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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of lengthening the distance in an adhesion molecule between the receptor binding site and the membrane anchor was studied by inserting four Ig-like domains into the two Ig domain lymphocyte function-associated antigen 3 (LFA-3) molecule. The extended molecule expressed in Chinese hamster ovary (CHO) cells bound to CD2 on T lymphocytes 4- to 20-fold more efficiently than the wild-type molecule at 4 degrees C. Treatment of the CHO clones with neuraminidase to remove sialic acid, or with deoxymannojirimycin to reduce the bulk of N-linked glycosylation, showed that adhesion to both the wild-type and the chimeric LFA-3 molecules was under the influence of cell-cell repulsive forces to a similar extent and that these treatments had less effect than lengthening LFA-3. At higher temperatures, such as 22 and 37 degrees C, the efficiency of binding to the wild-type LFA-3 increased to levels comparable with binding to extended LFA-3. Our results suggest that more distal locations of the adhesive binding site from the cell membrane anchor increase the efficiency of cell-cell adhesion by enhancing the frequency of receptor encounter with ligand and that more proximal locations of the adhesive binding site can provide efficient cell-cell adhesion at physiological temperatures.
Mol Biol Cell 1992 Feb
PMID:Effect of lengthening lymphocyte function-associated antigen 3 on adhesion to CD2. 134 6

AMOG, identified as an adhesion molecule that mediates neuron-astrocyte interaction, has structural similarity to the beta-subunit of Na,K ATPase. We have mapped the AMOG gene to human chromosome 17 and mouse chromosome 11 by somatic cell hybrid analysis. Recombinant inbred strain mapping has placed the Amog locus close to genes for zinc finger protein-3 and the asialoglycoprotein receptor in a region of mouse chromosome 11 that is homologous to human 17p.
Somat Cell Mol Genet 1990 Jul
PMID:Assignment of Amog (adhesion molecule on glia) gene to mouse chromosome 11 near Zfp-3 and Asgr-1,2 and to human chromosome 17. 169 90

Tst-1, a member of the POU domain gene family, is expressed in specific neurons and in myelinating glia in the mammalian nervous system. Bacterially expressed Tst-1 binds specifically to the promoter of the gene encoding myelin protein P0, a Schwann cell surface adhesion molecule. In cotransfection assays, Tst-1 can specifically repress the P0 promoter. The N-terminal part of Tst-1 protein is highly glycine- and alanine-rich, a structural feature shared by the helix-loop-helix protein TFEB.
Mol Cell Biol 1991 Mar
PMID:Tst-1, a member of the POU domain gene family, binds the promoter of the gene encoding the cell surface adhesion molecule P0. 170 13

Evidence from epidemiological and histopathologic studies in humans with autoimmune type 1 (insulin-dependent) diabetes suggests that beta-cell destruction within the islets of Langerhans progresses through a number of stages. In this review we draw on recent experimental evidence in an attempt to define the molecular pathology of these stages. Stage 1 is postulated to be initiated by modification of the beta cell by virus, chemical or other factors, leading to the production of interferon-alpha, hyperexpression of major histocompatibility complex (MHC) class I molecules and induction of MHC class II molecules. Experiments in transgenic mice suggest that overexpression of MHC molecules is in itself detrimental to beta-cell function. Shedding of antigen(s) from dying beta cells in combination with hyperexpression of MHC molecules may be a powerful immunogenic stimulus. Stage 2 commences with infiltration of the islets by immuno-inflammatory cells (termed insulitis). It is proposed that production of cytokines from the infiltrating cells induces "phenotypic switching" in beta cells, with further upregulation of MHC molecules and the induction of intracellular adhesion molecule-1 expression and interleukin-6 production. Together, these properties are seen as a prerequisite for the presentation of autoantigen by beta cells to adherent T lymphocytes and autoimmune activation. The final stage encompasses autoimmune-mediated destruction of the beta cells by the targeted delivery of cytotoxic cytokines and other mediators.
Mol Biol Med 1990 Aug
PMID:Molecular pathology of type 1 diabetes. 223 44

