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https://www.readbyqxmd.com/read/29739871/canonical-notch-signaling-directs-the-fate-of-differentiating-neurocompetent-progenitors-in-the-mammalian-olfactory-epithelium
#1
Daniel B Herrick, Zhen Guo, Woochan Jang, Nikolai Schnittke, James E Schwob
The adult olfactory epithelium (OE) has the remarkable capacity to regenerate fully both neurosensory and non-neuronal cell types after severe epithelial injury. Life-long persistence of two stem cell populations supports OE regeneration when damaged: the horizontal basal cells (HBCs) -- dormant and held in reserve, and globose basal cells (GBCs) -- a heterogeneous population most of which are actively dividing. Both populations regenerate all cell types of the OE after injury, but the mechanisms underlying neuronal vs...
May 8, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29593239/attenuated-notch-signaling-in-schizophrenia-and-bipolar-disorder
#2
Eva Z Hoseth, Florian Krull, Ingrid Dieset, Ragni H Mørch, Sigrun Hope, Erlend S Gardsjord, Nils Eiel Steen, Ingrid Melle, Hans-Richard Brattbakk, Vidar M Steen, Pål Aukrust, Srdjan Djurovic, Ole A Andreassen, Thor Ueland
The Notch signaling pathway plays a crucial role in neurodevelopment and in adult brain homeostasis. We aimed to further investigate Notch pathway activity in bipolar disorder (BD) and schizophrenia (SCZ) by conducting a pathway analysis. We measured plasma levels of Notch ligands (DLL1 and DLK1) using enzyme immunoassays in a large sample of patients (SCZ n = 551, BD n = 246) and healthy controls (HC n = 639). We also determined Notch pathway related gene expression levels by microarray analyses from whole blood in a subsample (SCZ n = 338, BD n = 241 and HC n = 263)...
March 28, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29575203/glucocorticoids-inhibit-notch-target-gene-expression-in-osteoblasts
#3
Stefano Zanotti, Jungeun Yu, Suyash Adhikari, Ernesto Canalis
Glucocorticoids in excess suppress osteoblast function and cause osteoporosis. We demonstrated that cortisol induces the expression of selected Notch receptors in osteoblasts, revealing a potential mechanism for the skeletal effects of glucocorticoids. However, it remains to be determined whether increased expression of Notch receptors results into enhanced signaling. Following activation of Notch, its intracellular domain (NICD) binds to the DNA-associated protein recombination signal binding protein for immunoglobulin kappa-J region (RBPJ) and induces the expression of target genes such as Hey1, Hey2, and HeyL...
March 25, 2018: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/29563122/epigenetic-programming-of-t-cells-impacts-immune-reconstitution-in-hematopoietic-stem-cell-transplant-recipients
#4
Kristine Hardy, Corey Smith, Wen Juan Tu, Robert McCuaig, Archana Panikkar, Vijayendra Dasari, Fan Wu, Siok-Keen Tey, Geoffrey R Hill, Rajiv Khanna, Sudha Rao
Immune reconstitution following hematopoietic stem cell transplantation (HSCT) is critical in preventing harmful sequelae in recipients with cytomegalovirus (CMV) infection. To understand the molecular mechanisms underlying immune reconstitution kinetics, we profiled the transcriptome-chromatin accessibility landscape of CMV-specific CD8+ T cells from HCST recipients with different immune reconstitution efficiencies. CMV-specific T cells from HSCT recipients with stable antiviral immunity expressed higher levels of interferon/defense response and cell cycle genes in an interconnected network involving PI3KCG , STAT5B , NFAT , RBPJ , and lower HDAC6 , increasing chromatin accessibility at the enhancer regions of immune and T-cell receptor signaling pathway genes...
