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  1. Article ; Online: Temporal and Spatial Patterns of Inflammation and Tissue Injury in Patients with Postoperative Respiratory Failure after Lung Resection Surgery: A Nested Case-Control Study.

    Kormish, Jay / Ghuman, Tejas / Liu, Richard Y / Srinathan, Sadeesh K / Tan, Lawrence / Graham, Kristen / Enns, Stephanie / Buduhan, Gordon / Halayko, Andrew J / Pascoe, Christopher D / Kidane, Biniam

    International journal of molecular sciences

    2023  Volume 24, Issue 12

    Abstract: Thoracic surgeries involving resection of lung tissue pose a risk of severe postoperative pulmonary complications, including acute respiratory distress syndrome (ARDS) and respiratory failure. Lung resections require one-lung ventilation (OLV) and, thus, ...

    Abstract Thoracic surgeries involving resection of lung tissue pose a risk of severe postoperative pulmonary complications, including acute respiratory distress syndrome (ARDS) and respiratory failure. Lung resections require one-lung ventilation (OLV) and, thus, are at higher risk of ventilator-induced lung injury (VILI) attributable to barotrauma and volutrauma in the one ventilated lung, as well as hypoxemia and reperfusion injury on the operated lung. Further, we also aimed to assess the differences in localized and systemic markers of tissue injury/inflammation in those who developed respiratory failure after lung surgery versus matched controls who did not develop respiratory failure. We aimed to assess the different inflammatory/injury marker patterns induced in the operated and ventilated lung and how this compared to the systemic circulating inflammatory/injury marker pattern. A case-control study nested within a prospective cohort study was performed. Patients with postoperative respiratory failure after lung surgery (
    MeSH term(s) Humans ; Case-Control Studies ; Prospective Studies ; Lung/surgery ; Lung/metabolism ; Respiratory Insufficiency/etiology ; Respiratory Insufficiency/metabolism ; Inflammation/etiology ; Inflammation/metabolism ; Postoperative Complications/etiology ; Postoperative Complications/metabolism ; Respiration, Artificial
    Language English
    Publishing date 2023-06-13
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms241210051
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Temporal and Spatial Patterns of Inflammation and Tissue Injury in Patients with Postoperative Respiratory Failure after Lung Resection Surgery

    Jay Kormish / Tejas Ghuman / Richard Y. Liu / Sadeesh K. Srinathan / Lawrence Tan / Kristen Graham / Stephanie Enns / Gordon Buduhan / Andrew J. Halayko / Christopher D. Pascoe / Biniam Kidane

    International Journal of Molecular Sciences, Vol 24, Iss 10051, p

    A Nested Case–Control Study

    2023  Volume 10051

    Abstract: Thoracic surgeries involving resection of lung tissue pose a risk of severe postoperative pulmonary complications, including acute respiratory distress syndrome (ARDS) and respiratory failure. Lung resections require one-lung ventilation (OLV) and, thus, ...

    Abstract Thoracic surgeries involving resection of lung tissue pose a risk of severe postoperative pulmonary complications, including acute respiratory distress syndrome (ARDS) and respiratory failure. Lung resections require one-lung ventilation (OLV) and, thus, are at higher risk of ventilator-induced lung injury (VILI) attributable to barotrauma and volutrauma in the one ventilated lung, as well as hypoxemia and reperfusion injury on the operated lung. Further, we also aimed to assess the differences in localized and systemic markers of tissue injury/inflammation in those who developed respiratory failure after lung surgery versus matched controls who did not develop respiratory failure. We aimed to assess the different inflammatory/injury marker patterns induced in the operated and ventilated lung and how this compared to the systemic circulating inflammatory/injury marker pattern. A case–control study nested within a prospective cohort study was performed. Patients with postoperative respiratory failure after lung surgery ( n = 5) were matched with control patients ( n = 6) who did not develop postoperative respiratory failure. Biospecimens (arterial plasma, bronchoalveolar lavage separately from ventilated and operated lungs) were obtained from patients undergoing lung surgery at two timepoints: (1) just prior to initiation of OLV and (2) after lung resection was completed and OLV stopped. Multiplex electrochemiluminescent immunoassays were performed for these biospecimen. We quantified 50 protein biomarkers of inflammation and tissue injury and identified significant differences between those who did and did not develop postoperative respiratory failure. The three biospecimen types also display unique biomarker patterns.
    Keywords one-lung ventilation (OLV) ; acute lung injury (ALI) ; ventilation-induced lung injury (VILI) ; acute respiratory distress syndrome (ARDS) ; postoperative pulmonary complications (PPCs) ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 610
    Language English
    Publishing date 2023-06-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Development of the C. elegans digestive tract.

