Disease relevance of Icam5

• To investigate the fate of ICAM-5 during focal brain injury, we induced hypoxia-ischemia (HI) damage in adult mice by right common carotid artery ligation followed by hypoxia [1].
• In addition to binding human immunodeficiency virus (HIV), this type II membrane protein binds with high affinity to the adhesion molecules ICAM-3 and -2 to promote important dendritic cell interactions with naive T cells and endothelial cells, respectively [2].
• At high doses SR 95195 induced clonic seizures in mice (threshold convulsant dose: 150 mg kg-1; CD50: 160 mg kg-1 i.p.) which were antagonized by Ro 15-1788 [3].
• Ehrlich ascites tumour cells grown in mice have a cell-surface trypsin-like neutral protease (TLNP) which is not inhibited by high-mol.-wt inhibitors of trypsin [4].
• The percentage of animals rendered cataleptic by administration of either GABA uptake inhibitor was reduced by treatment for as few as 4 days and treatment with SKF(R)-89976A for 14 days resulted in a 4-fold increase in the CD50 for induction of catalepsy [5].

Psychiatry related information on Icam5

• DBA mice had lower maximal electroshock seizure thresholds (MESTs, 15%) and CD50s for homocysteine thiolactone (HTL, 23%) and bicuculline (69%), and a higher CD50 for pentylenetetrazol (PTZ) at 3 weeks of age, the age of maximal audiogenic seizure (AGS) susceptibility [6].
• The effect of 50% convulsant (CD50) and 50% lethal (LD50) doses of lidocaine, bupivacaine and pentylenetetrazol were determined in mice stressed by paradoxical sleep deprivation (PSD) [7].

High impact information on Icam5

• This third ligand, designated ICAM-3 based on its functional relatedness to ICAM-1 and -2, is a highly glycosylated protein of 124,000 Mr. It is well expressed on all leukocytes and absent from endothelial cells [8].
• An ICAM-related neuronal glycoprotein, telencephalin, with brain segment-specific expression [9].
• TLN is an example of a dendrite-associated cell adhesion molecule involved in the brain's segmental organization, cell-cell interactions during dendritic development, and maintenance of functional neuronal networks [9].
• Telencephalin (TLN) is a 130 kd glycoprotein expressed exclusively in neurons of the telencephalon, the most rostral brain segment [9].
• The structural similarity of TLN with ICAMs provides a new and strong link between immunoglobulin superfamily molecules in the nervous and immune systems [9].

Chemical compound and disease context of Icam5

• At 8 weeks, when DBA mice are not susceptible to AGSs, significant differences were a lower minimal electroshock seizure threshold (mEST, 37%) and maximal EST (MEST) (19%), lower CD50s for N-methyl-D-aspartate (NMDA) (39%), kainic acid (KA, 50%), HTL (32%), strychnine (37%), and a higher CD50 for nicotine (55%) in DBA mice [6].
• However, Nomega-nitro-L-arginine methyl ester reduced the tonic CD50 of both picrotoxin and 4-aminopyridine in mice and failed to suppress tonus following maximal electroshock [10].
• The CD50 value for clonic seizures for Evans blue was 35(23-53) nmol [11].
• Neither L-NAME nor 7-NI affected the convulsions induced by PIL (clonic seizures) or PTZ (clonic and tonic seizures), having no effect on their CD50 values [12].
• Acute toxicity (LD50 and CD50) of lidocaine and prilocaine in combination with adrenaline and felypressin [13].

Biological context of Icam5

• The loss of Icam3 in rodent genomes might be relevant for rodent-specific properties of the T-cell-mediated immune response [14].
• The Tlcn gene spanned about 6.3 kb and consisted of 11 exons [15].
• A conserved amino acid motif including residues E37 and T38 form an integrin binding site (IBS) in ICAM-3 [16].
• Point mutation of Ser(487), Ser(489), and Ser(496) to alanine in the juxtamembrane region of ICAM-3 significantly impaired both ERM binding and polarization of ICAM-3 [17].
• Almost the same ICAM gene clusters were found in rodent genome, but only the ICAM-3 was not present [18].

Anatomical context of Icam5

• A novel phenylalanine-based targeting signal directs telencephalin to neuronal dendrites [19].
• In HI brain, dendritic ICAM-5 immunore-activity was abolished, but it was present in the neuropil and soma of hippocampal pyramidal, dentate granule, and some cortical and striatal neurons [1].
• Intracerebroventricular administration of lipopolysaccharide to activate microglia before HI injury resulted in elevated serum ICAM-5 levels compared with those in mice with only HI injury [1].
• Intercellular adhesion molecule (ICAM)-5 (telencephalin) is unique among the ICAMs, because it is only expressed in somatodendritic membranes of telencephalic neurons [1].
• Dendrite-associated cell adhesion molecule, telencephalin, promotes neurite outgrowth in mouse embryo [20].

Associations of Icam5 with chemical compounds

• The intercellular adhesion molecule-3 (ICAM-3) is a counter receptor for the integrin LFA-1 that supports cell-cell adhesion dependent functions [16].
• Protein-protein binding assays demonstrated a phosphatidylinositol 4,5-bisphosphate-induced association between ICAM-3 and the amino-terminal domain of ERM proteins [17].
• Our results underscore the key role of specific serine residues within the cytoplasmic region of ICAM-3 for its ERM-directed positioning at the trailing edge of motile lymphocytes [17].
• The CD50 of 7.0 mg/kg i.v. falls between that of picrotoxin and pentylenetetrazol [21].
• (-)Nicotine was the most potent agonist tested, with a CD50 of 7.9 X 10(-9) mol [22].

Physical interactions of Icam5

• LFA-1 binding site in ICAM-3 contains a conserved motif and non-contiguous amino acids [16].

Regulatory relationships of Icam5

• Six out of nine ICAM-3 Mab described blocked the interaction with LFA-1 to varying degrees [16].

Other interactions of Icam5

• Genomic organization and chromosomal localization of the mouse telencephalin gene, a neuronal member of the ICAM family [15].
• This motif has also been shown to function as an IBS in ICAM-3 and VCAM-1 and hence many form a common site of contact in all CAMs of this type [16].
• Pretreatment with anti-LFA-1 antibodies before HI injury or LFA-1 receptor knockout mice with HI injury had markedly reduced levels of serum ICAM-5 [1].
• This residue, Q75, is predicted to locate in a model of ICAM-3 to the same site as RGD in the immunoglobulin-like domain of fibronectin that binds several integrins [16].

Analytical, diagnostic and therapeutic context of Icam5

• Dynamic fluorescence videomicroscopy studies of cells demonstrated that moesin and ICAM-3 coordinately redistribute on the plasma membrane during lymphocyte migration [17].
• Epitope mapping and functional properties of anti-intercellular adhesion molecule-3 (CD50) monoclonal antibodies [23].
• We have investigated whether nitrous oxide antagonizes or augments the CNS stimulant action of laudanosine in mice by comparing the mean convulsive doses (CD50 (SE] of a control group and those following pretreatment with 65% nitrous oxide in oxygen for 20 and 180 min [24].

References