Ask about this productRelated genes to: INADL antibody
- Gene:
- PATJ NIH gene
- Name:
- PATJ crumbs cell polarity complex component
- Previous symbol:
- INADL
- Synonyms:
- Cipp
- Chromosome:
- 1p31.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-12-23
- Date modifiied:
- 2019-01-25
Related products to: INADL antibody
Related articles to: INADL antibody
- This study aims to elucidate the regulatory mechanisms of host genetics on the porcine gut microbiota and their subsequent impact on the feed conversion ratio (FCR). While initial genome-wide association studies (GWAS) did not identify significant SNPs directly associated with FCR, we investigated the gut microbiota as a potential intermediate phenotype influencing feed efficiency. Nonmetric multidimensional scaling (NMDS) based on Bray–Curtis distances demonstrated a distinct separation in microbial community structure between the high-feed conversion ratio (HFCR) and low-feed conversion ratio (LFCR) groups (stress = 0.19), suggesting a link between FCR and gut microbial composition. Furthermore, a significant, albeit weak, negative correlation was observed between the genomic relatedness matrices and microbial Bray‒Curtis dissimilarity ( = −0.0143, = 0.0031), indicating host genetic control over the microbiome. Microbiome genome-wide association study (mGWAS) identified 117 significant SNPs associated with 28 microbial taxa. Functional annotation highlighted eight candidate genes () involved in the regulation of taxa, including . Collectively, these findings establish that the gut microbiota is a heritable trait influenced by the host genome, providing novel targets for breeding strategies designed to optimize microbial composition for improved feed efficiency. - Source: PubMed
Publication date: 2026/03/12
Wu QitianWang XiaoqingMu QimingTian JingjingWang HailingYang JiayiPeng ZhenGao LiliGao PengfeiZhao Fuping - The molecular features determining the risk of metachronous metastases in clear cell renal cell carcinoma (ccRCC) are poorly defined. This study aimed to identify molecular factors associated with the risk of metachronous metastasis. - Source: PubMed
Publication date: 2026/02/25
M Naeini MarjanPang MengyuanRohatgi NehaKadioglu SinemGhoshdastider UmeshDiNatale Renzo GMano RoyHakimi A AriSkanderup Anders Jacobsen - Drought and water scarcity, exacerbated by global warming, are enormous threats to global food sustainability and security. Poultry, in particular, are highly impacted by adverse environmental stressors. As nutrient absorption and intestinal integrity are critical for growth and performance, understanding the impact on the broiler gastrointestinal tract is highly relevant. Here, we examined the effect of chronic cyclic heat stress (HS) on the jejunal expression profile of tight-junction, gap-junction, adherens, and desmosome genes in the 4th generation of broiler lines divergently selected for low (LWE)- and high-water efficiency (HWE). Male HWE and LWE broilers (n = 240/line) were allotted to 12 environmental chambers (2 floor pens/chamber, 6 chambers/line, 20 birds/pen) and were exposed to cyclic HS (36°C for 9h/day from 9:00 am to 6:00 pm) or thermoneutral conditions (25°C) from day 29 to 49 of age in a 2 × 2 factorial design. Growth performance and mortality were recorded. At day 49, jejunal tissues were collected for molecular analyses using real-time quantitative PCR and immunoblot. Jejunal gene expression of multiple gut integrity factors were higher (P < 0.05) in the HWE as compared to the LWE lines, including claudin 22 (CLDN22), -34, occluding (OCDN), zona-occludin-2 (ZO-2), gap junction alpha1 (GJA1), GJA3, GJC1, and cadherin 1 (CDH1). CLDN8, -20, -25, -4, GJC2, and GJD2 were also greater (P < 0.05) in HWE, but were additionally downregulated (P < 0.05) during HS. Conversely PALS1-associated tight junction protein (PATJ) and desmocollin 1 (DSC1) mRNAs were significantly downregulated in the HWE as compared to the LWE broilers. Significant interactions between the line and environment were seen in CLDN1, where the expression was decreased in the LWE but increased in the HWE in HS. Additionally, CLDN15 and -16 genes were greatest in the HWE under TN conditions, while catenin alpha 2 (CTNNA2) was highest in the HWE during HS. Overall, the jejunal expression profile of key genes associated with intestinal barrier integrity likely contributes to the water efficiency phenotype and the response of these birds to HS. - Source: PubMed
Publication date: 2025/12/16