    Kormish, Jay D / Gaudet, Jeb / McGhee, James D

    Current opinion in genetics & development

    2010  Volume 20, Issue 4, Page(s) 346–354

    Abstract: The C. elegans digestive tract (pharynx, intestine, and rectum) contains only approximately 100 cells but develops under the control of the same types of transcription factors (e.g. FoxA and GATA factors) that control digestive tract development in far ... ...

    Abstract The C. elegans digestive tract (pharynx, intestine, and rectum) contains only approximately 100 cells but develops under the control of the same types of transcription factors (e.g. FoxA and GATA factors) that control digestive tract development in far more complex animals. The GATA-factor dominated core regulatory hierarchy directing development of the homogenous clonal intestine from oocyte to mature organ is now known with some degree of certainty, setting the stage for more biochemical experiments to understand developmental mechanisms. The FoxA-factor dominated development of the pharynx (and rectum) is less well understood but is beginning to reveal how transcription factor combinations produce unique cell types within organs.
    MeSH term(s) Animals ; Caenorhabditis elegans/embryology ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Caenorhabditis elegans Proteins/physiology ; Cell Differentiation/genetics ; Cell Lineage ; Embryonic Development/genetics ; GATA Transcription Factors/genetics ; GATA Transcription Factors/metabolism ; GATA Transcription Factors/physiology ; Gastrointestinal Tract/cytology ; Gastrointestinal Tract/embryology ; Gene Expression Regulation, Developmental ; Intestines/cytology ; Intestines/embryology ; Pharynx/cytology ; Pharynx/embryology ; Rectum/cytology ; Rectum/embryology ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Trans-Activators/physiology
    Chemical Substances Caenorhabditis elegans Proteins ; GATA Transcription Factors ; Pha-4 protein, C elegans ; Trans-Activators
    Language English
    Publishing date 2010-08
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1077312-5
    ISSN 1879-0380 ; 0959-437X
    ISSN (online) 1879-0380
    ISSN 0959-437X
    DOI 10.1016/j.gde.2010.04.012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Interactions between SOX factors and Wnt/beta-catenin signaling in development and disease.

    Kormish, Jay D / Sinner, Débora / Zorn, Aaron M

    Developmental dynamics : an official publication of the American Association of Anatomists

    2009  Volume 239, Issue 1, Page(s) 56–68

    Abstract: The SOX family of transcription factors have emerged as modulators of canonical Wnt/beta-catenin signaling in diverse development and disease contexts. There are over 20 SOX proteins encoded in the vertebrate genome and recent evidence suggests that many ...