March 27, 2018: Blood Advances
https://www.readbyqxmd.com/read/29462212/epstein-barr-virus-nuclear-antigen-ebna-lp-is-essential-for-transforming-na%C3%A3-ve-b-cells-and-facilitates-recruitment-of-transcription-factors-to-the-viral-genome
#5
Agnieszka Szymula, Richard D Palermo, Amr Bayoumy, Ian J Groves, Mohammed Ba Abdullah, Beth Holder, Robert E White
The Epstein-Barr virus (EBV) nuclear antigen leader protein (EBNA-LP) is the first viral latency-associated protein produced after EBV infection of resting B cells. Its role in B cell transformation is poorly defined, but it has been reported to enhance gene activation by the EBV protein EBNA2 in vitro. We generated EBNA-LP knockout (LPKO) EBVs containing a STOP codon within each repeat unit of internal repeat 1 (IR1). EBNA-LP-mutant EBVs established lymphoblastoid cell lines (LCLs) from adult B cells at reduced efficiency, but not from umbilical cord B cells, which died approximately two weeks after infection...
February 2018: PLoS Pathogens
https://www.readbyqxmd.com/read/29449332/inhibition-of-endothelial-notch1-signaling-attenuates-inflammation-by-reducing-cytokine-mediated-histone-acetylation-at-inflammatory-enhancers
#6
Lars la Cour Poulsen, Reidunn Jetne Edelmann, Stig Krüger, Rodrigo Diéguez-Hurtado, Akshay Shah, Tor Espen Stav-Noraas, Anastasia Renzi, Monika Szymanska, Junbai Wang, Manuel Ehling, Rui Benedito, Monika Kasprzycka, Espen Bækkevold, Olav Sundnes, Kim S Midwood, Helge Scott, Philippe Collas, Christian W Siebel, Ralf H Adams, Guttorm Haraldsen, Eirik Sundlisæter, Johanna Hol
OBJECTIVE: Endothelial upregulation of adhesion molecules serves to recruit leukocytes to inflammatory sites and appears to be promoted by NOTCH1; however, current models based on interactions between active NOTCH1 and NF-κB components cannot explain the transcriptional selectivity exerted by NOTCH1 in this context. APPROACH AND RESULTS: Observing that Cre/Lox-induced conditional mutations of endothelial Notch modulated inflammation in murine contact hypersensitivity, we found that IL (interleukin)-1β stimulation induced rapid recruitment of RELA (v-rel avian reticuloendotheliosis viral oncogene homolog A) to genomic sites occupied by NOTCH1-RBPJ (recombination signal-binding protein for immunoglobulin kappa J region) and that NOTCH1 knockdown reduced histone H3K27 acetylation at a subset of NF-κB-directed inflammatory enhancers...
April 2018: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/29421235/analysis-of-rat-cardiac-myocytes-and-fibroblasts-identifies-combinatorial-enhancer-organization-and-transcription-factor-families
#7
Tal Golan-Lagziel, Yair E Lewis, Omer Shkedi, Guy Douvdevany, Lilac H Caspi, Izhak Kehat
Cardiac fibroblasts play key roles in both health and disease. Their regulatory elements, transcription factors (TFs), and mechanisms of expression control have not been fully elucidated. We used a differential open chromatin approach, coupled with active enhancer mark, transcriptomic, and computational TFs binding analysis to map cell-type-specific active enhancers in cardiac fibroblasts and cardiomyocytes, and outline the TFs families that control them. This approach was validated by its ability to uncover the known cardiomyocyte TF biology in an unbiased manner, and was then applied to cardiac fibroblasts...
March 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29413900/expression-of-the-human-timm23-and-timm23b-genes-is-regulated-by-the-gabp-transcription-factor
#8
Jesús A Prieto-Ruiz, Rafael Alis, Sandra García-Benlloch, Sara Sáez-Atiénzar, Ignacio Ventura, José M Hernández-Andreu, José Hernández-Yago, José R Blesa
The TIM23 protein is a key component of the mitochondrial import machinery in yeast and mammals. TIM23 is the channel-forming subunit of the translocase of the inner mitochondrial membrane (TIM23) complex, which mediates preprotein translocation across the mitochondrial inner membrane. In this paper, we aimed to characterize the promoter region of the highly similar human TIM23 orthologs: TIMM23 and TIMM23B. Bioinformatic analysis revealed putative sites for the GA-binding protein (GABP) and the recombination signal binding protein for immunoglobulin kappa J (RBPJ) transcription factors in both promoters...
