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  1. Article ; Online: Animal models of the immunology and pathogenesis of human babesiosis.

    Kumar, Abhinav / Kabra, Aditya / Igarashi, Ikuo / Krause, Peter J

    Trends in parasitology

    2022  Volume 39, Issue 1, Page(s) 38–52

    Abstract: Animal models of human babesiosis have provided a basic understanding of the immunological mechanisms that clear, or occasionally exacerbate, Babesia infection and those pathological processes that cause disease complications. Human Babesia infection can ...

    Abstract Animal models of human babesiosis have provided a basic understanding of the immunological mechanisms that clear, or occasionally exacerbate, Babesia infection and those pathological processes that cause disease complications. Human Babesia infection can cause asymptomatic infection, mild to moderate disease, or severe disease resulting in organ dysfunction and death. More than 100 Babesia species infect a wide array of wild and domestic animals, and many of the immunologic and pathologic responses to Babesia infection are similar in animals and humans. In this review, we summarize the knowledge gained from animal studies, their limitations, and how animal models or alternative approaches can be further leveraged to improve our understanding of human babesiosis.
    MeSH term(s) Animals ; Humans ; Babesiosis ; Babesia ; Models, Animal
    Language English
    Publishing date 2022-12-02
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2036227-4
    ISSN 1471-5007 ; 1471-4922
    ISSN (online) 1471-5007
    ISSN 1471-4922
    DOI 10.1016/j.pt.2022.11.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Age-Dependent Changes in Regulation of Water Inflow Into the Vitreous Body.

    Ueki, Satoshi / Suzuki, Yuji / Nakamura, Yukimi / Igarashi, Hironaka

    Investigative ophthalmology & visual science

    2023  Volume 64, Issue 12, Page(s) 22

    Abstract: ... H2O positron emission tomography (PET).: Methods: Forty-six normal adult volunteers underwent [15O ... H2O PET, and the standard uptake value (SUV) in the center of the vitreous body after 1000-MBq [15O ...

    Abstract Purpose: Water inflow into the vitreous body regulated by retinal aquaporin-4 distributed within Müller cells has been observed in mice; however, the changes in this phenomenon with age remain unknown. This study aimed to evaluate whether intravenously injected H2O also flows into the vitreous body of human subjects and to investigate whether water dynamics in the human posterior eye change with age using [15O]H2O positron emission tomography (PET).
    Methods: Forty-six normal adult volunteers underwent [15O]H2O PET, and the standard uptake value (SUV) in the center of the vitreous body after 1000-MBq [15O]H2O administration was assessed. The SUV was fitted to an exponential curve, and y0, the steady state of the SUV, and b, the speed of increase in the SUV, were calculated. The results for patients ranging from in age from 20 to 39, 40 to 59, and 60 to 79 years were compared using analyses of variance followed by Games to Howell tests.
    Results: For the parameter y0, statistical analysis revealed no statistically significant differences among the three groups. For parameter b, statistical analysis revealed statistically significant differences between the 20 to 39 and 60 to 79 age groups (P = 0.000), the 40 to 59 and 60 to 79 age groups (P = 0.025), and the 20 to 39 and 40 to 59 age groups (P = 0.037).
    Conclusions: The present study revealed that H2O injected into the vein flows into the human vitreous body and that the speed of increase in water flow into the vitreous body decreases with aging. This study suggests that water dynamics in the posterior eye, or the retinal glymphatic pathway, change significantly with aging.
    MeSH term(s) Adult ; Humans ; Animals ; Mice ; Young Adult ; Vitreous Body/diagnostic imaging ; Aging ; Aquaporin 4 ; Biological Transport
    Chemical Substances Oxygen-15 ; Aquaporin 4
    Language English
    Publishing date 2023-09-12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 391794-0
    ISSN 1552-5783 ; 0146-0404
    ISSN (online) 1552-5783
    ISSN 0146-0404
    DOI 10.1167/iovs.64.12.22
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: New insights into the role of HNF-1β in kidney (patho)physiology.

