G2Cdb::Gene report

Gene id
Gene symbol
Homo sapiens
intercellular adhesion molecule 5, telencephalin
G00001164 (Mus musculus)

Databases (9)

Curated Gene
OTTHUMG00000070935 (Vega human gene)
ENSG00000076662 (Ensembl human gene)
7087 (Entrez Gene)
338 (G2Cdb plasticity & disease)
ICAM5 (GeneCards)
601852 (OMIM)
Marker Symbol
HGNC:5348 (HGNC)
Protein Expression
2498 (human protein atlas)
Protein Sequence
Q9UMF0 (UniProt)

Synonyms (1)

  • TLN

Literature (20)

Pubmed - other

  • Association between genetic variants in VEGF, ERCC3 and occupational benzene haematotoxicity.

    Hosgood HD, Zhang L, Shen M, Berndt SI, Vermeulen R, Li G, Yin S, Yeager M, Yuenger J, Rothman N, Chanock S, Smith M and Lan Q

    Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892-7240, USA. hosgoodd@mail.nih.gov

    Introduction: Benzene is an established human haematotoxin, with substantial interindividual variation in benzene-induced toxicity.

    Methods: To further examine if genetic variation contributes to benzene haematotoxicity, we analysed 1023 tagSNPs in 121 gene regions important for benzene metabolism, haematopoiesis, leukaemia and lymphoma among 250 workers exposed to benzene and 140 unexposed controls in a cross-sectional study carried out in China. Linear regression was used to analyse the relationship between genetic polymorphisms and total white blood cell (WBC) count and its subtypes, adjusting for potential confounders and occupational exposure to benzene and toluene among exposed workers. The minp test assessed the association on the gene region level. The false discovery rate method was used to control for multiple comparisons.

    Results: VEGF (minp = 0.0030) and ERCC3 (minp = 0.0042) were the most significantly associated gene regions with altered WBC counts among benzene-exposed workers, after accounting for multiple comparisons. Highly significant changes were also found for WBC subtype counts, including granulocytes, CD4+ T cells and lymphocytes for VEGF and granulocytes and NK cells for ERCC3. Further, in workers exposed to <1 ppm, a SNP in VEGF was associated with changes in WBC and granulocyte counts, and SNPs in ERCC3 were associated with changes in WBC, NK cell and granulocyte counts.

    Discussion: Our findings suggest that genetic variation in VEGF, which plays an important role in blood vessel growth, and ERCC3, which is a member of the DNA repair pathway and is responsible for repairing bulky DNA adducts formed by chemicals, may contribute to individual susceptibility to benzene-induced haematotoxicity at relatively low levels of benzene exposure.

    Funded by: Intramural NIH HHS: Z99 CA999999; NIEHS NIH HHS: P30 ES001896, P30ES01896, P42 ES004705, P42ES04705, R01 ES006721, R01ES06721

    Occupational and environmental medicine 2009;66;12;848-53

  • Common genetic variation in candidate genes and susceptibility to subtypes of breast cancer.

    Mavaddat N, Dunning AM, Ponder BA, Easton DF and Pharoah PD

    Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom. nm274@cam.ac.uk

    Association studies have been widely used to search for common low-penetrance susceptibility alleles to breast cancer in general. However, breast cancer is a heterogeneous disease and it has been suggested that it may be possible to identify additional susceptibility alleles by restricting analyses to particular subtypes. We used data on 710 single nucleotide polymorphisms (SNP) in 120 candidate genes from a large candidate gene association study of up to 4,470 cases and 4,560 controls to compare the results of analyses of "overall" breast cancer with subgroup analyses based on the major clinicopathologic characteristics of breast cancer (stage, grade, morphology, and hormone receptor status). No SNP was highly significant in overall effects analysis. Subgroup analysis resulted in substantial reordering of ranks of SNPs, as assessed by the magnitude of the test statistics, and some associations that were not significant for an overall effect were detected in subgroups at a nominal 5% level adjusted for multiple testing. The most significant association of CCND1 SNP rs3212879 with estrogen receptor-negative tumor types (P = 0.001) did not reach genome-wide significance levels. These results show that it may be possible to detect associations using subgroup analysis that are missed in overall effects analysis. If the associations we found can be replicated in independent studies, they may provide important insights into disease mechanisms in breast cancer.

