hybridization identified a novel complex structural variation, including duplication-deletion-duplication rearrangement, which may have modified clinical manifestations. Case 2 involved a 10-year-old boy with AHC and developmental delay that was initially considered a consequence of adrenal crises. Genetic analysis confirmed an Xp21 deletion, including IL1RAPL1, implicating it in his intellectual disability. A literature review reveals that Xp21 deletions involving IL1RAPL1 are strongly associated with neurodevelopmental delays, suggesting a distinct phenotype within Xp21 deletion syndromes. Early genetic diagnosis via chromosomal microarray analysis facilitates precise delineation of deletion regions, aiding in clinical management, genetic counseling, and early intervention strategies. Further studies are needed to elucidate genotype-phenotype correlations in Xp21 deletion syndromes and optimize individualized medical care. - Source: PubMed
Publication date: 2025/11/22
Gau MakiIemura RyoseiOrimoto RyutaAdachi ErikoSaito YokoYamano HarukiNakatani HisaeKirino ShizukaKuno HarukaMoriyama KengoYamaguchi YoheiOitani YoshikiSugie ManabuMizuno TomokoIshii TakuYoshida MasayukiKashimada KenichiTakasawa Kei - Protein-tyrosine phosphatase receptor-type D (PTPRD) is an adhesion-coupled phosphatase that translates extracellular binding codes into intracellular phosphotyrosine signaling from embryogenesis through adulthood. Alternative inclusion of the Ig-domain mini-exons meA and meB tailors the ectodomain surface, thereby dictating high-affinity engagement with IL1RAPL1, IL1RAP, Slitrks, LRFN4/5 (SALM3/5), neuroligin-3, and other postsynaptic partners. Intracellularly, the catalytically active D1 domain and scaffold-like D2 module, anchored to liprin-α, coordinate presynaptic vesicle release, postsynaptic receptor composition, and synaptic plasticity. Beyond synapses, PTPRD restrains embryonic neurogenesis, promotes STAT3-dependent gliogenesis, accelerates oligodendrocyte myelination, and guides Sema3a/Fyn-mediated axon and dendrite patterning. In the adult brain it serves as the high-affinity hypothalamic and cerebellar receptor for asprosin, thereby coupling systemic energy and hydration states to feeding and drinking behavior. Human genetic studies and mouse models link these molecular activities to a spectrum of conditions-including restless legs syndrome, addiction, Alzheimer's disease, ADHD, OCD, autism spectrum disorder, and metabolic syndrome. Because PTPRD functions are pathway-specific and shaped by mini-exon usage or redundancy with other family members (PTPRS/PTPRF), domain- or ligand-selective interventions represent plausible therapeutic strategies. Elucidating its full ligand repertoire, substrate landscape, and structural basis for allosteric regulation will be critical for converting this versatile receptor from a mechanistic curiosity into a tractable target for neurodevelopmental, neuropsychiatric, and metabolic disorders. - Source: PubMed
Kim SeoyeongShin Jae JinKang MuwonYi YunhoKim Eunjoon