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    Jam3 junction adhesion molecule 3 [ Mus musculus (house mouse) ]

    Gene ID: 83964, updated on 2-Jul-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    JAM-C Is Important for Lens Epithelial Cell Proliferation and Lens Fiber Maturation in Murine Lens Development.

    JAM-C Is Important for Lens Epithelial Cell Proliferation and Lens Fiber Maturation in Murine Lens Development.
    Sun Q, Li J, Ma J, Zheng Y, Ju R, Li X, Ren X, Huang L, Chen R, Tan X, Luo L., Free PMC Article

    12/20/2023
    Junctional adhesion molecule C expression specifies a CD138low/neg multiple myeloma cell population in mice and humans.

    Junctional adhesion molecule C expression specifies a CD138low/neg multiple myeloma cell population in mice and humans.
    Brandl A, Solimando AG, Mokhtari Z, Tabares P, Medler J, Manz H, Da Vià MC, Croci GA, Kurzwart M, Thusek S, Schneider T, Ebert R, Jakob F, Einsele H, Beilhack A., Free PMC Article

    04/9/2022
    Junctional Adhesion Molecule-C Mediates the Recruitment of Embryonic-Endothelial Progenitor Cells to the Perivascular Niche during Tumor Angiogenesis.

    Junctional Adhesion Molecule-C Mediates the Recruitment of Embryonic-Endothelial Progenitor Cells to the Perivascular Niche during Tumor Angiogenesis.
    Czabanka M, Petrilli LL, Elvers-Hornung S, Bieback K, Albert Imhof B, Vajkoczy P, Vinci M., Free PMC Article

    11/21/2020
    CIRP induces neutrophil reverse transendothelial migration in sepsis by increasing neutrophil elastase and decreasing junctional adhesion molecule-C

    CIRP Induces Neutrophil Reverse Transendothelial Migration in Sepsis.
    Jin H, Aziz M, Ode Y, Wang P., Free PMC Article

    06/13/2020
    Jam-c gene deletion resulted in smaller eyes and decreased photoreceptor numbers.

    Neuronal Expression of Junctional Adhesion Molecule-C is Essential for Retinal Thickness and Photoreceptor Survival.
    Li Y, Zhang F, Lu W, Li X.

    06/15/2019
    The role of JAM-C on the aging of neutrophils to cause sepsis-induced acute lung injury was studied. JAM-C not only regulates neutrophil chemotaxis but also prolongs their survival by promoting anti-apoptotic function.

    Targeting junctional adhesion molecule-C ameliorates sepsis-induced acute lung injury by decreasing CXCR4(+) aged neutrophils.
    Hirano Y, Ode Y, Ochani M, Wang P, Aziz M., Free PMC Article

    05/18/2019
    this study shows that JAM-C promotes autoimmune-mediated liver fibrosis in mice

    Junctional adhesion molecules JAM-B and JAM-C promote autoimmune-mediated liver fibrosis in mice.
    Hintermann E, Bayer M, Conti CB, Fuchs S, Fausther M, Leung PS, Aurrand-Lions M, Taubert R, Pfeilschifter JM, Friedrich-Rust M, Schuppan D, Dranoff JA, Gershwin ME, Manns MP, Imhof BA, Christen U.

    04/13/2019
    the dimerization sites E66-K68 of JAM-C affected cell adhesion, polarization and migration and are essential for tumor cell metastasis.

    Junctional adhesion molecule C (JAM-C) dimerization aids cancer cell migration and metastasis.
    Garrido-Urbani S, Vonlaufen A, Stalin J, De Grandis M, Ropraz P, Jemelin S, Bardin F, Scheib H, Aurrand-Lions M, Imhof BA.

    06/2/2018
    JAM-C plays an important role in maintaining VEGR2 expression to promote retinal pigment epithelial cell survival under oxidative stress.

    JAM-C maintains VEGR2 expression to promote retinal pigment epithelium cell survival under oxidative stress.
    Jia X, Zhao C, Chen Q, Du Y, Huang L, Ye Z, Ren X, Wang S, Lee C, Tang Z, Li X, Ju R.