    Funded by: Cancer Research UK: 10118, 10119, 10124, A10119, A10124; Medical Research Council

    Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 2009;18;1;255-9

  • Shedded neuronal ICAM-5 suppresses T-cell activation.

    Tian L, Lappalainen J, Autero M, Hänninen S, Rauvala H and Gahmberg CG

    Department of Biologic and Environmental Sciences, Faculty of Biosciences, University of Helsinki, Finland. li.tian@helsinki.fi

    Intercellular adhesion molecules (ICAMs) bind to leukocyte beta2 integrins, which, among other functions, provide costimulatory signals for T-cell activation. ICAM-5 (telencephalin) is expressed in the somadendritic region of neurons of the mammalian brain. The receptor for ICAM-5 is the integrin LFA-1, a major leukocyte integ-rin expressed in lymphocytes and microglia. In conditions of brain ischemia, epilepsy, and encephalitis, the soluble form of ICAM-5 (sICAM-5) has been detected in physiologic fluids. Here, we report that sICAM-5 attenuates the T-cell receptor-mediated activation of T cells as demonstrated by the decreased expression of the activation markers CD69, CD40L, and CD25 (IL-2R). This effect is most clearly seen in CD45ROLow (naive), and not in CD45ROHigh (memory) T cells, and is most effective early in priming, but not in the presence of strong costimulatory signals. Furthermore, sICAM-5 promotes the mRNA expression of the cytokines TGF-beta1 and IFN-gamma, but not TNF. The formation of sICAM-5 is promoted by activated T cells through the cleavage of ICAM-5 from neurons. This suggests that ICAM-5 is involved in immune privilege of the brain and acts as an anti-inflammatory agent.

    Blood 2008;111;7;3615-25

  • A common coding variant in CASP8 is associated with breast cancer risk.

    Cox A, Dunning AM, Garcia-Closas M, Balasubramanian S, Reed MW, Pooley KA, Scollen S, Baynes C, Ponder BA, Chanock S, Lissowska J, Brinton L, Peplonska B, Southey MC, Hopper JL, McCredie MR, Giles GG, Fletcher O, Johnson N, dos Santos Silva I, Gibson L, Bojesen SE, Nordestgaard BG, Axelsson CK, Torres D, Hamann U, Justenhoven C, Brauch H, Chang-Claude J, Kropp S, Risch A, Wang-Gohrke S, Schürmann P, Bogdanova N, Dörk T, Fagerholm R, Aaltonen K, Blomqvist C, Nevanlinna H, Seal S, Renwick A, Stratton MR, Rahman N, Sangrajrang S, Hughes D, Odefrey F, Brennan P, Spurdle AB, Chenevix-Trench G, Kathleen Cunningham Foundation Consortium for Research into Familial Breast Cancer, Beesley J, Mannermaa A, Hartikainen J, Kataja V, Kosma VM, Couch FJ, Olson JE, Goode EL, Broeks A, Schmidt MK, Hogervorst FB, Van't Veer LJ, Kang D, Yoo KY, Noh DY, Ahn SH, Wedrén S, Hall P, Low YL, Liu J, Milne RL, Ribas G, Gonzalez-Neira A, Benitez J, Sigurdson AJ, Stredrick DL, Alexander BH, Struewing JP, Pharoah PD, Easton DF and Breast Cancer Association Consortium

    Sheffield University Medical School, Sheffield S10 2RX, UK.