    Abstract The SOX family of transcription factors have emerged as modulators of canonical Wnt/beta-catenin signaling in diverse development and disease contexts. There are over 20 SOX proteins encoded in the vertebrate genome and recent evidence suggests that many of these can physically interact with beta-catenin and modulate the transcription of Wnt-target genes. The precise mechanisms by which SOX proteins regulate beta-catenin/TCF activity are still being resolved and there is evidence to support a number of models including: protein-protein interactions, the binding of SOX factors to Wnt-target gene promoters, the recruitment of co-repressors or co-activators, modulation of protein stability, and nuclear translocation. In some contexts, Wnt signaling also regulates SOX expression resulting in feedback regulatory loops that fine-tune cellular responses to beta-catenin/TCF activity. In this review, we summarize the examples of Sox-Wnt interactions and examine the underlying mechanisms of this potentially widespread and underappreciated mode of Wnt-regulation.
    MeSH term(s) Animals ; Embryonic Development/physiology ; Gene Expression Regulation, Developmental/physiology ; Humans ; Models, Biological ; Neoplasms/metabolism ; SOX Transcription Factors/metabolism ; Sex Determination Processes ; Signal Transduction/physiology ; Wnt Proteins/metabolism ; beta Catenin/metabolism
    Chemical Substances SOX Transcription Factors ; Wnt Proteins ; beta Catenin
    Language English
    Publishing date 2009-08-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1102541-4
    ISSN 1097-0177 ; 1058-8388
    ISSN (online) 1097-0177
    ISSN 1058-8388
    DOI 10.1002/dvdy.22046
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: The C. elegans lethal gut-obstructed gob-1 gene is trehalose-6-phosphate phosphatase.

    Kormish, Jay D / McGhee, James D

    Developmental biology

    2005  Volume 287, Issue 1, Page(s) 35–47

    Abstract: We identified the gob-1 (gut-obstructed) gene in a forward genetic screen for intestinal defects in the nematode Caenorhabditis elegans. gob-1 loss of function results in early larval lethality, at least in part because of a blocked intestinal lumen and ... ...

    Abstract We identified the gob-1 (gut-obstructed) gene in a forward genetic screen for intestinal defects in the nematode Caenorhabditis elegans. gob-1 loss of function results in early larval lethality, at least in part because of a blocked intestinal lumen and consequent starvation. The gob-1 gene is first expressed in the 8E cell stage of the embryonic intestine, and the GATA factor ELT-2 is sufficient but not necessary for this early phase of gob-1 expression; gob-1 expression later becomes widespread in embryos, larvae, and adults. GOB-1 is a member of the HAD-like hydrolase superfamily and shows a robust and specific phosphatase activity for the substrate trehalose-6-phosphate. Trehalose is a glucose disaccharide found in bacteria, fungi, plants, insects, and nematodes but not in mammals. Trehalose plays a number of critical roles such as providing flexible energy reserves and contributing to thermal and osmotic stress resistance. In budding yeast and in plants, the intermediate in trehalose synthesis, trehalose-6-phosphate, has additional critical but less well-defined roles in controlling glycolysis and carbohydrate metabolism. Strong loss-of-function mutants in the C. elegans tps-1 and tps-2 genes (which encode the two trehalose phosphate synthases responsible for trehalose-6-phosphate synthesis) completely suppress the lethality associated with gob-1 loss of function. The suppression of gob-1 lethality by ablation of TPS-1 and TPS-2, the upstream enzymes in the trehalose synthesis pathway, suggests that gob-1 lethality results from a toxic build-up of the intermediate trehalose-6-phosphate, not from an absence of trehalose. GOB-1 is the first trehalose-6-phosphate phosphatase to be identified in nematodes and, because of its associated lethality and distinctive sequence properties, provides a new and attractive target for anti-parasitic drugs.
    MeSH term(s) Animals ; Caenorhabditis elegans/embryology ; Caenorhabditis elegans/enzymology ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Caenorhabditis elegans Proteins/physiology ; GATA Transcription Factors/physiology ; Genes, Lethal ; Hydrolases/genetics ; Intestinal Obstruction/enzymology ; Intestinal Obstruction/genetics ; Intestinal Obstruction/pathology ; Intestines/enzymology ; Intestines/pathology ; Phenotype ; Phosphoric Monoester Hydrolases/genetics ; Phosphoric Monoester Hydrolases/metabolism ; Sequence Analysis, DNA
    Chemical Substances Caenorhabditis elegans Proteins ; ELT-2 protein, C elegans ; GATA Transcription Factors ; Hydrolases (EC 3.-) ; trehalose-phosphatase (EC 3.1.3.12) ; Phosphoric Monoester Hydrolases (EC 3.1.3.2) ; 2-haloacid dehalogenase (EC 3.8.1.2)
    Language English
    Publishing date 2005-11-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1114-9
    ISSN 1095-564X ; 0012-1606
    ISSN (online) 1095-564X
    ISSN 0012-1606
    DOI 10.1016/j.ydbio.2005.08.027
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Ammonia excretion in Caenorhabditis elegans: Physiological and molecular characterization of the rhr-2 knock-out mutant.

