Extracellular Matrix
Cell-Matrix Junctions
Fibronectins
Extracellular Matrix Proteins
Cells, Cultured
Gap Junctions
Intercellular Junctions
Tight Junctions
Collagen
Laminin
Cell Movement
Endothelium, Vascular
Adherens Junctions
Matrix Metalloproteinase 2
Matrix Metalloproteinases
Nuclear Matrix
Connexins
Connexin 43
Bone Matrix
Matrix Metalloproteinase Inhibitors
Matrix Metalloproteinase 1
Zonula Occludens-1 Protein
Esophagogastric Junction
Occludin
Matrix Metalloproteinase 3
Holliday Junction Resolvases
Freeze Fracturing
Molecular Sequence Data
Cell Communication
Microscopy, Electron
Membrane Proteins
Cadherins
Matrix Metalloproteinase 14
Matrix Metalloproteinase 7
Matrix Metalloproteinase 13
Base Sequence
Epithelial Cells
DNA, Cruciform
Claudin-1
Matrix Metalloproteinases, Membrane-Associated
Amino Acid Sequence
Immunohistochemistry
Matrix Metalloproteinase 12
RNA, Messenger
Tissue Inhibitor of Metalloproteinase-1
Desmosomes
Matrix Metalloproteinases, Secreted
Viral Matrix Proteins
Fibroblasts
Tissue Inhibitor of Metalloproteinases
Zonula Occludens-2 Protein
Fluorescent Antibody Technique
Epithelium
Neuromuscular Junction Diseases
Models, Biological
Tissue Inhibitor of Metalloproteinase-2
Glycyrrhetinic Acid
Carbenoxolone
Microscopy, Fluorescence
Signal Transduction
Microscopy, Confocal
Dogs
Protein Binding
Cell Adhesion Molecules
Blotting, Western
Mutation
Cytoskeletal Proteins
Actins
alpha Catenin
Permeability
Gelatinases
Heptanol
Cell Membrane Permeability
Matrix Metalloproteinase 10
Desmoplakins
Cell Membrane
Microscopy, Electron, Scanning
Claudin-3
DNA
Cytoskeleton
Motor Endplate
Cartilage Oligomeric Matrix Protein
Reverse Transcriptase Polymerase Chain Reaction
Cell Differentiation
Basement Membrane
Integrins
Cell Polarity
Cattle
Claudin-4
Cartilage
Collagen Type I
Mice, Knockout
Catenins
Transfection
Receptors, Cholinergic
Nucleic Acid Conformation
Gene Expression Regulation
Tenascin
Protein Structure, Tertiary
Junctional Adhesion Molecules
beta Catenin
Calcium
Neuroeffector Junction
Gene Expression
Rats, Sprague-Dawley
Microscopy, Electron, Transmission
Microscopy, Immunoelectron
Binding Sites
Calcification, Physiologic
Cartilage, Articular
Matrix Metalloproteinase 11
Phenotype
Rabbits
Phosphorylation
Recombination, Genetic
Tissue Engineering
Endothelial Cells
Cloning, Molecular
Position-Specific Scoring Matrices
Rana pipiens
Stress, Mechanical
Immunoblotting
Matrilin Proteins
Disease Models, Animal
Protein Transport
gamma Catenin
Hyaluronic Acid
Electrophoresis, Polyacrylamide Gel
Glycosaminoglycans
Transforming Growth Factor beta
Caco-2 Cells
Synaptic Transmission
Morphogenesis
Gelatin
Vinculin
Chick Embryo
Membrane Potentials
Electrophysiology
Recombinant Fusion Proteins
Protease Inhibitors
MARVEL Domain Containing 2 Protein
Glycoproteins
Skin
Microfilament Proteins
Matrix Attachment Regions
DNA Primers
Synapses
Drosophila Proteins
Models, Molecular
Agrin
Antigens, CD29
Zonula Occludens Proteins
Fluorescent Dyes
Lens, Crystalline
Up-Regulation
Sertoli Cells
Tumor Cells, Cultured
Matrix Metalloproteinase 20
Tendons
Sequence Alignment
Tissue Scaffolds
Proteins
Lanthanum
Kidney
Fluorescent Antibody Technique, Indirect
Sequence Homology, Amino Acid
Cell Division
Seminiferous Epithelium
Blood-Brain Barrier
Exons
Cell Adhesion Molecules, Neuronal
Polymerase Chain Reaction
Enzyme Activation
Drosophila
Myocardium
Gene Expression Regulation, Developmental
Endodeoxyribonucleases
Matrix attachment regulates Fas-induced apoptosis in endothelial cells: a role for c-flip and implications for anoikis. (1/97)