    03/3/2018
    JAM-B/JAM-C mediated interaction between endothelial cells and stellate cells stabilizes vessel walls and may control the sinusoidal diameter.

    Murine junctional adhesion molecules JAM-B and JAM-C mediate endothelial and stellate cell interactions during hepatic fibrosis.
    Hintermann E, Bayer M, Ehser J, Aurrand-Lions M, Pfeilschifter JM, Imhof BA, Christen U., Free PMC Article

    08/5/2017
    Study provides evidence that JAM-C downregulation may contribute to acute pancreatitis-associated lung injury via reverse transendothelial migration of neutrophils.

    Reverse-migrated neutrophils regulated by JAM-C are involved in acute pancreatitis-associated lung injury.
    Wu D, Zeng Y, Fan Y, Wu J, Mulatibieke T, Ni J, Yu G, Wan R, Wang X, Hu G., Free PMC Article

    01/14/2017
    Endothelial-specific deletion of JAM-C promoted endothelial cell sprouting, and consequently vessel normalisation and revascularisation of the hypoxic retina without altering pathologic neovascularisation.

    Endothelial-specific deficiency of Junctional Adhesion Molecule-C promotes vessel normalisation in proliferative retinopathy.
    Economopoulou M, Avramovic N, Klotzsche-von Ameln A, Korovina I, Sprott D, Samus M, Gercken B, Troullinaki M, Grossklaus S, Funk RH, Li X, Imhof BA, Orlova VV, Chavakis T.

    09/24/2016
    JAM-C blockade can finely-tune the innate cell migration and accelerate the consequent immune response to L. major without changing the type of the T helper cell response.

    Blocking junctional adhesion molecule C enhances dendritic cell migration and boosts the immune responses against Leishmania major.
    Ballet R, Emre Y, Jemelin S, Charmoy M, Tacchini-Cottier F, Imhof BA., Free PMC Article

    11/7/2015
    Function of Jam-B/Jam-C interaction in homing and mobilization of human and mouse hematopoietic stem and progenitor cells.

    Function of Jam-B/Jam-C interaction in homing and mobilization of human and mouse hematopoietic stem and progenitor cells.
    Arcangeli ML, Bardin F, Frontera V, Bidaut G, Obrados E, Adams RH, Chabannon C, Aurrand-Lions M.

    02/14/2015
    These findings provide evidence for a role for endothelial cell JAM-C in tumor growth and aggressiveness as well as recruitment of pericytes to newly formed blood vessels in a model of ovarian cancer.

    Endothelial cell junctional adhesion molecule C plays a key role in the development of tumors in a murine model of ovarian cancer.
    Leinster DA, Colom B, Whiteford JR, Ennis DP, Lockley M, McNeish IA, Aurrand-Lions M, Chavakis T, Imhof BA, Balkwill FR, Nourshargh S., Free PMC Article

    12/21/2013
    JAM-C might be involved in the final steps of trafficking and transmigration of antigen-specific autoaggressive T-cells to the islets of Langerhans.

    Blockade but not overexpression of the junctional adhesion molecule C influences virus-induced type 1 diabetes in mice.
    Christen S, Coppieters K, Rose K, Holdener M, Bayer M, Pfeilschifter JM, Hintermann E, von Herrath MG, Aurrand-Lions M, Imhof BA, Christen U., Free PMC Article

    07/27/2013
    study suggests that JAM-C(-/-) C57BL/6 mice model the important role for JAM-C in brain development and CSF homeostasis as recently observed in humans with a loss-of-function mutation in JAM-C

    Junctional adhesion molecule (JAM)-C deficient C57BL/6 mice develop a severe hydrocephalus.
    Wyss L, Schäfer J, Liebner S, Mittelbronn M, Deutsch U, Enzmann G, Adams RH, Aurrand-Lions M, Plate KH, Imhof BA, Engelhardt B., Free PMC Article

    03/30/2013
    Data show that junctional adhesion molecule-B (JAM-B) expressed by endothelial cells contributes to murine B16 melanoma cells metastasis through its interaction with junctional adhesion molecule-C (JAM-C) on tumor cells.