    Adlimoghaddam, Aida / O'Donnell, Michael J / Kormish, Jay / Banh, Sheena / Treberg, Jason R / Merz, David / Weihrauch, Dirk

    Comparative biochemistry and physiology. Part A, Molecular & integrative physiology

    2016  Volume 195, Page(s) 46–54

    Abstract: Previous studies have shown the free living soil nematode Caenorhabditis elegans (N2 strain) to be ammonotelic. Ammonia excretion was suggested to take place partially via the hypodermis, involving the Na(+)/K(+)-ATPase (NKA), V-ATPase (VAT), carbonic ... ...

    Abstract Previous studies have shown the free living soil nematode Caenorhabditis elegans (N2 strain) to be ammonotelic. Ammonia excretion was suggested to take place partially via the hypodermis, involving the Na(+)/K(+)-ATPase (NKA), V-ATPase (VAT), carbonic anhydrase, NHX-3 and a functional microtubule network and at least one Rh-like ammonia transporter RHR-1. In the current study, we show that a second Rh-protein, RHR-2, is highly expressed in the hypodermis, here also in the apical membrane of that tissue. To further characterize the role of RHR-2 in ammonia excretion, a knock-out mutant rhr-2 (ok403), further referred to as ∆rhr-2, was employed. Compared to wild-type worms (N2), this mutant showed a lower rate of ammonia excretion and a lower hypodermal H(+) excretion rate. At the same time rhr-1, nka, vat, and nhx-3 showed higher mRNA expression levels when compared to N2. Also, in contrast to N2 worms, ∆rhr-2 did not show enhanced ammonia excretion rates when exposed to a low pH environment, suggesting that RHR-2 represents the apical NH3 pathway that allows ammonia trapping via the hypodermis in N2 worms. A hypothetical model for the mechanism of hypodermal ammonia excretion is proposed on the basis of data in this and previous investigations.
    MeSH term(s) Ammonia/metabolism ; Animals ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/metabolism ; Green Fluorescent Proteins/genetics ; Microscopy, Fluorescence ; Mutation
    Chemical Substances Green Fluorescent Proteins (147336-22-9) ; Ammonia (7664-41-7)
    Language English
    Publishing date 2016-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 121246-1
    ISSN 1531-4332 ; 0300-9629 ; 1095-6433
    ISSN (online) 1531-4332
    ISSN 0300-9629 ; 1095-6433
    DOI 10.1016/j.cbpa.2016.02.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Identification of vacuoles containing extraintestinal differentiated forms of Legionella pneumophila in colonized Caenorhabditis elegans soil nematodes.

    Hellinga, Jacqueline R / Garduño, Rafael A / Kormish, Jay D / Tanner, Jennifer R / Khan, Deirdre / Buchko, Kristyn / Jimenez, Celine / Pinette, Mathieu M / Brassinga, Ann Karen C

    MicrobiologyOpen

    2015  Volume 4, Issue 4, Page(s) 660–681

    Abstract: Legionella pneumophila, a causative agent of Legionnaires' disease, is a facultative intracellular parasite of freshwater protozoa. Legionella pneumophila features a unique developmental network that involves several developmental forms including the ... ...