February 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29390495/a-boy-with-13-34-mb-interstitial-deletion-of-chromosome-4p15-a-new-case-report-and-review-of-the-literature
#9
REVIEW
Anca Florentina Mitroi, Mariana Aschie, Adriana Apostol, Costel Brinzan, Georgeta Cozaru, Adrian Nelutu Mitroi
RATIONALE: To date, >40 cases have been described with interstitial deletions involving the 4p15 region. PATIENT CONCERNS AND DIAGNOSIS: We report a case of a 3-year-old boy with an interstitial de novo deletion of approximately 13.34 Mb in 4p15.1-15.31 having mild developmental delay and multiple minor congenital abnormalities. LESSONS: This case presents a clinical manifestation that is similar but not identical to other reported cases...
December 2017: Medicine (Baltimore)
https://www.readbyqxmd.com/read/29386140/notch2-signaling-maintains-nsc-quiescence-in-the-murine-ventricular-subventricular-zone
#10
Anna Engler, Chiara Rolando, Claudio Giachino, Ichiko Saotome, Andrea Erni, Callum Brien, Runrui Zhang, Ursula Zimber-Strobl, Freddy Radtke, Spyros Artavanis-Tsakonas, Angeliki Louvi, Verdon Taylor
Neurogenesis continues in the ventricular-subventricular zone (V-SVZ) of the adult forebrain from quiescent neural stem cells (NSCs). V-SVZ NSCs are a reservoir for new olfactory bulb (OB) neurons that migrate through the rostral migratory stream (RMS). To generate neurons, V-SVZ NSCs need to activate and enter the cell cycle. The mechanisms underlying NSC transition from quiescence to activity are poorly understood. We show that Notch2, but not Notch1, signaling conveys quiescence to V-SVZ NSCs by repressing cell-cycle-related genes and neurogenesis...
January 23, 2018: Cell Reports
https://www.readbyqxmd.com/read/29339402/canonical-notch-signaling-is-dispensable-for-adult-steady-state-and-stress-myelo-erythropoiesis
#11
Sara Duarte, Petter S Woll, Natalija Buza-Vidas, Desmond Wai Loon Chin, Hanane Boukarabila, Tiago C Luís, Laura Stenson, Tiphaine Bouriez-Jones, Helen Ferry, Adam J Mead, Deborah Atkinson, Shaobo Jin, Sally-Ann Clark, Bishan Wu, Emmanouela Repapi, Nicki Gray, Stephen Taylor, Anders P Mutvei, Yat Long Tsoi, Claus Nerlov, Urban Lendahl, Sten Eirik W Jacobsen
Although an essential role for canonical Notch signaling in generation of hematopoietic stem cells in the embryo and in thymic T-cell development is well established, its role in adult bone marrow (BM) myelopoiesis remains unclear. Some studies, analyzing myeloid progenitors in adult mice with inhibited Notch signaling, implicated distinct roles of canonical Notch signaling in regulation of progenitors for the megakaryocyte, erythroid, and granulocyte-macrophage cell lineages. However, these studies might also have targeted other pathways...
April 12, 2018: Blood
https://www.readbyqxmd.com/read/29305585/sumoylation-of-notch1-represses-its-target-gene-expression-during-cell-stress
#12
Christian J M Antila, Vilma Rraklli, Henri A Blomster, Käthe M Dahlström, Tiina A Salminen, Johan Holmberg, Lea Sistonen, Cecilia Sahlgren
The Notch signaling pathway is a key regulator of stem cells during development, and its deregulated activity is linked to developmental defects and cancer. Transcriptional activation of Notch target genes requires cleavage of the Notch receptor in response to ligand binding, production of the Notch intracellular domain (NICD1), NICD1 migration into the nucleus, and assembly of a transcriptional complex. Post-translational modifications of Notch regulate its trafficking, turnover, and transcriptional activity...
