Molecular cloning of a novel immunoglobulin superfamily gene preferentially expressed by brain and testis

Suzu, Shinya; Hayashi, Yokichi; Harumi, Tatsuo; Nomaguchi, Kouji; Yamada, Muneo; Hayasawa, Hirotoshi; Motoyoshi, Kazuo

doi:10.1016/s0006-291x(02)02025-9

Cited by 68 publications

(78 citation statements)

References 22 publications

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“…[32][33][34][35][36] Endothelial cell-selective adhesion molecule (ESAM) is a newly identified transmembrane junction protein with a similar structure to JAM proteins: extracellular region with variable type Ig domain and constant C2 type of Ig domain that share similarity with same domain of coxsackie and adenovirus receptor (CAR). [37][38][39] ESAM is indicated to play role in endothelial cellcell interaction crucial for vascular development and extravasation of neutrophils during the early phase of inflammation. 39 The TJ scaffolding proteins act as a core of a large protein network which includes structural connection to transmembrane proteins on one side and actin cytoskeleton proteins on the other side and associated group of signaling molecules which directly regulate the structural protein interactions.…”

Section: Blood-brain Barrier Junctional Complexmentioning

confidence: 99%

Junctional proteins of the blood-brain barrier: New insights into function and dysfunction

et al. 2016

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Section: Blood-brain Barrier Junctional Complexmentioning

confidence: 99%

Junctional proteins of the blood-brain barrier: New insights into function and dysfunction

et al. 2016

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“…The PCR product was subcloned into an expression vector, pEF-BOS. 29 The resultant plasmid was transfected into COS7 cells using LipofectAMINE2000 reagent (Invitrogen), 30 and the culture supernatant was used as a source of Flag-tagged M-CSF. For analysis, cells were incubated with the Flag-tagged M-CSF, followed by biotin-labeled anti-Flag M2 antibody (10 g/mL; Sigma) and PE-labeled streptavidin (5 g/mL; PharMingen).…”

Section: Cell Count and Flow Cytometrymentioning

confidence: 99%

HIV-1 Nef interferes with M-CSF receptor signaling through Hck activation and inhibits M-CSF bioactivities

Suzu

Harada

Μatsumoto

et al. 2005

Blood

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IntroductionNef is an accessory protein of HIV-1, a causative virus for AIDS. A number of reports, including studies of HIV-1-infected patients and of animal models, have demonstrated that the Nef protein is a major determinant of the pathogenicity of HIV-1. [1][2][3][4] Transgenic mice expressing the complete coding sequences of HIV-1 under the regulatory sequences of human CD4 gene developed severe AIDS-like abnormalities: loss of CD4 ϩ T cells, thymus atrophy, failure to thrive, diarrhea, wasting, premature death, interstitial pneumonitis, and tubulo-interstitial nephritis. 4 Using this mouse model and the introduction of mutation into selected HIV-1 gene(s), Hanna et al 4 clearly demonstrated that Nef harbored a major disease determinant. Therefore, much attention has been given to Nef to explain its contribution to HIV-1 pathogenesis and to investigate it as a target for antiviral drug development.CD4 ϩ T cells and monocytes/macrophages are the principal target cells for HIV-1, and the functions of Nef in CD4 ϩ T cells are generally accepted as accounting for many aspects of viral pathogenesis (reviewed in Fackler and Baur 5 and Peterlin and Trono 6 ). For example, Nef has been shown to cause the downregulation of cell surface molecules such as cell surface receptor CD4 7 and major histocompatibility complex (MHC) class I in CD4 ϩ T cells. 8 The down-regulation of MHC class I is considered to diminish the recognition of HIV-1-infected cells by cytotoxic T cells. In contrast, the contribution of monocytes/macrophages to viral pathogenesis is less well understood. Several lines of evidence support the idea that monocytes/macrophages and CD4 ϩ T cells are important for the development and progression of AIDS. Recent studies have demonstrated that Nef induces the production of CC chemokines (macrophage inflammatory proteins-1␣ and -1␤) and soluble forms of CD23 and intracellular adhesion molecule-1 by macrophages. 9,10 These Nef-induced factors from macrophages might stimulate the chemotaxis and activation of resting CD4 ϩ T cells, thereby promoting the permissiveness of CD4 ϩ T cells to HIV-1 infection. 9,10 This Nef function is likely to be mediated by the activation of NF-B transcription factor. 10 Another important feature of Nef is the binding at high affinity to myeloid lineage-specific Src family kinase Hck to activate its kinase activity. 11,12 The proline-rich (PxxP) motif in Nef binds to the Src homology 3 (SH3) domain of Hck. 11 Interestingly, Hck was found to bind preferentially and with higher affinity to Nef than other Src kinases. 11 The pathologic relevance of the molecular interaction in vivo was revealed by studies of HIV-1 transgenic mice. The mutation in the SH3-binding motif of Nef abolished the development of AIDS-like disease in the HIV-1 transgenic mice. 13 Moreover, the breeding of transgenic mice expressing the complete coding sequences of HIV-1 on a hck Ϫ/Ϫ background resulted in the delay of disease development. 13 These studies suggest that the modulation of macrophage functions by ...

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“…The JAMs have recently been renamed according to a new nomenclature (8), in which JAM-1-3 have been replaced by JAM-A-C, respectively. Other recently identified members are the endothelial cell-selective adhesion molecule (ESAM) (16) and the brain-and testis-specific immunoglobulin superfamily (BT-IgSF) (17). These genes/proteins share characteristics with CTX such as a specific exon/intron organization, in which both the V and the C2 domains are encoded by splicing of two half-domain exons, and an extra pair of cysteine residues flanking the C2 domain.…”

mentioning

confidence: 99%

CLMP, a Novel Member of the CTX Family and a New Component of Epithelial Tight Junctions

Raschperger

Engström

Pettersson

et al. 2004

Journal of Biological Chemistry

107

127

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The CTX family is a growing group of type I transmembrane proteins within the immunoglobulin superfamily (IgSF). They localize to junctional complexes between endothelial and epithelial cells and seem to participate in cell-cell adhesion and transmigration of leukocytes. Here, we report the identification of a new member of the CTX family. This protein, which was designated CLMP (coxsackie-and adenovirus receptor-like membrane protein), is composed of 373 amino acids including an extracellular part containing a V-and a C2-type domain, a transmembrane region and a cytoplasmic tail.

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Molecular cloning of a novel immunoglobulin superfamily gene preferentially expressed by brain and testis

Cited by 68 publications

References 22 publications

Junctional proteins of the blood-brain barrier: New insights into function and dysfunction

Junctional proteins of the blood-brain barrier: New insights into function and dysfunction

HIV-1 Nef interferes with M-CSF receptor signaling through Hck activation and inhibits M-CSF bioactivities

CLMP, a Novel Member of the CTX Family and a New Component of Epithelial Tight Junctions

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