    The Junctional Adhesion Molecule-B regulates JAM-C-dependent melanoma cell metastasis.
    Arcangeli ML, Frontera V, Bardin F, Thomassin J, Chetaille B, Adams S, Adams RH, Aurrand-Lions M.

    02/9/2013
    Results indicate that in vivo JAM-C shows enrichment at the apical surface and therefore is asymmetrically distributed during cell divisions.

    JAM-C is an apical surface marker for neural stem cells.
    Stelzer S, Worlitzer MM, Bahnassawy L, Hemmer K, Rugani K, Werthschulte I, Schön AL, Brinkmann BF, Bunk EC, Palm T, Ebnet K, Schwamborn JC.

    06/30/2012
    Data indicate deletion of JAM-C in deletion of JAM-C in Schwann cells (SCs) (JAM-C SC KO) mice showed electrophysiological defects, muscular weakness, and hypersensitivity to mechanical stimuli.

    Schwann cell-specific JAM-C-deficient mice reveal novel expression and functions for JAM-C in peripheral nerves.
    Colom B, Poitelon Y, Huang W, Woodfin A, Averill S, Del Carro U, Zambroni D, Brain SD, Perretti M, Ahluwalia A, Priestley JV, Chavakis T, Imhof BA, Feltri ML, Nourshargh S., Free PMC Article

    05/26/2012
    Endothelial cell JAM-C has a key role in supporting luminal-to-abluminal migration of neutrophils in vivo, suggsting that reverse transepithial cell migration of neutrophils can contribute to the dissemination of systemic inflammation.

    The junctional adhesion molecule JAM-C regulates polarized transendothelial migration of neutrophils in vivo.
    Woodfin A, Voisin MB, Beyrau M, Colom B, Caille D, Diapouli FM, Nash GB, Chavakis T, Albelda SM, Rainger GE, Meda P, Imhof BA, Nourshargh S., Free PMC Article

    10/8/2011
    Thrombomodulin and platelet-derived growth factor receptor alpha (PDGFRalpha) identify a population of fibroblastic reticular cells in lymph nodes where chemokine secretion is controlled by JAM-C.

    Cutting edge: JAM-C controls homeostatic chemokine secretion in lymph node fibroblastic reticular cells expressing thrombomodulin.
    Frontera V, Arcangeli ML, Zimmerli C, Bardin F, Obrados E, Audebert S, Bajenoff M, Borg JP, Aurrand-Lions M.

    09/24/2011
    JAM-C(-/-) mice as well as endothelial-specific JAM-C-deficient mice displayed significantly decreased B16 melanoma cell metastasis to the lung, whereas treatment of mice with soluble JAM-C prevented melanoma lung metastasis

    A novel function of junctional adhesion molecule-C in mediating melanoma cell metastasis.
    Langer HF, Orlova VV, Xie C, Kaul S, Schneider D, Lonsdorf AS, Fahrleitner M, Choi EY, Dutoit V, Pellegrini M, Grossklaus S, Nawroth PP, Baretton G, Santoso S, Hwang ST, Arnold B, Chavakis T., Free PMC Article

    08/20/2011
    role of JAM-3 in cardiac development studied in JAM-C deleted mice; mice have normal cardiac structure & function, indicating haplo-insufficiency of JAM-3 is unlikely to cause congenital heart defects that occur in 11q- patients

    Deletion of JAM-C, a candidate gene for heart defects in Jacobsen syndrome, results in a normal cardiac phenotype in mice.
    Ye M, Hamzeh R, Geddis A, Varki N, Perryman MB, Grossfeld P.

    01/21/2010
    role for endothelial cell JAM-C in mediating leukocyte adhesion and transmigration in response to I/R injury.

    Junctional adhesion molecule-C mediates leukocyte infiltration in response to ischemia reperfusion injury.
    Scheiermann C, Colom B, Meda P, Patel NS, Voisin MB, Marrelli A, Woodfin A, Pitzalis C, Thiemermann C, Aurrand-Lions M, Imhof BA, Nourshargh S., Free PMC Article

    01/21/2010
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