Mouse polyclonal to PKHD1L1, Host Mouse
- Known as:
- Mouse pab PKHD1L1, Host Mouse
- Catalog number:
- YF-PA26791
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Mouse polyclonal PKHD1L1 Host
Related genes to: Mouse polyclonal to PKHD1L1, Host Mouse
- Gene:
- PKHD1L1 NIH gene
- Name:
- PKHD1 like 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8q23.1-q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-03-28
- Date modifiied:
- 2018-02-13
Related products to: Mouse polyclonal to PKHD1L1, Host Mouse
Related articles to: Mouse polyclonal to PKHD1L1, Host Mouse
- Platelets express several glycophosphatidylinositol-(GPI-) anchored receptors, mainly involved in protection against lysis by activated complements. Most of these are well-characterised and are expressed on other blood cells. More recently, CD109 with a mass of 175 kDa was also shown to be a GPI-anchored receptor, surface expressed only on activated platelets, with a role as a co-receptor for transforming growth factor-β (TGF-β). CD109 is expressed on a wide range of cells and is a marker for various types of tumors. Activated platelets express an even larger GPI-anchored receptor at about 500 kDa. We have now isolated this and identified it as fibrocystin L, also known as polycystic kidney hepatic disease L1 (PKHD1L1). Fibrocystin L, like other platelet GPI-anchored receptors, is missing or deficient in paroxysmal nocturnal hemoglobinuria. Fibrocystin L is also expressed in activated T-cells and may be involved in immune responses. Recently, there have been additional reports of PKHD1L1 expression and roles as a coat protein of hair-cell stereocilia essential for normal hearing, as well as reports of them in the dentate gyrus in mice involved in susceptibility to seizure. In all these cases, GPI anchors were not reported, but neither were they tested for. During the fluorescence microscopy studies, we used CD109 as a control and observed that it is also a granule protein that had not been previously reported. - Source: PubMed
Publication date: 2026/08/31
Polgar JanosClemetson Jeannine MMagnenat EdithWells Timothy NRöss HelenaRochat SophieAlberio Lorenzo AClemetson Kenneth J - Lung lymphatic drainage of interstitial fluid is essential for preventing pulmonary edema, a condition characterized by the accumulation of extravascular fluid that impedes respiratory gas exchange and can be fatal. Beyond fluid regulation, lung lymphatics also serve as conduits for immune cell trafficking, supporting both surveillance and mounting of host immune responses during lung infection. Despite their essential roles, the cellular and functional heterogeneity of lung lymphatic endothelial cells (LECs) remains poorly defined. - Source: PubMed
Publication date: 2026/04/16
Crossey ErinCarty SenegalGarza IsabellaPerez MelizaShao FengzhiAl Abdullatif SalamCampbell Joshua DMizgerd Joseph PFine AlanJones Matthew R - PURPOSE: Impact of pre-treatment platelet-monocyte ratio on prognosis in patients with non-small cell lung cancer. 2. Screening and analyzing the relationship between NSCLC, platelet- and monocyte-associated genes and prognosis. 3. Expression of platelet- and monocyte-associated genes in NSCLC and the correlation between them and clinicopathological features and survival time. METHODS: The clinicopathological characteristics of the high and low PMR groups were compared by t-test and chi-square test. The Cox proportional hazards regression model was used to analyze univariate and multivariate factors, and statistical analysis was conducted using R language statistical software. The optimal PMR was obtained by using the surv_cutpoint function of the "survminer" software package. The optimal cut-off point of PMR was obtained by using the surv_cutpoint function of the "survminer" software package, and univariate and multivariate analyses were conducted by using its "Survival" software package. The survival data were fitted using the survfit function of the "survival" package, the survival curve was plotted using the ggsurvplot function of the "survival" package, and the cox regression model was constructed using the coxph function of the "survival" package. 2. The cox regression model was constructed using the coxph function of the "Survival" software package. The "limma" software package was used to perform deg analysis on tumor samples of patients and normal controls. Matching genes were used for single-gene COX regression analysis, gene grouping and KM survival analysis, etc. The ROC curve was used to evaluate the prognostic model test. 3. Laboratory verification: The expression of the target gene was observed by qPCR experiment. The correlation between the staining of the target gene and the clinicopathological characteristics and survival time was detected by immunohistochemical experiment. The experimental results were analyzed by SPSS and Graphpad Prism software. RESULTS: PMR is closely related to various clinicopathological characteristics of NSCLC patients. PMR is an independent risk factor for OS in patients with NSCLC. 