    Ferrè, Silvia / Igarashi, Peter

    Pediatric nephrology (Berlin, Germany)

    2018  Volume 34, Issue 8, Page(s) 1325–1335

    Abstract: Hepatocyte nuclear factor-1β (HNF-1β) is an essential transcription factor that regulates the development and function of epithelia in the kidney, liver, pancreas, and genitourinary tract. Humans who carry HNF1B mutations develop heterogeneous renal ... ...

    Abstract Hepatocyte nuclear factor-1β (HNF-1β) is an essential transcription factor that regulates the development and function of epithelia in the kidney, liver, pancreas, and genitourinary tract. Humans who carry HNF1B mutations develop heterogeneous renal abnormalities, including multicystic dysplastic kidneys, glomerulocystic kidney disease, renal agenesis, renal hypoplasia, and renal interstitial fibrosis. In the embryonic kidney, HNF-1β is required for ureteric bud branching, initiation of nephrogenesis, and nephron segmentation. Ablation of mouse Hnf1b in nephron progenitors causes defective tubulogenesis, whereas later inactivation in elongating tubules leads to cyst formation due to downregulation of cystic disease genes, including Umod, Pkhd1, and Pkd2. In the adult kidney, HNF-1β controls the expression of genes required for intrarenal metabolism and solute transport by tubular epithelial cells. Tubular abnormalities observed in HNF-1β nephropathy include hyperuricemia with or without gout, hypokalemia, hypomagnesemia, and polyuria. Recent studies have identified novel post-transcriptional and post-translational regulatory mechanisms that control HNF-1β expression and activity, including the miRNA cluster miR17 ∼ 92 and the interacting proteins PCBD1 and zyxin. Further understanding of the molecular mechanisms upstream and downstream of HNF-1β may lead to the development of new therapeutic approaches in cystic kidney disease and other HNF1B-related renal diseases.
    MeSH term(s) Down-Regulation ; Gene Expression Regulation, Developmental ; Hepatocyte Nuclear Factor 1-beta/genetics ; Hepatocyte Nuclear Factor 1-beta/metabolism ; Humans ; Hydro-Lyases/metabolism ; Kidney Diseases, Cystic/blood ; Kidney Diseases, Cystic/genetics ; Kidney Diseases, Cystic/pathology ; Kidney Diseases, Cystic/urine ; Kidney Tubules/abnormalities ; Kidney Tubules/pathology ; MicroRNAs/metabolism ; Mutation ; RNA, Long Noncoding ; Receptors, Cell Surface/genetics ; TRPP Cation Channels/genetics ; Uromodulin/genetics ; Urothelium/abnormalities ; Urothelium/pathology ; Zyxin/metabolism
    Chemical Substances HNF1B protein, human ; MIR17HG, human ; MicroRNAs ; PKHD1 protein, human ; RNA, Long Noncoding ; Receptors, Cell Surface ; TRPP Cation Channels ; UMOD protein, human ; Uromodulin ; ZYX protein, human ; Zyxin ; polycystic kidney disease 2 protein ; Hepatocyte Nuclear Factor 1-beta (138674-15-4) ; Hydro-Lyases (EC 4.2.1.-) ; pterin-4a-carbinolamine dehydratase (EC 4.2.1.96)
    Language English
    Publishing date 2018-07-01
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-018-3990-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Small hairpin inhibitory RNA delivery in the metanephric organ culture identifies long noncoding RNA

    Eckberg, Kara / Weisser, Ivan / Buttram, Daniel / Somia, Nikunj / Igarashi, Peter / Aboudehen, Karam S

    American journal of physiology. Renal physiology

    2022  Volume 323, Issue 3, Page(s) F335–F348

    Abstract: Autosomal dominant polycystic kidney disease (ADPKD) is a monogenic disorder characterized by the formation of kidney cysts that originate from the epithelial tubules of the nephron and primarily results from mutations in polycystin-1 ( ...