    Abstract Legionella pneumophila, a causative agent of Legionnaires' disease, is a facultative intracellular parasite of freshwater protozoa. Legionella pneumophila features a unique developmental network that involves several developmental forms including the infectious cyst forms. Reservoirs of L. pneumophila include natural and man-made freshwater systems; however, recent studies have shown that isolates of L. pneumophila can also be obtained directly from garden potting soil suggesting the presence of an additional reservoir. A previous study employing the metazoan Caenorhabditis elegans, a member of the Rhabditidae family of free-living soil nematodes, demonstrated that the intestinal lumen can be colonized with L. pneumophila. While both replicative forms and differentiated forms were observed in C. elegans, these morphologically distinct forms were initially observed to be restricted to the intestinal lumen. Using live DIC imaging coupled with focused transmission electron microscopy analyses, we report here that L. pneumophila is able to invade and establish Legionella-containing vacuoles (LCVs) in the intestinal cells. In addition, LCVs containing replicative and differentiated cyst forms were observed in the pseudocoelomic cavity and gonadal tissue of nematodes colonized with L. pneumophila. Furthermore, establishment of LCVs in the gonadal tissue was Dot/Icm dependent and required the presence of the endocytic factor RME-1 to gain access to maturing oocytes. Our findings are novel as this is the first report, to our knowledge, of extraintestinal LCVs containing L. pneumophila cyst forms in C. elegans tissues, highlighting the potential of soil-dwelling nematodes as an alternate environmental reservoir for L. pneumophila.
    MeSH term(s) Animals ; Caenorhabditis elegans/microbiology ; Gastrointestinal Tract/microbiology ; Gonads/microbiology ; Legionella pneumophila/isolation & purification ; Microscopy, Electron, Transmission ; Microscopy, Interference ; Soil/parasitology ; Vacuoles/microbiology
    Chemical Substances Soil
    Language English
    Publishing date 2015-08
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661368-2
    ISSN 2045-8827 ; 2045-8827
    ISSN (online) 2045-8827
    ISSN 2045-8827
    DOI 10.1002/mbo3.271
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Study of FoxA pioneer factor at silent genes reveals Rfx-repressed enhancer at Cdx2 and a potential indicator of esophageal adenocarcinoma development.

    Watts, Jason A / Zhang, Chaolin / Klein-Szanto, Andres J / Kormish, Jay D / Fu, Jian / Zhang, Michael Q / Zaret, Kenneth S

    PLoS genetics

    2011  Volume 7, Issue 9, Page(s) e1002277

    Abstract: Understanding how silent genes can be competent for activation provides insight into development as well as cellular reprogramming and pathogenesis. We performed genomic location analysis of the pioneer transcription factor FoxA in the adult mouse liver ... ...

