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  1. Buch ; Dissertation / Habilitation: Betreuung von Kindern mit konnataler Hypothyreose

    Christ, Annabel

    Erfahrungen der Universitätskinderklinik Erlangen

    2006  

    Verfasserangabe vorgelegt von Annabel Christ
    Sprache Deutsch
    Umfang 98, XXXV Bl. : Ill., graph. Darst.
    Erscheinungsland Deutschland
    Dokumenttyp Buch ; Dissertation / Habilitation
    Dissertation / Habilitation Erlangen, Nürnberg, Univ., Diss., 2006
    HBZ-ID HT014669082
    Datenquelle Katalog ZB MED Medizin, Gesundheit

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    SignaturLeihstatusStandort
    2006 E 450 bestellbar zur Ausleihe Magazin

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  2. Artikel ; Online: LRP2 controls sonic hedgehog-dependent differentiation of cardiac progenitor cells during outflow tract formation.

    Christ, Annabel / Marczenke, Maike / Willnow, Thomas E

    Human molecular genetics

    2020  Band 29, Heft 19, Seite(n) 3183–3196

    Abstract: Conotruncal malformations are a major cause of congenital heart defects in newborn infants. Recently, genetic screens in humans and in mouse models have identified mutations in LRP2, a multi-ligand receptor, as a novel cause of a common arterial trunk, a ...

    Abstract Conotruncal malformations are a major cause of congenital heart defects in newborn infants. Recently, genetic screens in humans and in mouse models have identified mutations in LRP2, a multi-ligand receptor, as a novel cause of a common arterial trunk, a severe form of outflow tract (OFT) defect. Yet, the underlying mechanism why the morphogen receptor LRP2 is essential for OFT development remained unexplained. Studying LRP2-deficient mouse models, we now show that LRP2 is expressed in the cardiac progenitor niche of the anterior second heart field (SHF) that contributes to the elongation of the OFT during separation into aorta and pulmonary trunk. Loss of LRP2 in mutant mice results in the depletion of a pool of sonic hedgehog-dependent progenitor cells in the anterior SHF due to premature differentiation into cardiomyocytes as they migrate into the OFT myocardium. Depletion of this cardiac progenitor cell pool results in aberrant shortening of the OFT, the likely cause of CAT formation in affected mice. Our findings identified the molecular mechanism whereby LRP2 controls the maintenance of progenitor cell fate in the anterior SHF essential for OFT separation, and why receptor dysfunction is a novel cause of conotruncal malformation.
    Mesh-Begriff(e) Animals ; Cell Differentiation ; Cell Lineage ; Cell Movement ; Cell Proliferation ; Female ; Heart Defects, Congenital/etiology ; Heart Defects, Congenital/metabolism ; Heart Defects, Congenital/pathology ; Hedgehog Proteins/genetics ; Hedgehog Proteins/metabolism ; Low Density Lipoprotein Receptor-Related Protein-2/physiology ; Mice ; Mice, Knockout ; Morphogenesis ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Signal Transduction ; Stem Cells/metabolism ; Stem Cells/pathology
    Chemische Substanzen Hedgehog Proteins ; Low Density Lipoprotein Receptor-Related Protein-2 ; Lrp2 protein, mouse ; Shh protein, mouse
    Sprache Englisch
    Erscheinungsdatum 2020-09-03
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1108742-0
    ISSN 1460-2083 ; 0964-6906
    ISSN (online) 1460-2083
    ISSN 0964-6906
    DOI 10.1093/hmg/ddaa200
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Endocytic receptor LRP2/megalin-of holoprosencephaly and renal Fanconi syndrome.

    Willnow, Thomas E / Christ, Annabel

    Pflugers Archiv : European journal of physiology

    2017  Band 469, Heft 7-8, Seite(n) 907–916

    Abstract: Megalin (or LRP2) is an endocytic receptor that plays a central role in embryonic development and adult tissue homeostasis. Loss of this receptor in congenital or acquired diseases results in multiple organ dysfunctions, including forebrain malformation ( ...