The adhesion of leukocytes to endothelium is a physiological phenomenon which is the first step for leukocyte emigration. The adhesion can be dramatically increased in pathological situations such as inflammation and vascular diseases. The molecular basis of leukocyte-endothelium interaction has been largely investigated in the last ten years. Using monoclonal antibodies it is possible to characterize the leukocyte adhesion molecule (LeuCAM) also named CD11/CD18 complex. These molecules responsible for leukocyte adhesion are heterodimers consisting of a common beta subunit and different subunit CD11a/CD18 corresponding to LFA-1; CD11b/CD18 to Mac1/Mol; CD11c/CD18 to GP150-95. Beside these receptors, other leukocyte structures such as the fibronectin receptors are involved in the adhesive process. On the endothelial cell side specialized structures implicated in leukocyte adhesion have been identified. Structures like Intercellular Adhesion Molecule (ICAM) are expressed on endothelial cells in the absence of stimulation, while other receptors Endothelial Leukocyte Adhesion Molecule (ELAM) are only detectable on activated endothelial cells. Cytokines such as IL-1 induced the expression of ELAM, increased the number of ICAM and Human Leukocyte Antigens (HLA) DR, DP, DQ. In various pathological circumstances, namely extracorporeal circulation, Acute Respiratory Distress Syndrome (ARDS), hypercholesterolemia and diabetes mellitus increased leukocyte adhesion has been reported and is potentially responsible for vascular damage. Therefore, the modulation of leukocyte-endothelial cell interactions is a possible target for antithrombotic and antiatherosclerotic therapy.
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PMID:Leukocyte adhesion to endothelial cells. 226 8

This interpretive review attempts to dovetail advanced work by different groups of investigators on blood group and carcinoma (CA) glycoconjugates that have terminal, immunoreactive Tn epitopes (GalNAc alpha-O-Ser/Thr), and on the interaction of those structures with complementary antibodies and lectins. Fenlon et al. (1987) and Leathem and Brooks (1987) found a positive correlation between primary breast CA aggressiveness and its affinity for Helix pomatia (HPA) lectin. This phenomenon was used successfully to accurately predict, in studies on 305 breast CA patients, early or late CA recurrence and patient survival time. The innate specificity of the large HPA combining groove (aside from its avid reactivity with appropriately spaced GalNAc alpha-O-) remains obscure, despite careful investigation for more than a decade (Baker et al., 1983). Leathem and Brooks presumed that HPA recognizes a hitherto "undefined biological marker" that indicates a breast CA's aggressiveness. Our own work has shown that the chemically fully defined Tn epitope, as measured with human polyclonal and murine monoclonal anti-Tn antibodies, occurs in immunoreactive form in approximately 90% of all breast and lung adenoCAs studied. Tn is occluded and non-reactive in healthy and non-CA-diseased tissues. We found that CA-associated Tn is an adhesion molecule in attachment to healthy cells; an increase in its density on breast CA cell membranes parallels greater aggressiveness of breast tumors in both humans and mice (the only species studied). Thus, Tn may be all or a major part of the postulated "as yet undefined biological marker" associated with high breast CA aggressiveness. Besides being helpful in the elucidation of some aspects of breast CA pathogenesis, these findings on primary breast CA have clinical implications in that they should facilitate stratification of breast CA patients for adjuvant treatment.
Mol Immunol 1989 Jan
PMID:Tn epitope (N-acetyl-D-galactosamine alpha-O-serine/threonine) density in primary breast carcinoma: a functional predictor of aggressiveness. 246 92

Effect of mAb against the CD11a-c, CD18, and GP84 adhesion molecules on the binding and cytotoxicity of human NK cells was studied. The target cells were K562, MOLT-4, Raji, and fresh uncultured autologous endometrial carcinoma cells. Antibodies against adhesion relevant epitopes of CD11a(TA-1/LFA-1), CD11b(Mol/OKM1/Mac1), or CD11c (Leu-M5) did not inhibit NK function. The mAb 60.3 against CD18, the common beta-chain associated to CD11a-c, strongly inhibited both the binding and cytotoxicity of large granular lymphocytes (LGL) against all the target cells tested. Also the antibody LB-2 against the GP84 adhesion molecule inhibited NK function to some degree. 60.3 and LB-2 antibodies exerted an additive effect in the inhibition of both binding and cytotoxicity. However, even this antibody combination did not completely block NK activity, suggesting a heterogeneity of adhesion structures in the NK system. According to both FACS analyses and immunoprecipitation studies, all the tested antibodies recognized either a subpopulation or all of LGL. On the other hand, antibodies against CD11b, CD11c, and LB-2 showed only marginal reactivity with highly purified LGL-free T cells.
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PMID:CD11a-c/CD18 and GP84 (LB-2) adhesion molecules on human large granular lymphocytes and their participation in natural killing. 289 96