March 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29302047/functional-and-association-analysis-of-an-amerindian-derived-population-specific-p-thr280met-variant-in-rbpjl-a-component-of-the-ptf1-complex
#13
Anup K Nair, Jeff R Sutherland, Michael Traurig, Paolo Piaggi, Peng Chen, Sayuko Kobes, Robert L Hanson, Clifton Bogardus, Leslie J Baier
PTF1 complex is critical for pancreatic development and maintenance of adult exocrine pancreas. As a part of our ongoing studies to identify genetic variation that contributes to type 2 diabetes (T2D) in American Indians, we analyzed variation in genes that form this complex, namely PTF1A, RBPJ, and its paralogue RBPJL. A c.839C>T (p.(Thr280Met)) variant (rs200998587:C>T, risk allele frequency = 0.03) in RBPJL, identified only in Amerindian-derived populations, associated with T2D (OR = 1.60[1...
February 2018: European Journal of Human Genetics: EJHG
https://www.readbyqxmd.com/read/29248546/accelerated-endothelial-to-mesenchymal-transition-increased-fibrosis-via-deleting-notch-signaling-in-wound-vasculature
#14
Jatin Patel, Betoul Baz, Ho Yi Wong, James S Lee, Kiarash Khosrotehrani
Skin wound healing in adults is characterized by a peak of angiogenesis followed by regression of the excessive vasculature in parallel with collagen deposition and fibrosis in the wound. We hypothesized that regressing vessels in healing wounds were in fact entering an endothelial to mesenchymal transition contributing to scarring. Using vascular-specific fate tracking (Cdh5-creERt2 /ROSA-YFP mice), full-thickness excisional wounds were analyzed to reveal a time-dependent transition from endothelial phenotype characterized by vascular endothelial-cadherin, CD31, and CD34 toward a mesenchymal phenotype characterized by alpha-smooth muscle actin and fibroblast-specific protein 1 expression...
December 14, 2017: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/29242273/rbpj-mediates-uterine-repair-in-the-mouse-and-is-reduced-in-women-with-recurrent-pregnancy-loss
#15
Michael R Strug, Ren-Wei Su, Tae Hoon Kim, Alessandro Mauriello, Carlo Ticconi, Bruce A Lessey, Steven L Young, Jeong Mook Lim, Jae-Wook Jeong, Asgerally T Fazleabas
Unexplained recurrent pregnancy loss (uRPL) is associated with repeated embryo loss and endometrial repair with elevated endometrial expression of inflammatory cytokines, including IFN-γ. Notch signaling through its transcription factor recombination signal binding protein Jκ (RBPJ) regulates mechanisms including the immune response and repair after tissue injury. Initially, null mutation of RBPJ in the mouse uterus ( Pgrcre/+ Rbpjf/f ; Rbpj c-KO) results in subfertility, but we have found that these mice become infertile after pregnancy as a result of dysfunctional postpartum uterine repair, including delayed endometrial epithelial and myometrial regeneration...
January 8, 2018: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/29241683/notch-pathway-signaling-in-the-skin-antagonizes-merkel-cell-development
#16
Gregory J Logan, Margaret C Wright, Adam C Kubicki, Stephen M Maricich
Merkel cells are mechanosensitive skin cells derived from the epidermal lineage whose development requires expression of the basic helix-loop-helix transcription factor Atoh1. The genes and pathways involved in regulating Merkel cell development during embryogenesis are poorly understood. Notch pathway signaling antagonizes Atoh1 expression in many developing body regions, so we hypothesized that Notch signaling might inhibit Merkel cell development. We found that conditional, constitutive overexpression of the Notch intracellular domain (NICD) in mouse epidermis significantly decreased Merkel cell numbers in whisker follicles and touch domes of hairy skin...