    Abstract Megalin (or LRP2) is an endocytic receptor that plays a central role in embryonic development and adult tissue homeostasis. Loss of this receptor in congenital or acquired diseases results in multiple organ dysfunctions, including forebrain malformation (holoprosencephaly) and renal reabsorption defects (renal Fanconi syndrome). Here, we describe current concepts of the mode of receptor action that include co-receptors and a repertoire of different ligands, and we discuss how these interactions govern functional integrity of the kidney and the brain, and cause disease when defective.
    Sprache Englisch
    Erscheinungsdatum 2017-08
    Erscheinungsland Germany
    Dokumenttyp Journal Article ; Review
    ZDB-ID 6380-0
    ISSN 1432-2013 ; 0031-6768
    ISSN (online) 1432-2013
    ISSN 0031-6768
    DOI 10.1007/s00424-017-1992-0
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

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    Uc I Zs.35: Hefte anzeigen Standort:
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  4. Artikel ; Online: LRP2 contributes to planar cell polarity-dependent coordination of motile cilia function.

    Bunatyan, Lena / Margineanu, Anca / Boutin, Camille / Montcouquiol, Mireille / Bachmann, Sebastian / Ilsø Christensen, Erik / Willnow, Thomas E / Christ, Annabel

    Cell and tissue research

    2023  Band 392, Heft 2, Seite(n) 535–551

    Abstract: Motile cilia are protruding organelles on specialized epithelia that beat in a synchronous fashion to propel extracellular fluids. Coordination and orientation of cilia beating on individual cells and across tissues is a complex process dependent on ... ...

    Abstract Motile cilia are protruding organelles on specialized epithelia that beat in a synchronous fashion to propel extracellular fluids. Coordination and orientation of cilia beating on individual cells and across tissues is a complex process dependent on planar cell polarity (PCP) signaling. Asymmetric sorting of PCP pathway components, essential to establish planar polarity, involves trafficking along the endocytic path, but the underlying regulatory processes remain incompletely understood. Here, we identified the endocytic receptor LRP2 as regulator of PCP component trafficking in ependyma, a multi-ciliated cell type that is involved in facilitating flow of the cerebrospinal fluid in the brain ventricular system. Lack of receptor expression in gene-targeted mice results in a failure to sort PCP core proteins to the anterior or posterior cell side and, consequently, in the inability to coordinate cilia arrangement and to aligned beating (loss of rotational and translational polarity). LRP2 deficiency coincides with a failure to sort NHERF1, a cytoplasmic LRP2 adaptor to the anterior cell side. As NHERF1 is essential to translocate PCP core protein Vangl2 to the plasma membrane, these data suggest a molecular mechanism whereby LRP2 interacts with PCP components through NHERF1 to control their asymmetric sorting along the endocytic path. Taken together, our findings identified the endocytic receptor LRP2 as a novel regulator of endosomal trafficking of PCP proteins, ensuring their asymmetric partition and establishment of translational and rotational planar cell polarity in the ependyma.
    Mesh-Begriff(e) Animals ; Mice ; Cilia/metabolism ; Cell Polarity ; Ependyma/metabolism ; Cerebral Ventricles/metabolism ; Carrier Proteins/metabolism ; Wnt Signaling Pathway ; Low Density Lipoprotein Receptor-Related Protein-2/metabolism
    Chemische Substanzen Carrier Proteins ; Lrp2 protein, mouse ; Low Density Lipoprotein Receptor-Related Protein-2
    Sprache Englisch
    Erscheinungsdatum 2023-02-11
    Erscheinungsland Germany
    Dokumenttyp Journal Article
    ZDB-ID 125067-x
    ISSN 1432-0878 ; 0302-766X
    ISSN (online) 1432-0878
    ISSN 0302-766X
    DOI 10.1007/s00441-023-03757-7
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

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    Ub I Zs.94: Hefte anzeigen Standort:
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  5. Artikel ; Online: LRP2 controls sonic hedgehog-dependent differentiation of cardiac progenitor cells during outflow tract formation

    Christ, Annabel / Willnow, Thomas E.

    bioRxiv

    Abstract: Conotruncal malformations are a major cause of congenital heart defects in newborn infants. Recently, genetic screens in humans and mouse models have identified mutations in LRP2 as a novel cause of a common arterial trunk, a severe form of outflow tract ...