    The Breast Cancer Association Consortium (BCAC) has been established to conduct combined case-control analyses with augmented statistical power to try to confirm putative genetic associations with breast cancer. We genotyped nine SNPs for which there was some prior evidence of an association with breast cancer: CASP8 D302H (rs1045485), IGFBP3 -202 C --> A (rs2854744), SOD2 V16A (rs1799725), TGFB1 L10P (rs1982073), ATM S49C (rs1800054), ADH1B 3' UTR A --> G (rs1042026), CDKN1A S31R (rs1801270), ICAM5 V301I (rs1056538) and NUMA1 A794G (rs3750913). We included data from 9-15 studies, comprising 11,391-18,290 cases and 14,753-22,670 controls. We found evidence of an association with breast cancer for CASP8 D302H (with odds ratios (OR) of 0.89 (95% confidence interval (c.i.): 0.85-0.94) and 0.74 (95% c.i.: 0.62-0.87) for heterozygotes and rare homozygotes, respectively, compared with common homozygotes; P(trend) = 1.1 x 10(-7)) and weaker evidence for TGFB1 L10P (OR = 1.07 (95% c.i.: 1.02-1.13) and 1.16 (95% c.i.: 1.08-1.25), respectively; P(trend) = 2.8 x 10(-5)). These results demonstrate that common breast cancer susceptibility alleles with small effects on risk can be identified, given sufficiently powerful studies.

    Funded by: Intramural NIH HHS; NCI NIH HHS: CA-95-003, CA82267; Wellcome Trust: 068545/Z/02

    Nature genetics 2007;39;3;352-8

  • ICAM gene cluster SNPs and prostate cancer risk in African Americans.

    Chen H, Hernandez W, Shriver MD, Ahaghotu CA and Kittles RA

    Human Cancer Genetics, Comprehensive Cancer Center, The Ohio State University, 494 Tzagournis Medical Research Facility, 420 W. 12th Avenue, Columbus, OH 43210, USA.

    Intercellular adhesion molecules (ICAMs) are known to be involved in various human cancers. An ICAM gene cluster lying within a 26 kb region on chromosome 19p13.2, and containing ICAM1, ICAM4, and ICAM5 has recently been identified as harboring a breast and prostate cancer susceptibility locus in two populations of European ancestry from Germany and Australia. The objective of this study was to confirm the ICAM association with prostate cancer in a sample of African American prostate cancer cases (N = 286) and controls (N = 391). Six single nucleotide polymorphisms (SNPs) within the three ICAM genes were genotyped. To control for potential population stratification an ancestry-adjusted association analysis was performed. We found that ICAM1 SNPs, -9A/C (rs5490) and K469E (rs5498) were associated with prostate cancer risk in men with a family history of prostate cancer (P = 0.008). Specifically, increased risk was observed for individuals who possessed the CC genotype of the -9 A/C variant (odds ratio = 2.5; 95% CI = 1.0-6.3) and at least one G allele of non-synonymous K469E variant (odds ratio = 1.8; 95% CI = 1.2-3.1). Strong linkage disequilibrium was observed across the ICAM region (P < 0.001). A common haplotype within the ICAM gene cluster, harboring the -9A/C variant was significantly associated with prostate cancer (P = 0.03), mainly due to men with family history (P = 0.01). Our results replicate previous findings of association of the ICAM gene cluster with prostate cancer and suggest that common genetic variation within ICAM1 and not ICAM5 may be an important risk factor for prostate cancer.

    Funded by: NCI NIH HHS: 5U54CA91431-01; NHGRI NIH HHS: HG02154-04A2; NIGMS NIH HHS: S06GM08016

    Human genetics 2006;120;1;69-76

  • Polymorphisms in the ICAM gene locus are not associated with breast cancer Risk.

    Cox DG, Hankinson SE and Hunter DJ

    Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA. dcox@hsph.harvard.edu

    Funded by: NCI NIH HHS: CA 09001-27, CA49449, CA65725, CA87969

    Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 2006;15;1;178-9

  • Robust phosphoproteomic profiling of tyrosine phosphorylation sites from human T cells using immobilized metal affinity chromatography and tandem mass spectrometry.

    Brill LM, Salomon AR, Ficarro SB, Mukherji M, Stettler-Gill M and Peters EC

    Genomics Institute of the Novartis Research Foundation, 10675 John Jay Hopkins Drive, San Diego, California 92121, USA. lbrill@gnf.org