Survival of endothelial cells is critical for cellular processes such as angiogenesis. Cell attachment to extracellular matrix inhibits apoptosis in endothelial cells both in vitro and in vivo, but the molecular mechanisms underlying matrix-induced survival signals or detachment-induced apoptotic signals are unknown. We demonstrate here that matrix attachment is an efficient regulator of Fas-mediated apoptosis in endothelial cells. Thus, matrix attachment protects cells from Fas-induced apoptosis, whereas matrix detachment results in susceptibility to Fas-mediated cell death. Matrix attachment modulates Fas-mediated apoptosis at two different levels: by regulating the expression level of Fas, and by regulating the expression level of c-Flip, an endogenous antagonist of caspase-8. The extracellular signal-regulated kinase (Erk) cascade functions as a survival pathway in adherent cells by regulating c-Flip expression. We further show that detachment-induced cell death, or anoikis, itself results from activation of the Fas pathway by its ligand, Fas-L. Fas-L/Fas interaction, Fas-FADD complex formation, and caspase-8 activation precede the bulk of anoikis in endothelial cells, and inhibition of any of these events blocks anoikis. These studies identify matrix attachment as a survival factor against death receptor-mediated apoptosis and provide a molecular mechanism for anoikis and previously observed Fas resistance in endothelial cells. (+info)Ezrin interacts with focal adhesion kinase and induces its activation independently of cell-matrix adhesion. (2/97)
Ezrin, a membrane-cytoskeleton linker, is required for cell morphogenesis, motility, and survival through molecular mechanisms that remain to be elucidated. Using the N-terminal domain of ezrin as a bait, we found that p125 focal adhesion kinase (FAK) interacts with ezrin. We show that the two proteins coimmunoprecipitate from cultured cell lysates. However, FAK does not interact with full-length ezrin in vitro, indicating that the FAK binding site on ezrin is cryptic. Mapping experiments showed that the entire N-terminal domain of FAK (amino acids 1-376) is required for optimal ezrin binding. While investigating the role of the ezrin-FAK interaction, we observed that, in suspended kidney-derived epithelial LLC-PK1 cells, overproduction of ezrin promoted phosphorylation of FAK Tyr-397, the major autophosphorylation site, creating a docking site for FAK signaling partners. Treatment of the cells with a Src family kinase inhibitor reduced the phosphorylation of Tyr-577 but not that of Tyr-397, indicating that ezrin-mediated FAK activation does not require the activity of Src kinases. Altogether, these observations indicate that ezrin is able to trigger FAK activation in signaling events that are not elicited by cell-matrix adhesion. (+info)pp60(c-src) and related tyrosine kinases: a role in the assembly and reorganization of matrix adhesions. (3/97)
Activation of tyrosine kinases during integrin-mediated cell-matrix adhesion is involved both in the regulation of focal contact assembly and in the initiation of signaling processes at the cell-matrix adhesive interface. In order to determine the role of pp60(c-src) and related kinases in these processes, we have compared the dynamic reorganization of phosphotyrosine, vinculin, focal adhesion kinase and tensin in cells with altered expression of Src-family kinases. Both null cells for pp60(c-src) and triple knockout cells for pp60(c-src), pp59(fyn), and pp62(c-yes) exhibited decreased phosphotyrosine levels in focal contacts when compared with wild-type cells. pp60(c-src)-null cells also exhibited faster assembly of cell-matrix adhesions and a more exuberant recruitment of FAK to these sites. Tensin, which normally segregates into fibrillar adhesions was localized in large focal contacts in the two mutant cell lines, suggesting involvement of pp60(c-src) in the segregation of focal contacts and fibrillar adhesions. Moreover, treatment of wild-type cells with tyrphostin AG1007, which inhibits both pp60(c-src) and FAK activity, induced accumulation of tensin in peripheral focal adhesions. These findings demonstrate that Src family kinases, and pp60(c-src) in particular, have a central role in regulating protein dynamics at cell-matrix interfaces, both during early stages of interaction and in mature focal contacts. (+info)Members of the Jagged/Notch gene families are expressed in injured arteries and regulate cell phenotype via alterations in cell matrix and cell-cell interaction. (4/97)