    Abstract Autosomal dominant polycystic kidney disease (ADPKD) is a monogenic disorder characterized by the formation of kidney cysts that originate from the epithelial tubules of the nephron and primarily results from mutations in polycystin-1 (
    MeSH term(s) Animals ; Cysts/genetics ; Cysts/metabolism ; Humans ; Kidney/metabolism ; Mice ; Organ Culture Techniques ; Polycystic Kidney, Autosomal Dominant/genetics ; Polycystic Kidney, Autosomal Dominant/metabolism ; RNA, Long Noncoding/genetics ; RNA, Small Interfering/metabolism ; TRPP Cation Channels/genetics ; TRPP Cation Channels/metabolism
    Chemical Substances RNA, Long Noncoding ; RNA, Small Interfering ; TRPP Cation Channels
    Language English
    Publishing date 2022-07-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00016.2022
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Role of transcription factor hepatocyte nuclear factor-1β in polycystic kidney disease.

    Shao, Annie / Chan, Siu Chiu / Igarashi, Peter

    Cellular signalling

    2020  Volume 71, Page(s) 109568

    Abstract: Hepatocyte nuclear factor-1β (HNF-1β) is a DNA-binding transcription factor that is essential for normal kidney development. Mutations of HNF1B in humans produce cystic kidney diseases, including renal cysts and diabetes, multicystic dysplastic kidneys, ... ...

    Abstract Hepatocyte nuclear factor-1β (HNF-1β) is a DNA-binding transcription factor that is essential for normal kidney development. Mutations of HNF1B in humans produce cystic kidney diseases, including renal cysts and diabetes, multicystic dysplastic kidneys, glomerulocystic kidney disease, and autosomal dominant tubulointerstitial kidney disease. Expression of HNF1B is reduced in cystic kidneys from humans with ADPKD, and HNF1B has been identified as a modifier gene in PKD. Genome-wide analysis of chromatin binding has revealed that HNF-1β directly regulates the expression of known PKD genes, such as PKHD1 and PKD2, as well as genes involved in PKD pathogenesis, including cAMP-dependent signaling, renal fibrosis, and Wnt signaling. In addition, a role of HNF-1β in regulating the expression of noncoding RNAs (microRNAs and long noncoding RNAs) has been identified. These findings indicate that HNF-1β regulates a transcriptional and post-transcriptional network that plays a central role in renal cystogenesis.
    MeSH term(s) Animals ; Hepatocyte Nuclear Factor 1-beta/chemistry ; Hepatocyte Nuclear Factor 1-beta/genetics ; Hepatocyte Nuclear Factor 1-beta/metabolism ; Humans ; Models, Biological ; Mutation/genetics ; Polycystic Kidney Diseases/genetics ; Polycystic Kidney Diseases/metabolism ; RNA, Untranslated/genetics ; RNA, Untranslated/metabolism ; Signal Transduction
    Chemical Substances RNA, Untranslated ; Hepatocyte Nuclear Factor 1-beta (138674-15-4)
    Language English
    Publishing date 2020-02-14
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1002702-6
    ISSN 1873-3913 ; 0898-6568
    ISSN (online) 1873-3913
    ISSN 0898-6568
    DOI 10.1016/j.cellsig.2020.109568
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Multiomics analysis reveals that hepatocyte nuclear factor 1β regulates axon guidance genes in the developing mouse kidney.

    Shao, Annie / Gearhart, Micah D / Chan, Siu Chiu / Miao, Zhen / Susztak, Katalin / Igarashi, Peter

    Scientific reports

    2022  Volume 12, Issue 1, Page(s) 17586

    Abstract: The transcription factor hepatocyte nuclear factor 1β (HNF-1β) is essential for normal development of the kidney and other epithelial organs. In the developing mouse kidney, HNF-1β is required for the differentiation and patterning of immature nephrons ... ...