    Abstract Understanding how silent genes can be competent for activation provides insight into development as well as cellular reprogramming and pathogenesis. We performed genomic location analysis of the pioneer transcription factor FoxA in the adult mouse liver and found that about one-third of the FoxA bound sites are near silent genes, including genes without detectable RNA polymerase II. Virtually all of the FoxA-bound silent sites are within conserved sequences, suggesting possible function. Such sites are enriched in motifs for transcriptional repressors, including for Rfx1 and type II nuclear hormone receptors. We found one such target site at a cryptic "shadow" enhancer 7 kilobases (kb) downstream of the Cdx2 gene, where Rfx1 restricts transcriptional activation by FoxA. The Cdx2 shadow enhancer exhibits a subset of regulatory properties of the upstream Cdx2 promoter region. While Cdx2 is ectopically induced in the early metaplastic condition of Barrett's esophagus, its expression is not necessarily present in progressive Barrett's with dysplasia or adenocarcinoma. By contrast, we find that Rfx1 expression in the esophageal epithelium becomes gradually extinguished during progression to cancer, i.e, expression of Rfx1 decreased markedly in dysplasia and adenocarcinoma. We propose that this decreased expression of Rfx1 could be an indicator of progression from Barrett's esophagus to adenocarcinoma and that similar analyses of other transcription factors bound to silent genes can reveal unanticipated regulatory insights into oncogenic progression and cellular reprogramming.
    MeSH term(s) Adenocarcinoma/genetics ; Adenocarcinoma/metabolism ; Adenocarcinoma/pathology ; Animals ; Barrett Esophagus/metabolism ; Barrett Esophagus/pathology ; Base Sequence ; Binding Sites ; CDX2 Transcription Factor ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/pathology ; DNA-Binding Proteins/genetics ; Enhancer Elements, Genetic ; Esophageal Neoplasms/genetics ; Esophageal Neoplasms/metabolism ; Esophageal Neoplasms/pathology ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Genome ; Hepatocyte Nuclear Factor 3-alpha/genetics ; Hepatocyte Nuclear Factor 3-alpha/metabolism ; Hepatocyte Nuclear Factor 3-beta/genetics ; Hepatocyte Nuclear Factor 3-beta/metabolism ; Homeodomain Proteins/genetics ; Humans ; Liver/metabolism ; Mice ; Molecular Sequence Data ; Promoter Regions, Genetic ; Receptors, Cytoplasmic and Nuclear/genetics ; Receptors, Cytoplasmic and Nuclear/metabolism ; Regulatory Factor X Transcription Factors ; Regulatory Factor X1 ; Transcription Factors/genetics ; Transcriptional Activation
    Chemical Substances CDX2 Transcription Factor ; Cdx2 protein, mouse ; DNA-Binding Proteins ; Foxa1 protein, mouse ; Foxa2 protein, mouse ; Hepatocyte Nuclear Factor 3-alpha ; Homeodomain Proteins ; RFX1 protein, human ; Receptors, Cytoplasmic and Nuclear ; Regulatory Factor X Transcription Factors ; Regulatory Factor X1 ; Rfx1 protein, mouse ; Transcription Factors ; Hepatocyte Nuclear Factor 3-beta (135845-92-0)
    Language English
    Publishing date 2011-09-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2186725-2
    ISSN 1553-7404 ; 1553-7390
    ISSN (online) 1553-7404
    ISSN 1553-7390
    DOI 10.1371/journal.pgen.1002277
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Pax3 regulation of FGF signaling affects the progression of embryonic progenitor cells into the myogenic program.

    Lagha, Mounia / Kormish, Jay D / Rocancourt, Didier / Manceau, Marie / Epstein, Jonathan A / Zaret, Kenneth S / Relaix, Frédéric / Buckingham, Margaret E

    Genes & development

    2008  Volume 22, Issue 13, Page(s) 1828–1837

    Abstract: Pax3/7-dependent stem cells play an essential role in skeletal muscle development. We now show that Fgfr4 lies genetically downstream from Pax3 and is a direct target. In chromatin immunoprecipitation (ChIP)-on-chip experiments, Pax3 binds to a sequence ... ...