    Abstract Conotruncal malformations are a major cause of congenital heart defects in newborn infants. Recently, genetic screens in humans and mouse models have identified mutations in LRP2 as a novel cause of a common arterial trunk, a severe form of outflow tract (OFT) defect. Yet, the underlying mechanism why the morphogen receptor LRP2 is essential for OFT development remained unexplained. Studying LRP2-deficient mouse models, we now show that LRP2 is expressed in the cardiac progenitor niche of the anterior second heart field (SHF) that contributes to elongation of the OFT during separation into aorta and pulmonary trunk. Loss of LRP2 in mutant mice results in depletion of a pool of sonic hedgehog-dependent progenitor cells in the SHF due to premature differentiation into cardiomyocytes as they migrate into the OFT myocardium. Depletion of this cardiac progenitor cell pool results in aberrant shortening of the OFT, the cause of CAT formation in affected mice. Our findings identified the molecular mechanism whereby LRP2 controls maintenance of progenitor cell fate in the anterior SHF essential for OFT separation, and why receptor dysfunction is a novel cause of conotruncal malformation.
    Schlagwörter covid19
    Verlag BioRxiv
    Dokumenttyp Artikel ; Online
    DOI 10.1101/801910
    Datenquelle COVID19

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  6. Artikel: LRP2 controls sonic hedgehog-dependent differentiation of cardiac progenitor cells during outflow tract formation

    Christ, Annabel / Marczenke, Maike / Willnow, Thomas E

    Hum. mol. genet

    Abstract: Conotruncal malformations are a major cause of congenital heart defects in newborn infants. Recently, genetic screens in humans and in mouse models have identified mutations in LRP2, a multi-ligand receptor, as a novel cause of a common arterial trunk, a ...

    Abstract Conotruncal malformations are a major cause of congenital heart defects in newborn infants. Recently, genetic screens in humans and in mouse models have identified mutations in LRP2, a multi-ligand receptor, as a novel cause of a common arterial trunk, a severe form of outflow tract (OFT) defect. Yet, the underlying mechanism why the morphogen receptor LRP2 is essential for OFT development remained unexplained. Studying LRP2-deficient mouse models, we now show that LRP2 is expressed in the cardiac progenitor niche of the anterior second heart field (SHF) that contributes to elongation of the OFT during separation into aorta and pulmonary trunk. Loss of LRP2 in mutant mice results in depletion of a pool of sonic hedgehog-dependent progenitor cells in the anterior SHF due to premature differentiation into cardiomyocytes as they migrate into the OFT myocardium. Depletion of this cardiac progenitor cell pool results in aberrant shortening of the OFT, the likely cause of CAT formation in affected mice. Our findings identified the molecular mechanism whereby LRP2 controls maintenance of progenitor cell fate in the anterior SHF essential for OFT separation, and why receptor dysfunction is a novel cause of conotruncal malformation.
    Schlagwörter covid19
    Verlag WHO
    Dokumenttyp Artikel
    Anmerkung WHO #Covidence: #32901292
    Datenquelle COVID19

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  7. Artikel ; Online: Cdon

    Hong, Mingi / Christ, Annabel / Christa, Anna / Willnow, Thomas E / Krauss, Robert S

    eLife

    2020  Band 9

    Abstract: Holoprosencephaly (HPE), a defect in midline patterning of the forebrain and midface, arises ~1 in 250 conceptions. It is associated with predisposing mutations in the Nodal and Hedgehog (HH) pathways, with penetrance and expressivity graded by genetic ... ...