    Abstract The transcription factor hepatocyte nuclear factor 1β (HNF-1β) is essential for normal development of the kidney and other epithelial organs. In the developing mouse kidney, HNF-1β is required for the differentiation and patterning of immature nephrons and branching morphogenesis of the ureteric bud (UB). Here, we used ChIP-sequencing (ChIP-seq) and RNA sequencing (RNA-seq) to identify genes that are regulated by HNF-1β in embryonic mouse kidneys. ChIP-seq revealed that HNF-1β binds to 8284 sites in chromatin from E14.5 mouse kidneys. Comparison with previous ATAC-seq and histone modification studies showed that HNF-1β binding peaks colocalized with open chromatin and epigenetic marks of transcriptional activation (H3K27 acetylation, H3K4 trimethylation, H3K4 monomethylation), indicating that the binding sites were functional. To investigate the relationship between HNF-1β binding and HNF-1β-dependent gene regulation, RNA-seq was performed on UB cells purified from wild-type and HNF-1β mutant embryonic kidneys. A total of 1632 genes showed reduced expression in HNF-1β-deficient UB cells, and 485 genes contained nearby HNF-1β binding sites indicating that they were directly activated by HNF-1β. Conversely, HNF-1β directly repressed the expression of 526 genes in the UB. Comparison with snATAC-seq analysis of UB-derived cells showed that both HNF-1β-dependent activation and repression correlated with chromatin accessibility. Pathway analysis revealed that HNF-1β binds near 68 axon guidance genes in the developing kidney. RNA-seq analysis showed that Nrp1, Sema3c, Sema3d, Sema6a, and Slit2 were activated by HNF-1β, whereas Efna1, Epha3, Epha4, Epha7, Ntn4, Plxna2, Sema3a, Sema4b, Slit3, Srgap1, Unc5c and Unc5d were repressed by HNF-1β. RNAscope in situ hybridization showed that Nrp1, Sema3c, Sema3d, Sema6a, and Slit2 were expressed in wild-type UB and were dysregulated in HNF-1β mutant UB. These studies show that HNF-1β directly regulates the expression of multiple axon guidance genes in the developing mouse kidney. Dysregulation of axon guidance genes may underlie kidney defects in HNF-1β mutant mice.
    MeSH term(s) Animals ; Mice ; Axon Guidance/genetics ; Chromatin/genetics ; Chromatin/metabolism ; Ephrin-A1/genetics ; Hepatocyte Nuclear Factor 1-beta/genetics ; Hepatocyte Nuclear Factor 1-beta/metabolism ; Kidney/metabolism ; Membrane Proteins/metabolism ; Nerve Tissue Proteins/metabolism ; Receptors, Cell Surface/metabolism ; Semaphorin-3A/genetics ; Semaphorins/genetics ; Transcription Factors/metabolism
    Chemical Substances Chromatin ; Ephrin-A1 ; Hepatocyte Nuclear Factor 1-beta (138674-15-4) ; Membrane Proteins ; Nerve Tissue Proteins ; Plxna2 protein, mouse ; Receptors, Cell Surface ; Sema6a protein, mouse ; Semaphorin-3A ; Semaphorins ; Slit3 protein, mouse ; Transcription Factors ; Hnf1b protein, mouse
    Language English
    Publishing date 2022-10-20
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-022-22327-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Host Resistance to Monilinia vaccinii-corymbosi in Flowers and Fruits of Highbush Blueberry.

    Lehman, Jeffrey S / Igarashi, Suzu / Oudemans, Peter V

    Plant disease

    2019  Volume 91, Issue 7, Page(s) 852–856

    Abstract: Monilinia vaccinii-corymbosi, the causal agent of mummy berry disease, infects blueberry flowers via the gynoecial pathway. To describe the expression of host resistance in highbush blueberry (Vaccinium corymbosum), fungal growth in the styles and ... ...

    Abstract Monilinia vaccinii-corymbosi, the causal agent of mummy berry disease, infects blueberry flowers via the gynoecial pathway. To describe the expression of host resistance in highbush blueberry (Vaccinium corymbosum), fungal growth in the styles and colonization of the locules were compared among five blueberry cultivars in a series of controlled greenhouse experiments. Styles were harvested 1 and 4 days postinoculation, and the length colonized by hyphae was determined using fluorescence microscopy. At 8 weeks after inoculation, fruit were harvested and scored for the presence of hyphae in the locules. The infection frequency of styles ranged from 0.33 to 0.71, and only cv. Weymouth had significantly lower infection frequency than the other cultivars. The mean length of the colonized portion of the stylar canal ranged from 0.126 to 0.434 mm after 1 day and 1.62 to 3.59 mm after 4 days. Hyphae in the styles of cv. Weymouth exhibited the least growth, whereas hyphae in the styles of cultivars Jersey and Rancocas were significantly longer. The distance of style penetrated for cultivars Bluecrop and Coville was intermediate. The mean disease incidence of locules differed significantly. Values for cultivars Weymouth and Jersey were the smallest (0.038 and 0.039) and largest (0.249 and 0.236), respectively. The results demonstrate that a component of resistance to infection by M. vaccinii-corymbosi is expressed during growth in the gynoecial pathway.
    Language English
    Publishing date 2019-02-19
    Publishing country United States
    Document type Journal Article
    ZDB-ID 754182-x
    ISSN 0191-2917
    ISSN 0191-2917
    DOI 10.1094/PDIS-91-7-0852
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Blood Cerebrospinal Fluid Barrier Function Disturbance Can Be Followed by Amyloid-β Accumulation.