Macrophage adhesion molecule is a surface molecule of guinea pig macrophages and neutrophils. It is the counterpart of mouse Mac-1 and human CD11b/CD18 (Mol/OKM-1/Mac-1/Leu-CAM) and is member of a family of heterodimer glycoproteins with a common beta-subunit. Macrophage adhesion molecule is a prevalent molecule in nonactivated macrophages, but it is dramatically decreased in macrophages activated in vivo. The experimental system of activated vs nonactivated guinea pig peritoneal macrophages was used to examine the mechanisms that down-regulate synthesis of this heterodimer molecule. [35S]Methionine labeling of nonactivated macrophages and chase incubation revealed that synthesis involves separate translation of the alpha- and beta-glycopeptides of "high mannose"-containing monomeric precursors, then refolding/assembly to form a heterodimer, and, finally, a maturation process that includes conversion of carbohydrate to "complex" units. Two lines of evidence demonstrate that down-regulation in activated macrophages occurs via restriction of the alpha-species. First, pre-beta is detected at 3 h only in activated macrophages. Second, the amount of newly translated pre-alpha averaged 16% in activated macrophages relative to nonactivated macrophages, which is close to the value of 12% for the mature heterodimer. The amount of newly translated pre-beta averaged 62%. These findings identify the regulatory step as a restriction of the alpha-species at, or before, translation. A model is proposed to explain regulation of synthesis of heterodimer membrane glycoproteins.
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PMID:Regulation of synthesis of macrophage adhesion molecule, a heterodimeric membrane glycoprotein. 334 13

We have investigated the molecular changes which occur during pressure overload hypertrophy of the RV in swine. Animals were banded on the pulmonary artery so that right ventricular pressure was increased two-fold. The heart was harvested at 3, 7, 24 and 72 h after surgery. Between 7 and 72 h there was evidence of muscle damage and inflammation. Northern blot experiments showed that pressure overload induced a transient increase in the expression of the immediate early genes and in the developmentally regulated atrial natriuretic factor and skeletal muscle alpha actin genes. Consistent with the histological observations of inflammation, increases in the expression of the gene for intercellular adhesion molecule, which encodes a protein involved in the binding of leukocytes by endothelial cells and myocytes, was observed between 3 and 24 h. In addition, the expression of vascular endothelial growth factor, a growth and permeability factor specific for endothelial cells was increased at 3 and 7 h of pressure overload. An increase in the expression of urokinase plasminogen activator and its inhibitors, plasminogen activator inhibitors I and II, was also observed between 3 and 24 h. This was associated with an increase in urokinase activity in the myocardial tissue. These results indicate that hypertrophy in a large mammal such as swine induces a program of gene expression similar to that previously described in rodents and suggests that up-regulation of a variety of other genes is an early response to pressure overload.
J Mol Cell Cardiol 1995 Jul
PMID:Gene expression in a swine model of right ventricular hypertrophy: intercellular adhesion molecule, vascular endothelial growth factor and plasminogen activators are upregulated during pressure overload. 747 88

P0, the major structural protein of peripheral myelin, is a homophilic adhesion molecule with a single immunoglobulin (Ig) domain, which contains a single N-linked glycosylation site and two cysteines. We have previously reported four different mutations of the myelin P0 gene in four families of Charcot-Marie-Tooth neuropathy type 1 (CMT1). In this study we found a new mutation of the myelin P0 gene in a small family of CMT1. The affected persons had an A - to - G substitution of nucleotide 245 of the myelin P0 gene in one allele, leading to a cysteine substitution for tyrosine82 in the extracellular Ig-domain. An additional cysteine in the extracellular domain may form a disulfide bond and cause an inappropriate change in the tertiary structure of the functional Ig-domain of P0.
Biochem Mol Biol Int 1993 Sep
PMID:New mutation of the myelin P0 gene in a pedigree of Charcot-Marie-Tooth neuropathy 1. 750 51


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