    Abstract Holoprosencephaly (HPE), a defect in midline patterning of the forebrain and midface, arises ~1 in 250 conceptions. It is associated with predisposing mutations in the Nodal and Hedgehog (HH) pathways, with penetrance and expressivity graded by genetic and environmental modifiers, via poorly understood mechanisms. CDON is a multifunctional co-receptor, including for the HH pathway. In mice,
    Mesh-Begriff(e) Animals ; Cell Adhesion Molecules/genetics ; Cell Adhesion Molecules/metabolism ; Disease Models, Animal ; Ethanol/adverse effects ; Female ; Holoprosencephaly/chemically induced ; Holoprosencephaly/genetics ; Holoprosencephaly/pathology ; Maternal Exposure ; Mice ; Mutation/genetics ; Nodal Protein/genetics ; Nodal Protein/metabolism ; Signal Transduction/drug effects
    Chemische Substanzen Cdon protein, mouse ; Cell Adhesion Molecules ; Nodal Protein ; Nodal protein, mouse ; Ethanol (3K9958V90M)
    Sprache Englisch
    Erscheinungsdatum 2020-09-02
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.60351
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Buch ; Online ; Dissertation / Habilitation: The role of LRP2 in forebrain development of the mouse

    Christ, Annabel [Verfasser]

    2011  

    Verfasserangabe Annabel Christ
    Schlagwörter Biowissenschaften, Biologie ; Life Science, Biology
    Thema/Rubrik (Code) sg570
    Sprache Englisch
    Verlag Freie Universität Berlin
    Erscheinungsort Berlin
    Dokumenttyp Buch ; Online ; Dissertation / Habilitation
    Datenquelle Digitale Dissertationen im Internet

    Volltext online

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  9. Artikel ; Online: LRP2, an auxiliary receptor that controls sonic hedgehog signaling in development and disease.

    Christ, Annabel / Herzog, Katja / Willnow, Thomas E

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

    2016  Band 245, Heft 5, Seite(n) 569–579

    Abstract: To fulfill their multiple roles in organ development and adult tissue homeostasis, hedgehog (HH) morphogens act through their receptor Patched (PTCH) on target cells. However, HH actions also require HH binding proteins, auxiliary cell surface receptors ... ...

    Abstract To fulfill their multiple roles in organ development and adult tissue homeostasis, hedgehog (HH) morphogens act through their receptor Patched (PTCH) on target cells. However, HH actions also require HH binding proteins, auxiliary cell surface receptors that agonize or antagonize morphogen signaling in a context-dependent manner. Here, we discuss recent findings on the LDL receptor-related protein 2 (LRP2), an exemplary HH binding protein that modulates sonic hedgehog activities in stem and progenitor cell niches in embryonic and adult tissues. LRP2 functions are crucial for developmental processes in a number of tissues, including the brain, the eye, and the heart, and defects in this receptor pathway are the cause of devastating congenital diseases in humans. Developmental Dynamics 245:569-579, 2016. © 2016 Wiley Periodicals, Inc.
    Sprache Englisch
    Erscheinungsdatum 2016-05
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Review
    ZDB-ID 1102541-4
    ISSN 1097-0177 ; 1058-8388
    ISSN (online) 1097-0177
    ISSN 1058-8388
    DOI 10.1002/dvdy.24394
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

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    Zs.MG 64: Hefte anzeigen

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  10. Buch ; Dissertation / Habilitation: Betreuung von Kindern mit konnataler Hypothyreose

    Christ, Annabel

    Erfahrungen der Universitätskinderklinik Erlangen

    2006  

    Verfasserangabe vorgelegt von Annabel Christ
    Sprache Deutsch
    Umfang 2 Mikrofiches, Ill., graph. Darst
    Dokumenttyp Buch ; Dissertation / Habilitation
    Dissertation / Habilitation Nürnberg, Univ., Diss--Erlangen, 2006
    Datenquelle Ehemaliges Sondersammelgebiet Küsten- und Hochseefischerei

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