The Jagged/Notch signaling pathways control cell fate determination and differentiation, and their dysfunction is associated with human pathologies involving cardiovascular abnormalities. To determine the presence of these genes during vascular response to injury, we analyzed expression of Jagged1, Jagged2, and Notch1 through 4 after balloon catheter denudation of the rat carotid artery. Although low levels of Jagged1, Jagged2, and constitutive expression of Notch1 were seen in uninjured endothelium, expression of all was significantly increased in injured vascular cells. High Jagged1 expression was restricted to the regenerating endothelial wound edge, whereas Notch transcripts were abundant in endothelial and smooth muscle cells. To understand the basis for Jagged/Notch control of cellular phenotype, we studied an in vitro model of NIH3T3 cells transfected with a secreted form of the extracellular domain of Jagged1. We report that the soluble Jagged1 protein caused decreased cell-matrix adhesion and cell migration defects. Cadherin-mediated intercellular junctions as well as focal adhesions were modified in soluble Jagged1 transfectants, demonstrating that cell-cell contacts and adhesion plaques may be targets of Jagged/Notch activity. We suggest that Jagged regulation of cell-cell and cell-matrix interactions may contribute to the control of cell migration in situations of tissue remodeling in vivo. (+info)Molecular complexity and dynamics of cell-matrix adhesions. (5/97)
Currently >50 proteins have been reported to be associated with focal contacts and related ECM adhesions. Most of these contain multiple domains through which they can interact with different molecular partners, potentially forming a dense and heterogeneous protein network at the cytoplasmic faces of the adhesion site. The molecular and structural diversity of this 'submembrane plaque' is regulated by a wide variety of mechanisms, including competition between different partner proteins for the same binding sites, interactions triggered or suppressed by tyrosine phosphorylation, and conformational changes in component proteins, which can affect their reactivity. Indeed, integrin-mediated adhesions can undergo dynamic changes in structure and molecular properties from dot-like focal complexes to stress-fiber-associated focal contacts, which can further 'mature' to form fibronectin-bound fibrillar adhesions. These changes are driven by mechanical force generated by the actin- and myosin-containing contractile machinery of the cells, or by external forces applied to the cells, and regulated by matrix rigidity. (+info)Cdk5 regulates cell-matrix and cell-cell adhesion in lens epithelial cells. (6/97)
Cdk5 is a member of the cyclin-dependent kinase family, which is expressed predominantly in terminally differentiated neurons. Lower levels of Cdk5 are also found in a wide variety of cell types, including the lens. Although Cdk5 has been shown to play an important role in neuronal migration and neurite outgrowth, its function in non-neuronal cells is not known. Therefore, this study was undertaken to explore the role of Cdk5 in the lens. Results showed that, within the adult mouse lens, Cdk5 was localized to the cytoplasm, especially along the lateral membranes of differentiating primary fiber cells, which suggests a role in cell-cell adhesion. Staining at the tips of elongating fiber cells was also particularly strong, suggesting a role in cell-matrix adhesion. To examine the possible role of Cdk5 in lens epithelial cell adhesion, we stably transfected N/N1003A rabbit lens epithelial cells with cDNAs for Cdk5 or a dominant-negative mutation, Cdk5-T33. Attachment to a fibronectin matrix, as measured with substrate-coated cell adhesion strips, was increased by Cdk5 overexpression, while an equivalent overexpression of Cdk5-T33 had no effect. Cdk5 also increased the rate of cell attachment and spreading as measured by electric cell-substrate impedance sensing (ECIS). In addition, Cdk5 overexpression decreased cell-cell adhesion as measured by a cell aggregation assay. These findings suggest that Cdk5 plays a role in regulating both cell-matrix and cell-cell interactions in the lens. (+info)PLC-gamma1 is required for IGF-I protection from cell death induced by loss of extracellular matrix adhesion. (7/97)
