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  1. Artikel ; Online: Ectodysplasin Signaling through XEDAR Is Required for Mammary Gland Morphogenesis.

    Wark, Abigail R / Aldea, Daniel / Tomizawa, Reiko R / Kokalari, Blerina / Warder, Bailey / Kamberov, Yana G

    The Journal of investigative dermatology

    2023  Band 143, Heft 8, Seite(n) 1529–1537.e2

    Abstract: XEDAR is a member of the TNF receptor subfamily and a mediator of the ectodysplasin (EDA) pathway. EDA signaling plays evolutionarily conserved roles in the development of the ectodermal appendage organ class, which includes hair, eccrine sweat glands, ... ...

    Abstract XEDAR is a member of the TNF receptor subfamily and a mediator of the ectodysplasin (EDA) pathway. EDA signaling plays evolutionarily conserved roles in the development of the ectodermal appendage organ class, which includes hair, eccrine sweat glands, and mammary glands. Loss-of-function sequence variants of EDA, which encodes the two major ligand isoforms, EDA-A1 and EDA-A2, result in X-linked hypohidrotic ectodermal dysplasia characterized by defects in two or more types of ectodermal appendages. EDA-A1 and EDA-A2 signal through the receptors EDAR and XEDAR, respectively. Although the contributions of the EDA-A1/EDAR signaling pathway to EDA-dependent ectodermal appendage phenotypes have been extensively characterized, the significance of the EDA-A2/XEDAR branch of the pathway has remained obscure. In this study, we report the phenotypic consequences of disrupting the EDA-A2/XEDAR pathway on mammary gland differentiation and growth. Using a mouse Xedar knockout model, we show that Xedar has a specific and temporally restricted role in promoting late pubertal growth and branching of the mammary epithelium that can be influenced by genetic background. Our findings implicate Xedar in ectodermal appendage development and suggest that the EDA-A2/XEDAR signaling axis contributes to the etiology of EDA-dependent mammary phenotypes.
    Mesh-Begriff(e) Ectodysplasins/genetics ; Ectodysplasins/metabolism ; Membrane Proteins/genetics ; Morphogenesis ; Receptors, Tumor Necrosis Factor ; Signal Transduction ; Animals ; Mice
    Chemische Substanzen Ectodysplasins ; Membrane Proteins ; Receptors, Tumor Necrosis Factor
    Sprache Englisch
    Erscheinungsdatum 2023-02-18
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 80136-7
    ISSN 1523-1747 ; 0022-202X
    ISSN (online) 1523-1747
    ISSN 0022-202X
    DOI 10.1016/j.jid.2023.02.007
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: L-type voltage-gated Ca

    Atsuta, Yuji / Tomizawa, Reiko R / Levin, Michael / Tabin, Clifford J

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

    2019  Band 116, Heft 43, Seite(n) 21592–21601

    Abstract: All cells, including nonexcitable cells, maintain a discrete transmembrane potential ( ...

    Abstract All cells, including nonexcitable cells, maintain a discrete transmembrane potential (
    Mesh-Begriff(e) Aggrecans/metabolism ; Animals ; Calcium Channels, L-Type/metabolism ; Cartilage/embryology ; Chick Embryo ; Chickens ; Chondrogenesis/physiology ; Collagen Type II/metabolism ; Extremities/embryology ; Gene Expression Regulation, Developmental/genetics ; Membrane Potentials/physiology ; Mice ; Mice, Transgenic ; NFATC Transcription Factors/metabolism ; SOX9 Transcription Factor/metabolism
    Chemische Substanzen Acan protein, mouse ; Aggrecans ; CACNA1C protein, mouse ; Calcium Channels, L-Type ; Col2a1 protein, mouse ; Collagen Type II ; NFATC Transcription Factors ; Nfatc2 protein, mouse ; SOX9 Transcription Factor ; Sox9 protein, mouse
    Sprache Englisch
    Erscheinungsdatum 2019-10-07
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1908981116
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Direct reprogramming of non-limb fibroblasts to cells with properties of limb progenitors.