February 15, 2018: Developmental Biology
https://www.readbyqxmd.com/read/29180399/diminished-microrna-29b-level-is-associated-with-brd4-mediated-activation-of-oncogenes-in-cutaneous-t-cell-lymphoma
#17
Rebecca Kohnken, Jing Wen, Bethany Mundy-Bosse, Kathleen McConnell, Ashleigh Keiter, Leah Grinshpun, Alex Hartlage, Max Yano, Betina McNeil, Nitin Chakravarti, Basem William, James E Bradner, Michael A Caligiuri, Pierluigi Porcu, Anjali Mishra
MicroRNA (miRNA) dysregulation is a hallmark of cutaneous T-cell lymphoma (CTCL), an often-fatal malignancy of skin-homing CD4+ T cells for which there are few effective therapies. The role of microRNAs (miRs) in controlling epigenetic modifier-dependent transcriptional regulation in CTCL is unknown. In this study, we characterize a novel miR dysregulation that contributes to overexpression of the epigenetic reader bromodomain-containing protein 4 (BRD4). We used patient CD4+ T cells to show diminished levels of miR-29b compared with healthy donor cells...
February 15, 2018: Blood
https://www.readbyqxmd.com/read/29126263/notch-signaling-regulates-differentiation-and-steroidogenesis-in-female-mouse-ovarian-granulosa-cells
#18
Rexxi D Prasasya, Kelly E Mayo
The Notch pathway is a highly conserved juxtacrine signaling mechanism that is important for many cellular processes during development, including differentiation and proliferation. Although Notch is important during ovarian follicle formation and early development, its functions during the gonadotropin-dependent stages of follicle development are largely unexplored. We observed positive regulation of Notch activity and expression of Notch ligands and receptors following activation of the luteinizing hormone-receptor in prepubertal mouse ovary...
January 1, 2018: Endocrinology
https://www.readbyqxmd.com/read/29057904/the-ank-repeats-of-notch-4-int3-activate-nf-%C3%AE%C2%BAb-canonical-pathway-in-the-absence-of-rbpj-and-causes-mammary-tumorigenesis
#19
Ahmed Raafat, Sharon Bargo, David McCurdy, Robert Callahan
Transgenic mice expressing the Notch-4 intracellular domain (designated Int3) in the mammary gland have two phenotypes exhibited with 100% penetrance: arrest of mammary alveolar/lobular development and mammary tumorigenesis. Notch-4 signaling is mediated primarily through the interaction of Int3 with the transcription repressor/activator Rbpj. Interestingly, WAP-Int3/Rbpj knockout mice have normal mammary gland development but still developed mammary tumors with a slightly longer latency than the WAP-Int3 mice...
October 20, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29038527/blood-vessel-control-of-macrophage-maturation-promotes-arteriogenesis-in-ischemia
#20
Kashyap Krishnasamy, Anne Limbourg, Tamar Kapanadze, Jaba Gamrekelashvili, Christian Beger, Christine Häger, Vladimir J Lozanovski, Christine S Falk, L Christian Napp, Johann Bauersachs, Matthias Mack, Hermann Haller, Christian Weber, Ralf H Adams, Florian P Limbourg
Ischemia causes an inflammatory response that is intended to restore perfusion and homeostasis yet often aggravates damage. Here we show, using conditional genetic deletion strategies together with adoptive cell transfer experiments in a mouse model of hind limb ischemia, that blood vessels control macrophage differentiation and maturation from recruited monocytes via Notch signaling, which in turn promotes arteriogenesis and tissue repair. Macrophage maturation is controlled by Notch ligand Dll1 expressed in vascular endothelial cells of arteries and requires macrophage canonical Notch signaling via Rbpj, which simultaneously suppresses an inflammatory macrophage fate...
October 16, 2017: Nature Communications
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