    Protein tyrosine phosphorylation cascades are difficult to analyze and are critical for cell signaling in higher eukaryotes. Methodology for profiling tyrosine phosphorylation, considered herein as the assignment of multiple protein tyrosine phosphorylation sites in single analyses, was reported recently (Salomon, A. R.; Ficarro, S. B.; Brill, L. M.; Brinker, A.; Phung, Q. T.; Ericson, C.; Sauer, K.; Brock, A.; Horn, D. M.; Schultz, P. G.; Peters, E. C. Proc. Natl. Acad. Sci. U.S.A. 2003, 100, 443-448). The technology platform included the use of immunoprecipitation, immobilized metal affinity chromatography (IMAC), liquid chromatography, and tandem mass spectrometry. In the present report, we show that when using complex mixtures of peptides from human cells, methylation improved the selectivity of IMAC for phosphopeptides and eliminated the acidic bias that occurred with unmethylated peptides. The IMAC procedure was significantly improved by desalting methylated peptides, followed by gradient elution of the peptides to a larger IMAC column. These improvements resulted in assignment of approximately 3-fold more tyrosine phosphorylation sites, from human cell lysates, than the previous methodology. Nearly 70 tyrosine-phosphorylated peptides from proteins in human T cells were assigned in single analyses. These proteins had unknown functions or were associated with a plethora of fundamental cellular processes. This robust technology platform should be broadly applicable to profiling the dynamics of tyrosine phosphorylation.

    Analytical chemistry 2004;76;10;2763-72

  • Exploring proteomes and analyzing protein processing by mass spectrometric identification of sorted N-terminal peptides.

    Gevaert K, Goethals M, Martens L, Van Damme J, Staes A, Thomas GR and Vandekerckhove J

    Department of Medical Protein Research, Flanders Interuniversity Institute for Biotechnology, Ghent University, A. Baertsoenkaai 3, B-9000 Ghent, Belgium. kris.gevaert@rug.ac.be

    Current non-gel techniques for analyzing proteomes rely heavily on mass spectrometric analysis of enzymatically digested protein mixtures. Prior to analysis, a highly complex peptide mixture is either separated on a multidimensional chromatographic system or it is first reduced in complexity by isolating sets of representative peptides. Recently, we developed a peptide isolation procedure based on diagonal electrophoresis and diagonal chromatography. We call it combined fractional diagonal chromatography (COFRADIC). In previous experiments, we used COFRADIC to identify more than 800 Escherichia coli proteins by tandem mass spectrometric (MS/MS) analysis of isolated methionine-containing peptides. Here, we describe a diagonal method to isolate N-terminal peptides. This reduces the complexity of the peptide sample, because each protein has one N terminus and is thus represented by only one peptide. In this new procedure, free amino groups in proteins are first blocked by acetylation and then digested with trypsin. After reverse-phase (RP) chromatographic fractionation of the generated peptide mixture, internal peptides are blocked using 2,4,6-trinitrobenzenesulfonic acid (TNBS); they display a strong hydrophobic shift and therefore segregate from the unaltered N-terminal peptides during a second identical separation step. N-terminal peptides can thereby be specifically collected for further liquid chromatography (LC)-MS/MS analysis. Omitting the acetylation step results in the isolation of non-lysine-containing N-terminal peptides from in vivo blocked proteins.

    Nature biotechnology 2003;21;5;566-9

  • Interaction with telencephalin and the amyloid precursor protein predicts a ring structure for presenilins.

    Annaert WG, Esselens C, Baert V, Boeve C, Snellings G, Cupers P, Craessaerts K and De Strooper B

    Laboratory for Neuronal Cell Biology, Department of Human Genetics, Flanders Interuniversity Institute for Biotechnology, KUL-Gasthuisberg, B-3000 Leuven, Belgium. ad@med.kuleuven.ac.be

    The carboxyl terminus of presenilin 1 and 2 (PS1 and PS2) binds to the neuron-specific cell adhesion molecule telencephalin (TLN) in the brain. PS1 deficiency results in the abnormal accumulation of TLN in a yet unidentified intracellular compartment. The first transmembrane domain and carboxyl terminus of PS1 form a binding pocket with the transmembrane domain of TLN. Remarkably, APP binds to the same regions via part of its transmembrane domain encompassing the critical residues mutated in familial Alzheimer's disease. Our data surprisingly indicate a spatial dissociation between the binding site and the proposed catalytic site near the critical aspartates in PSs. They provide important experimental evidence to support a ring structure model for PS.

    Neuron 2001;32;4;579-89

  • Intercellular adhesion molecule-5 induces dendritic outgrowth by homophilic adhesion.