    Atsuta, Yuji / Lee, ChangHee / Rodrigues, Alan R / Colle, Charlotte / Tomizawa, Reiko R / Lujan, Ernesto G / Tschopp, Patrick / Galan, Laura / Zhu, Meng / Gorham, Joshua M / Vannier, Jean-Pierre / Seidman, Christine E / Seidman, Jonathan G / Ros, Marian A / Pourquié, Olivier / Tabin, Clifford J

    Developmental cell

    2024  Band 59, Heft 3, Seite(n) 415–430.e8

    Abstract: The early limb bud consists of mesenchymal limb progenitors derived from the lateral plate mesoderm (LPM). The LPM also gives rise to the mesodermal components of the flank and neck. However, the cells at these other levels cannot produce the variety of ... ...

    Abstract The early limb bud consists of mesenchymal limb progenitors derived from the lateral plate mesoderm (LPM). The LPM also gives rise to the mesodermal components of the flank and neck. However, the cells at these other levels cannot produce the variety of cell types found in the limb. Taking advantage of a direct reprogramming approach, we find a set of factors (Prdm16, Zbtb16, and Lin28a) normally expressed in the early limb bud and capable of imparting limb progenitor-like properties to mouse non-limb fibroblasts. The reprogrammed cells show similar gene expression profiles and can differentiate into similar cell types as endogenous limb progenitors. The further addition of Lin41 potentiates the proliferation of the reprogrammed cells. These results suggest that these same four factors may play pivotal roles in the specification of endogenous limb progenitors.
    Mesh-Begriff(e) Mice ; Animals ; Extremities ; Proteins/metabolism ; Fibroblasts ; Mesoderm/metabolism ; Limb Buds
    Chemische Substanzen Proteins
    Sprache Englisch
    Erscheinungsdatum 2024-02-04
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2023.12.010
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Sweat gland development requires an eccrine dermal niche and couples two epidermal programs.

    Dingwall, Heather L / Tomizawa, Reiko R / Aharoni, Adam / Hu, Peng / Qiu, Qi / Kokalari, Blerina / Martinez, Serenity M / Donahue, Joan C / Aldea, Daniel / Mendoza, Meryl / Glass, Ian A / Wu, Hao / Kamberov, Yana G

    Developmental cell

    2023  Band 59, Heft 1, Seite(n) 20–32.e6

    Abstract: Eccrine sweat glands are indispensable for human thermoregulation and, similar to other mammalian skin appendages, form from multipotent epidermal progenitors. Limited understanding of how epidermal progenitors specialize to form these vital organs has ... ...

    Abstract Eccrine sweat glands are indispensable for human thermoregulation and, similar to other mammalian skin appendages, form from multipotent epidermal progenitors. Limited understanding of how epidermal progenitors specialize to form these vital organs has precluded therapeutic efforts toward their regeneration. Herein, we applied single-nucleus transcriptomics to compare the expression content of wild-type, eccrine-forming mouse skin to that of mice harboring a skin-specific disruption of Engrailed 1 (En1), a transcription factor that promotes eccrine gland formation in humans and mice. We identify two concurrent but disproportionate epidermal transcriptomes in the early eccrine anlagen: one that is shared with hair follicles and one that is En1 dependent and eccrine specific. We demonstrate that eccrine development requires the induction of a dermal niche proximal to each developing gland in humans and mice. Our study defines the signatures of eccrine identity and uncovers the eccrine dermal niche, setting the stage for targeted regeneration and comprehensive skin repair.
    Mesh-Begriff(e) Humans ; Mice ; Animals ; Epidermis/metabolism ; Eccrine Glands/metabolism ; Skin ; Hair Follicle/metabolism ; Gene Expression Regulation ; Mammals
    Sprache Englisch
    Erscheinungsdatum 2023-12-13
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2023.11.015
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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