2. We identified five genes independently associated with the prognosis of non-small cell lung cancer through analysis: FSTL3, MYLIP, PKHD1L1, C8B and EREG. Compared with adjacent tissues, the expression of these five genes was consistently and significantly downregulated in tumor tissues. CONCLUSIONS: PMR value may be a potential prognostic indicator for non-small cell lung cancer. Combining PMR with clinicopathological characteristics, it can be considered to further refine the treatment and prognosis plans for patients based on this proportion. 2. These key genes are all related to the process of tumor occurrence and development, providing a basis for the early and accurate diagnosis of NSCLC patients and promising the discovery of potential targets for tumor treatment. 3. The FSTL3, MYLIP, ppkhd1l1 and C8B genes in NSCLC tissues may be potential carcinogenic factors, potential biological markers and potential targets for the treatment of NSCLC tumors, and EREG may be a biomarker with significant prognostic value. - Source: PubMed
Publication date: 2026/04/06
Tang YonglianHuang YiliChen LeiHuang ZiguiHuang XiaoliangHe Zhiyi - Autosomal recessive polycystic kidney disease (ARPKD) is the prototype of the hepato-renal fibrocystic diseases, a subset of the broader ciliopathy disorders. As a severe form of PKD, ARPKD typically manifests in utero with 21% perinatal mortality and progressive loss of kidney function in most post-natal survivors. Congenital hepatic fibrosis is an invariant feature of ARPKD. PKHD1-encoded fibrocystin/polyductin (FPC) is a large 4074 amino acid glycoprotein that likely functions as a receptor molecule and appears to play a key role in maintaining differentiated renal tubular epithelium. The molecular mechanisms by which defects in FPC contribute to ARPKD pathogenesis are just beginning to be elucidated. FPC is a novel protein that likely evolved as vertebrates transitioned from aquatic to semi-terrestrial ecosystems. Full-length human FPC shares a phylogenetically conserved, multi-motif N-terminal region with its ancestral homolog, PKHD1L1, and contains a single-pass transmembrane domain and a novel C-terminal tail that harbors a ciliary targeting motif as well as mitochondrial and nuclear localization sequences. This review synthesizes the full range of recent experimental data about PKHD1/FPC to provide a current functional perspective about this complex protein. We also discuss the clinical relevance of these emerging functional insights for both kidney health and ARPKD pathogenesis. - Source: PubMed
Publication date: 2026/01/28
Gulati AshimaCaldovic LjubicaGuay-Woodford Lisa M - Considering the lack of molecular background of the metastatic process in pancreatic ductal adenocarcinoma (PDAC) and the fact that the location of the metastasis may carry prognostic information and potential therapeutic opportunities, we aimed to explore genomic profiles of metastases from diverse loci and their value for the patients' therapeutic management. DNA samples from paired primary and metastatic tissue of 20 patients were microdissected and sequenced using whole exome target enrichment. Somatic genetic variability, copy number variations (CNVs), and mutational signatures were assessed for associations with clinical data of patients. KRAS (78% in primary tumors, 74% in metastases), TP53 (67%-68%), CDKN2A (28%-37%), and SMAD4 (22%-26%) were the most commonly mutated oncodrivers in primary tumors and metastases. Other frequently mutated genes were CCDC187 (50%-58%), MUC5AC (50%-53%), EPPK1 (39%-63%), SYN2 (39%-26%), MUC19 (33%-47%), MUC3A (33%-26%), DNAH12 (28%-37%), ZBED3 (22%-26%), PKHD1L1 (28%-16%), and GTPBP6 (11%-32%). Lung metastases differed from other metastatic sites (liver, stomach, and locoregional) in a higher frequency of nonsense mutations in the MH2 domain of SMAD4, oncodriver comutations, gains on chromosomes 2 and 20, CNV counts, and share of signature SBS5. Somatic alterations of KRAS in metastases (P = .041) and MUC3A in both loci (P = .041 and P = .011, respectively) and CNVs count and size in metastases (P = .024 and P = .011) associated with response to systemic chemotherapy. Patients with mutated KRAS (P = .045), high mutational load (P = .004), and frequent CNVs (P = .004) in metastatic loci had shortened survival after metastasis resection. Interestingly, the personalized treatment targetable alterations, such as microsatellite instability and mismatch repair or homologous recombination deficiencies did not differ between the primary tumors and paired metastases or between the metastases from different secondary sites and had no prognostic value. The results suggest a potential prognostic role of KRAS mutations, mutation load, and CNVs in PDAC patients after metastasectomy and encourage further molecular profiling for personalized treatment of PDAC patients with different metastasis localization. - Source: PubMed
Publication date: 2025/06/20
Loveček MartinStrouhal OndřejČervenková LenkaŠůsová SimonaHlaváč ViktorChottova Dvorakova MagdalenaHolý PetrLiška VáclavSkalický PavelSkanderová DanielaLanger AlešMohelníková-Duchoňová BeatriceSouček Pavel