    Tian L, Nyman H, Kilgannon P, Yoshihara Y, Mori K, Andersson LC, Kaukinen S, Rauvala H, Gallatin WM and Gahmberg CG

    Department of Biosciences, Division of Biochemistry, Viikinkaari 5, University of Helsinki, Helsinki 00014, Finland.

    Intercellular adhesion molecule-5 (ICAM-5) is a dendritically polarized membrane glycoprotein in telencephalic neurons, which shows heterophilic binding to leukocyte beta(2)-integrins. Here, we show that the human ICAM-5 protein interacts in a homophilic manner through the binding of the immunoglobulin domain 1 to domains 4-5. Surface coated ICAM-5-Fc promoted dendritic outgrowth and arborization of ICAM- 5-expressing hippocampal neurons. During dendritogenesis in developing rat brain, ICAM-5 was in monomer form, whereas in mature neurons it migrated as a high molecular weight complex. The findings indicate that its homophilic binding activity was regulated by nonmonomer/monomer transition. Thus, ICAM-5 displays two types of adhesion activity, homophilic binding between neurons and heterophilic binding between neurons and leukocytes.

    The Journal of cell biology 2000;150;1;243-52

  • Binding of T lymphocytes to hippocampal neurons through ICAM-5 (telencephalin) and characterization of its interaction with the leukocyte integrin CD11a/CD18.

    Tian L, Kilgannon P, Yoshihara Y, Mori K, Gallatin WM, Carpén O and Gahmberg CG

    Department of Biosciences, University of Helskinki, Finland.

    Intercellular adhesion molecule-5 (ICAM-5, telencephalin) is a member of the immunoglobulin superfamily expressed on telencephalic neurons, and serves as a ligand for the leukocyte integrin CD11 a/CD18. We studied here the binding site in ICAM-5 for CD11a/CD18. Protein constructs containing the first immunoglobulin domain of ICAM-5 were able to support CD11a/CD18 interaction, while deletion of the first domain abolished binding. Monoclonal antibodies reacting with the first domain of ICAM-5 also completely blocked the interaction. The soluble first domain of ICAM-5 inhibited the binding of T cells to immobilized ICAM-5 at concentrations of 50 nM and higher. Interestingly, the sixth domain of ICAM-5 was also able to support leukocyte binding, but this binding activity may not involve leukocyte integrins. To test the involvement of ICAM-5 in leukocyte-neuron interactions, an assay using human T cells binding to rat hippocampal neurons was established. This binding was blocked by monoclonal antibodies against CD11a/CD18 and ICAM-5. Thus ICAM-5 may act as a major adhesion molecule for leukocyte binding to neurons in the central nervous system.

    European journal of immunology 2000;30;3;810-8

  • Neuronal adhesion molecule telencephalin induces rapid cell spreading of microglia.

    Mizuno T, Yoshihara Y, Kagamiyama H, Ohsawa K, Imai Y, Kohsaka S and Mori K

    Laboratory for Neurobiology of Synapse, RIKEN Brain Science Institute, Wako, Japan.

    Telencephalin (TLCN) is a neuronal surface glycoprotein whose expression is restricted to the telencephalon, the most rostral segment of the brain. TLCN binds to lymphocyte function-associated antigen-1 (LFA-1) integrin. In the central nervous system, LFA-1 is selectively and constitutively expressed by microglia, suggesting that TLCN/LFA-1 binding may mediate cell-cell interactions between telencephalic neurons and microglia. In the present study, we investigated the effects of recombinant TLCN protein on the morphology of microglia. TLCN induced an intensive spreading of lamellipodia, causing a rapid change in microglial morphology. In contrast, TLCN induced no significant change in morphology of neuroblastoma and fibroblasts. Furthermore, the TLCN-induced spreading of microglia was accompanied by a clustering of LFA-1 on cell surface membrane. These results provide evidence that TLCN binding to the surface of microglia transduces signals into microglia that mediate or accelerate cell spreading and LFA-1 redistribution, implying that neuronal TLCN may control the state and/or function of microglia in both physiological and pathological conditions.

    Brain research 1999;849;1-2;58-66

  • Development of telencephalin in the human cerebrum.