    Suzuki, Yuji / Nakamura, Yukimi / Igarashi, Hironaka

    Journal of clinical medicine

    2022  Volume 11, Issue 20

    Abstract: ... Methods: Twenty-five normal older adult volunteers (60-81 years old) participated in this PET study ...

    Abstract Background: Elucidation of the mechanism of amyloid-β accumulation plays an important role in therapeutic strategies for Alzheimer's disease (AD). The aim of this study is to elucidate the relationship between the function of the blood-cerebrospinal fluid barrier (BCSFB) and the clearance of amyloid-β (Aβ).
    Methods: Twenty-five normal older adult volunteers (60-81 years old) participated in this PET study for clarifying the relationship between interstitial water flow and Aβ accumulation. Water dynamics were analyzed using two indices in [
    Results: [
    Conclusions: Our results indicated that BCSFB function disturbances could be followed by Aβ accumulation, because the reduced interstitial flow preceded amyloid accumulation in the positive-change subjects, and amyloid accumulation was not observed in the older adults with sufficiently high values for the two indices. We believe that further elucidation of interstitial water flow will be the key to developing therapeutic strategies for AD, especially with regard to prevention.
    Language English
    Publishing date 2022-10-17
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2662592-1
    ISSN 2077-0383
    ISSN 2077-0383
    DOI 10.3390/jcm11206118
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  9. Article ; Online: Hepatocyte nuclear factor 1β suppresses canonical Wnt signaling through transcriptional repression of lymphoid enhancer-binding factor 1.

    Chan, Siu Chiu / Hajarnis, Sachin S / Vrba, Sophia M / Patel, Vishal / Igarashi, Peter

    The Journal of biological chemistry

    2021  Volume 295, Issue 51, Page(s) 17560–17572

    Abstract: Hepatocyte nuclear factor-1β (HNF-1β) is a tissue-specific transcription factor that is required for normal kidney development and renal epithelial differentiation. Mutations of HNF-1β produce congenital kidney abnormalities and inherited renal ... ...