    Abstract Pax3/7-dependent stem cells play an essential role in skeletal muscle development. We now show that Fgfr4 lies genetically downstream from Pax3 and is a direct target. In chromatin immunoprecipitation (ChIP)-on-chip experiments, Pax3 binds to a sequence 3' of the Fgfr4 gene that directs Pax3-dependent expression at sites of myogenesis in transgenic mouse embryos. The activity of this regulatory element is also partially dependent on E-boxes, targets of the myogenic regulatory factors, which are expressed as progenitor cells enter the myogenic program. Other FGF signaling components, notably Sprouty1, are also regulated by Pax3. In vivo manipulation of Sprouty expression reveals that FGF signaling affects the balance between Pax-positive progenitor cells and committed myoblasts. These results provide new insight into the Pax-initiated regulatory network that modulates stem cell maintenance versus tissue differentiation.
    MeSH term(s) 3' Flanking Region ; Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Cell Differentiation ; Embryonic Stem Cells/cytology ; Embryonic Stem Cells/metabolism ; Fibroblast Growth Factors/physiology ; Membrane Proteins/metabolism ; Mice ; Molecular Sequence Data ; Muscle Development ; Myoblasts/cytology ; Myoblasts/metabolism ; PAX3 Transcription Factor ; Paired Box Transcription Factors/physiology ; Phosphoproteins/metabolism ; Receptor, Fibroblast Growth Factor, Type 4/metabolism ; Response Elements ; Signal Transduction
    Chemical Substances Adaptor Proteins, Signal Transducing ; Membrane Proteins ; PAX3 Transcription Factor ; Paired Box Transcription Factors ; Phosphoproteins ; Spry1 protein, mouse ; Pax3 protein, mouse (138016-91-8) ; Fibroblast Growth Factors (62031-54-3) ; Fgfr4 protein, mouse (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 4 (EC 2.7.10.1)
    Language English
    Publishing date 2008-07-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 806684-x
    ISSN 1549-5477 ; 0890-9369
    ISSN (online) 1549-5477
    ISSN 0890-9369
    DOI 10.1101/gad.477908
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Itm2a is a Pax3 target gene, expressed at sites of skeletal muscle formation in vivo.

    Lagha, Mounia / Mayeuf-Louchart, Alicia / Chang, Ted / Montarras, Didier / Rocancourt, Didier / Zalc, Antoine / Kormish, Jay / Zaret, Kenneth S / Buckingham, Margaret E / Relaix, Frederic

    PloS one

    2013  Volume 8, Issue 5, Page(s) e63143

    Abstract: The paired-box homeodomain transcription factor Pax3 is a key regulator of the nervous system, neural crest and skeletal muscle development. Despite the important role of this transcription factor, very few direct target genes have been characterized. We ...

    Abstract The paired-box homeodomain transcription factor Pax3 is a key regulator of the nervous system, neural crest and skeletal muscle development. Despite the important role of this transcription factor, very few direct target genes have been characterized. We show that Itm2a, which encodes a type 2 transmembrane protein, is a direct Pax3 target in vivo, by combining genetic approaches and in vivo chromatin immunoprecipitation assays. We have generated a conditional mutant allele for Itm2a, which is an imprinted gene, by flanking exons 2-4 with loxP sites and inserting an IRESnLacZ reporter in the 3' UTR of the gene. The LacZ reporter reproduces the expression profile of Itm2a, and allowed us to further characterize its expression at sites of myogenesis, in the dermomyotome and myotome of somites, and in limb buds, in the mouse embryo. We further show that Itm2a is not only expressed in adult muscle fibres but also in the satellite cells responsible for regeneration. Itm2a mutant mice are viable and fertile with no overt phenotype during skeletal muscle formation or regeneration. Potential compensatory mechanisms are discussed.
    MeSH term(s) Animals ; Cell Nucleus/metabolism ; Female ; Gene Expression Regulation, Developmental ; Male ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Muscle Development ; Muscle, Skeletal/cytology ; Muscle, Skeletal/embryology ; Muscle, Skeletal/metabolism ; Myogenic Regulatory Factor 5/metabolism ; PAX3 Transcription Factor ; Paired Box Transcription Factors/metabolism ; Satellite Cells, Skeletal Muscle/metabolism
    Chemical Substances Itm2a protein, mouse ; Membrane Proteins ; Myf5 protein, mouse ; Myogenic Regulatory Factor 5 ; PAX3 Transcription Factor ; Paired Box Transcription Factors ; Pax3 protein, mouse (138016-91-8)
    Language English
    Publishing date 2013-05-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0063143
    Database MEDical Literature Analysis and Retrieval System OnLINE

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