    Arii N, Mizuguchi M, Mori K and Takashima S

    Department of Mental Retardation and Birth Defect Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kadario, Tokyo 187-8502 Japan. arii@ncnaxp.ncnp.go.jp

    Telencephalin (TLN) is a 130kDa, type 1 integral membrane glycoprotein of the immunoglobulin superfamily found in the mammalian central nervous system. TLN shows a molecular structure resembling intercellular adhesion molecules-1 and -3, and binds to the CD11a/CD18 leukocyte integrin. TLN was localized to neuronal dendrites in the telencephalic gray matter: cerebral cortex and basal ganglia. We studied immunohistochemically the expression of TLN in the developing human brain. In the hippocampus, TLN immunoreactivity appeared at 29 gestational weeks (GW), intensified subsequently, and persisted into adulthood. In the temporal cortex, labeling was weak and restricted to the cytoplasm of pyramidal neurons from 35 to 39 GW, but thereafter became diffuse and intense in the cortical layers, especially the molecular layer, by 5 months of postnatal age. The development of TLN was late compared to synaptophysin and microtubule-associated protein 2, suggesting its involvement in the functional maturation of neuronal dendrites and synapses.

    Microscopy research and technique 1999;46;1;18-23

  • Mapping of the ICAM-5 (telencephalin) gene, a neuronal member of the ICAM family, to a location between ICAM-1 and ICAM-3 on human chromosome 19p13.2.

    Kilgannon P, Turner T, Meyer J, Wisdom W and Gallatin WM

    ICOS Corporation, Bothell, Washington, 98021, USA. pkilgannon@icos.com

    Intercellular adhesion molecule 5 (ICAM-5, telencephalin) is a cell adhesion molecule expressed on neurons in the most rostral segment of the mammalian brain, the telencephalon. Antibody studies in rodents and rabbits have demonstrated expression of this molecule on the cell body and dendrites of these neurons. We have examined the expression pattern in human brain by Northern blot analysis of 16 human brain segments. This analysis has confirmed the unique expression pattern of this ICAM in human. In addition, we report the mapping of the human ICAM-5 gene to an 80-kb region on chromosome 19p13.2 that also contains ICAM-1 and ICAM-3.

    Genomics 1998;54;2;328-30

  • Telencephalin as an indicator for temporal-lobe dysfunction.

    Rieckmann P, Turner T, Kligannon P and Steinhoff BJ

    Lancet (London, England) 1998;352;9125;370-1

  • Polarized distribution and cell type-specific localization of telencephalin, an intercellular adhesion molecule.

    Benson DL, Yoshihara Y and Mori K

    Fishberg Research Center for Neurobiology, Mount Sinai School of Medicine, New York, New York 10029, USA. benson@cortex.neuro.mssm.edu

    Telencephalin is an intercellular adhesion molecule (ICAM) restricted to the telencephalon. This study demonstrates that immunolabeled telencephalin is targeted to the somatodendritic domain of cultured hippocampal pyramidal neurons beginning with the first stages of dendritic differentiation. In contrast, it is entirely excluded from all gamma-aminobutyric acid (GABA)ergic inhibitory interneurons at all stages of development. Prior to the stage at which nearly all pyramidal neurons express telencephalin, labeled neurons possess more extensive dendritic arbors than unlabeled pyramidal neurons. More synaptic boutons form with the larger, more elaborate telencephalin-expressing dendritic trees, but bouton number per unit length is similar between neurons with and without telencephalin. These findings suggest that telencephalin identifies pyramidal neurons, it may identify plasma membrane as dendritic, and it may be generally adhesive or stabilize dendritic membranes, but it is probably not specifically synaptic. Such characteristics would be expected to be important for the formation of cell type-specific dendritic arbors.

    Funded by: NIA NIH HHS: AG15204-01

    Journal of neuroscience research 1998;52;1;43-53

  • The intercellular adhesion molecule (ICAM) family of proteins. New members and novel functions.

    Hayflick JS, Kilgannon P and Gallatin WM

    ICOS Corp., Bothell, WA 98021, USA. jhayflick@icos.com

    Macromolecular adhesive associations between cells are important for transmitting spatial and temporal information that is critical for immune system function. One such group of proteins, the intercellular adhesion molecules (ICAMs), has grown as newly identified members are revealed. In addition, the functions of the ICAMs, in general, have begun to be better understood, including intracellular signaling events. This information has led to the design of novel therapeutic agents that may prove effective in a variety of disease states.