Phospholipase C-gamma1, a tyrosine kinase substrate, hydrolyses phosphatidylinositol 4,5-bisphosphate to produce inositol 1,4,5-trisphosphate and diacylglycerol, which act as second messenger moleculesto mobilize intracellular calcium and activate protein kinase C, respectively. We have investigated the role of phospholipase C-gamma1 in anoikis, or cell death, induced by the loss of extracellular matrix adhesion. Spontaneously immortalized mouse embryonic fibroblasts nullizygous at the Plcg1 locus (Plcg1(-/-)), referred to as Null cells, were derived from targeted gene disruption experiments. Subsequently, phospholipase C-gamma1 was re-expressed in these cells to derive Null+ cells. The Null and Null+ cells were then placed in suspension to induce cell death, which was measured directly as well as by the induction of caspase 3, as an index of programmed cell death or apoptosis. The results demonstrate that insulin-like growth factor can rescue Null+ cells but not Null cells from suspension-induced cell death. This demonstrates that phospholipase C-gamma1 is required for insulin-like growth factor dependent cell survival under these conditions. Lastly, the data demonstrate that insulinlike growth factor stimulated tyrosine phosphorylation of phospholipase C-gamma1 in both adherent and suspension cells. (+info)Fibronectin polymerization regulates the composition and stability of extracellular matrix fibrils and cell-matrix adhesions. (8/97)
Remodeling of extracellular matrices occurs during development, wound healing, and in a variety of pathological processes including atherosclerosis, ischemic injury, and angiogenesis. Thus, identifying factors that control the balance between matrix deposition and degradation during tissue remodeling is essential for understanding mechanisms that regulate a variety of normal and pathological processes. Using fibronectin-null cells, we found that fibronectin polymerization into the extracellular matrix is required for the deposition of collagen-I and thrombospondin-1 and that the maintenance of extracellular matrix fibronectin fibrils requires the continual polymerization of a fibronectin matrix. Further, integrin ligation alone is not sufficient to maintain extracellular matrix fibronectin in the absence of fibronectin deposition. Our data also demonstrate that the retention of thrombospondin-1 and collagen I into fibrillar structures within the extracellular matrix depends on an intact fibronectin matrix. An intact fibronectin matrix is also critical for maintaining the composition of cell-matrix adhesion sites; in the absence of fibronectin and fibronectin polymerization, neither alpha5beta1 integrin nor tensin localize to fibrillar cell-matrix adhesion sites. These data indicate that fibronectin polymerization is a critical regulator of extracellular matrix organization and stability. The ability of fibronectin polymerization to act as a switch that controls the organization and composition of the extracellular matrix and cell-matrix adhesion sites provides cells with a means of precisely controlling cell-extracellular matrix signaling events that regulate many aspects of cell behavior including cell proliferation, migration, and differentiation. (+info)Types of NMJ Diseases:
1. Myasthenia Gravis (MG): An autoimmune disorder that causes muscle weakness and fatigue due to the immune system attacking the NMJs.
2. Lambert-Eaton Myasthenic Syndrome (LEMS): A rare autoimmune disorder that affects the NMJ and can cause muscle weakness, fatigue, and other symptoms.
3. Congenital Myasthenic Syndromes (CMS): A group of rare genetic disorders that affect the development and function of the NMJ, leading to muscle weakness and other symptoms.
4. Neuronal Ceroid Lipofuscinosis (NCL): A group of rare genetic disorders that affect the nervous system and can cause muscle weakness, seizures, and vision loss.