    Abstract Hepatocyte nuclear factor-1β (HNF-1β) is a tissue-specific transcription factor that is required for normal kidney development and renal epithelial differentiation. Mutations of HNF-1β produce congenital kidney abnormalities and inherited renal tubulopathies. Here, we show that ablation of HNF-1β in mIMCD3 renal epithelial cells results in activation of β-catenin and increased expression of lymphoid enhancer-binding factor 1 (LEF1), a downstream effector in the canonical Wnt signaling pathway. Increased expression and nuclear localization of LEF1 are also observed in cystic kidneys from Hnf1b mutant mice. Expression of dominant-negative mutant HNF-1β in mIMCD3 cells produces hyperresponsiveness to exogenous Wnt ligands, which is inhibited by siRNA-mediated knockdown of Lef1. WT HNF-1β binds to two evolutionarily conserved sites located 94 and 30 kb from the mouse Lef1 promoter. Ablation of HNF-1β decreases H3K27 trimethylation repressive marks and increases β-catenin occupancy at a site 4 kb upstream to Lef1. Mechanistically, WT HNF-1β recruits the polycomb-repressive complex 2 that catalyzes H3K27 trimethylation. Deletion of the β-catenin-binding domain of LEF1 in HNF-1β-deficient cells abolishes the increase in Lef1 transcription and decreases the expression of downstream Wnt target genes. The canonical Wnt target gene, Axin2, is also a direct transcriptional target of HNF-1β through binding to negative regulatory elements in the gene promoter. These findings demonstrate that HNF-1β regulates canonical Wnt target genes through long-range effects on histone methylation at Wnt enhancers and reveal a new mode of active transcriptional repression by HNF-1β.
    MeSH term(s) Animals ; Axin Protein/genetics ; Axin Protein/metabolism ; Binding Sites ; Epithelial Cells/cytology ; Epithelial Cells/metabolism ; Gene Expression Regulation ; Hepatocyte Nuclear Factor 1-beta/deficiency ; Hepatocyte Nuclear Factor 1-beta/genetics ; Hepatocyte Nuclear Factor 1-beta/metabolism ; Histones/metabolism ; Kidney/cytology ; Lymphoid Enhancer-Binding Factor 1/antagonists & inhibitors ; Lymphoid Enhancer-Binding Factor 1/genetics ; Lymphoid Enhancer-Binding Factor 1/metabolism ; Methylation ; Mice ; Mice, Knockout ; Mutagenesis ; Promoter Regions, Genetic ; RNA Interference ; RNA, Small Interfering/metabolism ; Regulatory Elements, Transcriptional/genetics ; Wnt Signaling Pathway ; Wnt3A Protein/metabolism ; beta Catenin/metabolism
    Chemical Substances Axin Protein ; Axin2 protein, mouse ; Histones ; Lymphoid Enhancer-Binding Factor 1 ; RNA, Small Interfering ; Wnt3A Protein ; beta Catenin ; Hepatocyte Nuclear Factor 1-beta (138674-15-4)
    Language English
    Publishing date 2021-01-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.RA120.015592
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Hepatocyte nuclear factor-1β regulates Wnt signaling through genome-wide competition with β-catenin/lymphoid enhancer binding factor.

    Chan, Siu Chiu / Zhang, Ying / Pontoglio, Marco / Igarashi, Peter

    Proceedings of the National Academy of Sciences of the United States of America

    2019  Volume 116, Issue 48, Page(s) 24133–24142

    Abstract: Hepatocyte nuclear factor-1β (HNF-1β) is a tissue-specific transcription factor that is essential for normal kidney development and renal tubular function. Mutations of HNF-1β produce cystic kidney disease, a phenotype associated with deregulation of ... ...

    Abstract Hepatocyte nuclear factor-1β (HNF-1β) is a tissue-specific transcription factor that is essential for normal kidney development and renal tubular function. Mutations of HNF-1β produce cystic kidney disease, a phenotype associated with deregulation of canonical (β-catenin-dependent) Wnt signaling. Here, we show that ablation of HNF-1β in mIMCD3 renal epithelial cells produces hyperresponsiveness to Wnt ligands and increases expression of Wnt target genes, including
    MeSH term(s) Animals ; Cell Line ; Enhancer Elements, Genetic ; Epithelial Cells/metabolism ; Extracellular Matrix Proteins/genetics ; Extracellular Matrix Proteins/metabolism ; Gene Expression Regulation ; Genome-Wide Association Study ; Hepatocyte Nuclear Factor 1-beta/genetics ; Hepatocyte Nuclear Factor 1-beta/metabolism ; Kidney Medulla/cytology ; Lymphoid Enhancer-Binding Factor 1/genetics ; Lymphoid Enhancer-Binding Factor 1/metabolism ; Mice, Knockout ; Mice, Transgenic ; Mutation ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism ; Wnt Signaling Pathway/genetics ; Wnt3A Protein/genetics ; Wnt3A Protein/metabolism ; beta Catenin/genetics ; beta Catenin/metabolism
    Chemical Substances CTNNB1 protein, mouse ; Ccdc80 protein, mouse ; Extracellular Matrix Proteins ; Hnf1b protein, mouse ; Lef1 protein, mouse ; Lymphoid Enhancer-Binding Factor 1 ; Wnt3A Protein ; Wnt3a protein, mouse ; beta Catenin ; Hepatocyte Nuclear Factor 1-beta (138674-15-4) ; RNF43 protein, mouse (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
    Language English
    Publishing date 2019-11-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1909452116
    Database MEDical Literature Analysis and Retrieval System OnLINE

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