Greene Elizabeth SOrlowski SaraDridi Sami - Heat stress (HS) has long posed a significant challenge to the poultry industry due to its adverse effects, such as depressed feed intake, decreased growth performance, and increased water consumption. Water efficiency (WE, conversion of water intake into body weight gain), although often neglected, is a key economic and production trait that is significantly affected by HS. Recently, we selected two broiler lines for high WE (HWE) and low WE (LWE) and showed a differential hypothalamic expression of genes involved in water homeostasis regulation. As the gut also plays a significant role in water absorption, the present study aimed to determine the effect of chronic HS on duodenal barrier integrity in LWE and HWE broilers. Male HWE and LWE chicks (240 chicks/line) were individually wing-banded for line identification, weighed, and placed in 12 controlled environmental chambers (2 pens/chambers). On day 29, birds were subjected to thermoneutral conditions (TN, 25 °C) or cyclic HS conditions (HS, 36 °C for 9 h/day from 9:00 a.m. to 6:00 p.m.) (120 birds/line/environment) for 3 weeks. On day 49, duodenal tissues were collected for histological, biochemical, and molecular analyses. Hematoxylin and eosin (H&E) staining revealed that HS significantly reduced villus height in the duodenum. Further analysis using qPCR showed that the mRNA expressions of intestinal barrier integrity-related genes, including claudins (CLDN1, 4, 5, 8, 16, and 22), PALS1-associated tight junction protein (), gap junction alpha 1 and 3 (), cadherin 2 (), and catenin alpha 2 (), were significantly upregulated by HS, and this effect was more pronounced in the HWE line than in its LWE counterpart. The findings of this study indicate that HS induces duodenal morphometric alterations. Based on the reduced serum fluorescein isothiocyanate-dextran (FITC-D) levels previously reported in the HWE line, the increased abundances of , , , , and mRNAs in the HWE line suggest an enhancement of its duodenal barrier integrity for better nutrient and water absorption and, consequently, better growth efficiency. - Source: PubMed
Publication date: 2025/11/13
Liu LuluGreene Elizabeth SRoach BrookleeOrlowski SaraDridi Sami - Ischemic stroke (IS) remains a leading cause of long-term disability and mortality worldwide, with recovery outcomes shaped by the interplay between acute vascular injury, pre-existing comorbidities, and individual molecular profiles. Common risk factors-such as diabetes mellitus, atrial fibrillation, hypertension, and dyslipidemia-not only increase stroke susceptibility but also impair neurovascular repair by perpetuating systemic inflammation, endothelial dysfunction, and impaired neuroplasticity. Aging remains an underexplored determinant of epigenetic remodeling in stroke. Beyond these clinical determinants, genetic and epigenetic mechanisms contribute substantially to stroke heterogeneity. Genome-wide association studies (GWAS) have identified loci such as HDAC9, PATJ, PTCH1, and ABO that modulate inflammation, oxidative stress, and vascular remodeling. Complementary epigenetic pathways, including DNA methylation, histone acetylation, and circular RNAs (circRNAs), dynamically regulate gene expression in response to ischemia and comorbid influences, encoding a persistent "molecular memory" that shapes both injury and repair. Functional studies reveal that circRNAs orchestrate apoptosis, angiogenesis, and synaptic remodeling, while selective DNMT and HDAC inhibition can restore neurovascular integrity in experimental models. Recent multi-omics and longitudinal approaches demonstrate that these molecular signatures evolve across acute, subacute, and chronic phases of recovery, yet clinical translation remains limited. Aging and chronic comorbidities further modify epigenetic programs, reducing repair capacity. Although genotype-guided antiplatelet therapy illustrates the feasibility of personalized stroke care, broader genomics- and epigenetics-informed interventions require rigorous validation. This review integrates current knowledge on the interplay between vascular comorbidities, genetic predisposition, and epigenetic regulation in shaping stroke recovery. Understanding these interactions is essential for developing precision medicine approaches that enhance functional outcomes and reduce recurrence in stroke survivors.Integrating multi-omics profiling with comorbidity stratification, functional validation, and longitudinal biomarker tracking will be pivotal to achieving actionable precision medicine and improving outcomes in stroke survivors. - Source: PubMed
Publication date: 2025/11/21
Cercel AndreeaMihaela AbuzanDoeppner Thorsten RHermann Dirk MMartin LiviuPopa-Wagner Aurel