5. Inflammatory Myopathies: A group of muscle disorders caused by inflammation, such as polymyositis or dermatomyositis, which can affect the NMJ and cause muscle weakness.
Symptoms of NMJ Diseases:
1. Muscle weakness or paralysis
2. Fatigue and exhaustion
3. Difficulty swallowing or breathing (in severe cases)
4. Droopy eyelids or double vision
5. Slurred speech or difficulty speaking
6. Weakness in the arms and legs
7. Muscle wasting and loss of muscle mass
8. Seizures or fits
9. Vision loss or blurred vision
10. Cramps or spasms
Diagnosis of NMJ Diseases:
1. Medical history and physical examination
2. Electromyography (EMG) to test muscle activity and strength
3. Nerve conduction studies (NCS) to test nerve function
4. Imaging tests such as MRI or CT scans to rule out other conditions
5. Blood tests to check for autoantibodies or other signs of inflammation
6. Genetic testing to diagnose inherited forms of NMJ diseases
Treatment of NMJ Diseases:
1. Medications such as steroids, immunosuppressants, and anticonvulsants to reduce inflammation and muscle weakness
2. Physical therapy to improve muscle strength and function
3. Occupational therapy to improve daily living skills
4. Speech therapy to improve communication and swallowing difficulties
5. Surgery to relieve compression or repair damaged nerves or muscles
6. Plasmapheresis (plasma exchange) to remove harmful antibodies from the blood
7. Intravenous immunoglobulin (IVIG) therapy to reduce inflammation and modulate the immune system
8. Immunoadsorption therapy to remove antibodies from the blood and restore immune balance
9. Stem cell transplantation to replace damaged cells with healthy ones
10. Gene therapy to repair genetic defects causing NMJ diseases.
It's important to note that the treatment of NMJ diseases is highly individualized and may vary depending on the specific diagnosis, severity of symptoms, and overall health of the patient. A multidisciplinary approach involving neurologists, physical therapists, occupational therapists, speech therapists, and other specialists may be necessary to provide comprehensive care.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
1. Tumor size and location: Larger tumors that have spread to nearby tissues or organs are generally considered more invasive than smaller tumors that are confined to the original site.
2. Cellular growth patterns: The way in which cancer cells grow and divide can also contribute to the overall invasiveness of a neoplasm. For example, cells that grow in a disorganized or chaotic manner may be more likely to invade surrounding tissues.
3. Mitotic index: The mitotic index is a measure of how quickly the cancer cells are dividing. A higher mitotic index is generally associated with more aggressive and invasive cancers.
4. Necrosis: Necrosis, or the death of cells, can be an indication of the level of invasiveness of a neoplasm. The presence of significant necrosis in a tumor is often a sign that the cancer has invaded surrounding tissues and organs.
5. Lymphovascular invasion: Cancer cells that have invaded lymphatic vessels or blood vessels are considered more invasive than those that have not.
6. Perineural invasion: Cancer cells that have invaded nerve fibers are also considered more invasive.
7. Histological grade: The histological grade of a neoplasm is a measure of how abnormal the cancer cells look under a microscope. Higher-grade cancers are generally considered more aggressive and invasive than lower-grade cancers.
8. Immunohistochemical markers: Certain immunohistochemical markers, such as Ki-67, can be used to evaluate the proliferative activity of cancer cells. Higher levels of these markers are generally associated with more aggressive and invasive cancers.
Overall, the degree of neoplasm invasiveness is an important factor in determining the likelihood of the cancer spreading to other parts of the body (metastasizing) and in determining the appropriate treatment strategy for the patient.
Fibrosis can occur in response to a variety of stimuli, including inflammation, infection, injury, or chronic stress. It is a natural healing process that helps to restore tissue function and structure after damage or trauma. However, excessive fibrosis can lead to the loss of tissue function and organ dysfunction.
There are many different types of fibrosis, including:
* Cardiac fibrosis: the accumulation of scar tissue in the heart muscle or walls, leading to decreased heart function and potentially life-threatening complications.