    Immunologic research 1998;17;3;313-27

  • cDNA cloning and chromosomal localization of the human telencephalin and its distinctive interaction with lymphocyte function-associated antigen-1.

    Mizuno T, Yoshihara Y, Inazawa J, Kagamiyama H and Mori K

    Department of Neuroscience, Osaka Bioscience Institute, Suita, Japan.

    We have isolated cDNA encoding human telencephalin (TLN), a brain segment-specific neuronal adhesion molecule. Human TLN comprises an NH2-terminal signal peptide, an extracellular region with nine Ig-like domains, a single transmembrane region, and a COOH-terminal cytoplasmic tail. The NH2-terminal five Ig-like domains of TLN were closely related to those of intercellular adhesion molecules (ICAMs)-1 and -3. The TLN gene was mapped to the human chromosome 19p13.2, where the ICAM-1, -3, and -4 (LW) genes are located. Furthermore, we observed lymphocyte function-associated antigen-1 (LFA-1)-mediated adhesion of HL-60 cells on recombinant TLN protein, as well as on ICAM-1. However, the interaction of TLN with LFA-1 on HL-60 cells was divalent cation-independent and phorbol 12-myristate 13-acetate stimulation-independent. We conclude that TLN is a unique neuronal member of ICAM subgroup of the Ig superfamily and propose a novel type of interaction between the Ig superfamily molecule and integrin, which does not require the activation of integrin. TLN on the surface of telencephalic neurons may be a target molecule in the brain for LFA-1-expressing microglia and leukocytes in physiological or pathological conditions.

    The Journal of biological chemistry 1997;272;2;1156-63

  • Telencephalin: a neuronal area code molecule?

    Yoshihara Y and Mori K

    Department of Neuroscience, Osaka Bioscience Institute, Japan.

    Cell adhesion molecules (CAMs) with expression restricted to specific developmental and structural units of the brain and/or selective neuronal types would play critical roles in the formation of functional neuronal networks. In this article, we summarize recent progress in knowledge on a brain segment-specific CAM, telencephalin (TLN). TLN has the following characteristic properties. (1) TLN is a neuronal glycoprotein whose expression is restricted within telencephalon, the most rostal segment of the brain. (2) TLN is localized to the soma-dendritic membrane of subsets of telencephalic neurons, but not to the axonal membrane. (3) Abrupt appearance of TLN around birth parallels the timing of dendritic development and synapse formation in the telencephalon. (4) TLN belongs to the immunoglobulin superfamily and its structure is most closely related to intercellular adhesion molecules (ICAMs)-1 and -3. These findings suggest that TLN is the first example of dendrite-associated cell adhesion molecules (DenCAMs) and that TLN may be involved in the brain segmental organization, cell-cell interactions during dendritic development, and maintenance of functional neuronal networks. We discuss the possibility that TLN is an area code-like address signal that is displayed selectively by telencephalic neurons and is decoded by specific subsets of growing axons to make proper synaptic connections.

    Neuroscience research 1994;21;2;119-24

Gene lists (4)

Gene List Source Species Name Description Gene count
L00000059 G2C Homo sapiens BAYES-COLLINS-HUMAN-PSD-CONSENSUS Human cortex PSD consensus 748
L00000061 G2C Homo sapiens BAYES-COLLINS-MOUSE-PSD-CONSENSUS Mouse cortex PSD consensus (ortho) 984
L00000069 G2C Homo sapiens BAYES-COLLINS-HUMAN-PSD-FULL Human cortex biopsy PSD full list 1461
L00000071 G2C Homo sapiens BAYES-COLLINS-MOUSE-PSD-FULL Mouse cortex PSD full list (ortho) 1556
© G2C 2014. The Genes to Cognition Programme received funding from The Wellcome Trust and the EU FP7 Framework Programmes:
EUROSPIN (FP7-HEALTH-241498), SynSys (FP7-HEALTH-242167) and GENCODYS (FP7-HEALTH-241995).

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