Map Key
Generic Enzyme
Generic kinase
Protein kinase
Lipid kinase
Generic phosphatase
Protein phosphatase
Lipid phosphatase
Generic phospholipase
Generic protease
Metalloprotease
G-alpha
RAS - superfamily
G beta/gamma
Regulators (GDI, GAP, GEF)
Generic channel
Ligand-gated channel
Voltage-gated channel
Transporter
Normal process
Pathological process
Positive effect
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Unspecified effect
Technical link
Disrupts in disease
Emerges in disease
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Organsim specific interaction

Generic binding protein
Receptor ligand
Cell membrane glycoprotein
Transcription factor
DNA
RNA
Compound
Inorganic ion
Predicted metabolite or user's structure
Reaction
Generic receptor
GPCR
Receptors with enzyme activity
Mitochondria
EPR
Golgi
Nucleus
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Peroxisome
Cytoplasm
Extracellular

Normal process
Pathological process
Binding
Cleavage
Covalent modifications
Phosphorylation
Dephosphorylation
Transformation
Transport
Catalysis
Transcription regulation
MicroRNA binding
Competition
Influence on expression
Unspecified interactions
Pharmacological effect
Toxic effect
Group relation
Complex subunit
Similarity reaction
A complex or a group
Organism specific object

Cell adhesion Cell-matrix glycoconjugates


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Cell adhesion Cell-matrix glycoconjugates

Cell- matrix glycoconjugates

Extracellular matrix (ECM) is composed of several macromolecules bound together in acomplex network. This structure allows cells to adhere, migrate and interact.Hyaluronic acid, a glycosaminoglycan, is a major component of ECM. Hyaluronicacid -binding proteins such as hyaluronic acid receptor LYVE-1, CD44,cartilage link protein CRTL1, Aggrecan, Brevican ( BCAN ) ,Neurocan and Versican, are implicated in cell-matrix interactions and instructurization of the ECM via stabilizing large macromolecular aggregates. They alsoplay an important role in tumor metastasis and cell motility [1], [2], [3], [4].

Aggrecan, Versican, Neurocan, and BCAN are chondroitinsulfate proteoglycans of the ECM. Their interactions with cell surface proteins, as wellas with chemokines such as CCL8, CCL5 and Lymphotactin, playimportant role in cell adhesion [5].

Fibulins are another family of the ECM proteins. Fibulins cross-linkhyaluronan-proteoglycan complexes that play an essential role in supramolecularorganization of cartilaginous and other extracellular matrices [6].

Tenascins are a family of large oligomeric ECM glycoproteins. They all modulatecell-matrix interactions and define the state of matrix attachment that promotes cellmotility [7].

Galectins are a family of beta-galactoside-binding proteins implicated inmodulating cell-cell and cell-matrix interactions. Galectins exist inintracellular and extracellular milieu. In extracellular space, they link withbeta-galactoside containing glycoconjugates of the ECM and cell surface adhesionmolecules that regulate cell adhesion and differentiation [8], [9], [10].

ECM remodeling is regulated by a huge number of proteinases and their inhibitors.Alpha-1-microglobulin ( A1M ) is a serine-proteinase inhibitor. It forms complexeswith one or two heavy chains, Inter-alpha (globulin) inhibitors H1, H2 and H3 (ITIH, ITIH2 and ITIH3 ) [11]. The heavy chains arelinked to hyaluronic acid, and this attachment greatly improves ECM stability[1]. A1M exerts an inhibitory activity towards Elastase-2 andPlasmin and it thus suspected of playing a key role in ECM biology [12].

Plasmin takes part in the processing of the matrix metallopreoteinases (MMPs),such as MMP-1. It also cleaves ECM proteins [13], [14].Plasmin, MMPs (such as MMP-1, MMP-9 and Stromelysin-1 ),and inhibitors of MMPs (such as TIMP2) directly participate in regulation of celladhesion, migration, and ECM remodeling [15], [16].