* Pulmonary fibrosis: the accumulation of scar tissue in the lungs, leading to decreased lung function and difficulty breathing.
* Hepatic fibrosis: the accumulation of scar tissue in the liver, leading to decreased liver function and potentially life-threatening complications.
* Neurofibromatosis: a genetic disorder characterized by the growth of benign tumors (neurofibromas) made up of fibrous connective tissue.
* Desmoid tumors: rare, slow-growing tumors that are made up of fibrous connective tissue and can occur in various parts of the body.
Fibrosis can be diagnosed through a variety of methods, including:
* Biopsy: the removal of a small sample of tissue for examination under a microscope.
* Imaging tests: such as X-rays, CT scans, or MRI scans to visualize the accumulation of scar tissue.
* Blood tests: to assess liver function or detect specific proteins or enzymes that are elevated in response to fibrosis.
There is currently no cure for fibrosis, but various treatments can help manage the symptoms and slow the progression of the condition. These may include:
* Medications: such as corticosteroids, immunosuppressants, or chemotherapy to reduce inflammation and slow down the growth of scar tissue.
* Lifestyle modifications: such as quitting smoking, exercising regularly, and maintaining a healthy diet to improve overall health and reduce the progression of fibrosis.
* Surgery: in some cases, surgical removal of the affected tissue or organ may be necessary.
It is important to note that fibrosis can progress over time, leading to further scarring and potentially life-threatening complications. Regular monitoring and follow-up with a healthcare professional are crucial to managing the condition and detecting any changes or progression early on.
Treatment for ureteral obstruction depends on the underlying cause and may include medications, endoscopic procedures, or surgery. In some cases, a temporary drainage catheter may be placed in the ureter to help relieve symptoms until the blockage can be fully treated.
Ureteral obstruction can be acute or chronic, and may occur in adults or children. It is important to seek medical attention if symptoms persist or worsen over time, as untreated ureteral obstruction can lead to complications such as kidney damage or sepsis.
Causes of Ureteral Obstruction:
Ureteral obstruction can be caused by a variety of factors, including:
1. Kidney stones: Small, hard mineral deposits that form in the urine and can block the flow of urine through the ureters.
2. Tumors: Cancerous or non-cancerous growths that can block the ureters.
3. Scar tissue: Scarring from previous surgeries or injuries can cause narrowing or blockages in the ureters.
4. Prostate enlargement: In men, an enlarged prostate gland can press on the urethra and ureters, causing blockages.
5. Bladder neck obstruction: A condition where the bladder neck is narrow or blocked, preventing urine from flowing through the urethra.
6. Trauma: Injuries to the ureters or bladder can cause blockages.
7. Inflammation: Inflammation in the ureters or kidneys can cause swelling and blockages.
8. Congenital conditions: Some people may be born with abnormalities that cause blockages in the urinary tract.
9. Neurological disorders: Conditions such as multiple sclerosis, Parkinson's disease, or spinal cord injuries can affect the nerves that control the bladder and ureters, leading to blockages.
10. Medications: Certain medications, such as certain antibiotics and chemotherapy drugs, can cause damage to the ureters and lead to blockages.
What's New for 2001 MeSH. NLM Technical Bulletin. Nov-Dec 2000
DeCS - Termos Novos
Budding epithelial morphogenesis driven by cell-matrix versus cell-cell adhesion - PubMed
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Extracellular matrix14
- Differences in architecture and cell-surface morphology were observed in biofilms formed by the M1- and M41-wild-type strains, accompanied by varying amounts of deposited extracellular matrix and differences in cell-to-cell junctions within each biofilm. (cdc.gov)
- Specialized areas at the CELL MEMBRANE where a cell attaches to the EXTRACELLULAR MATRIX or other substratum. (bvsalud.org)
- Matrix metalloproteinases are proteases that degrade the extracellular matrix as well as tight junctions between endothelial cells and have been implicated in … blood-brain barrier breakdown in neurodegenerative diseases. (iospress.com)
- Fibroblast cell lines carrying the T3257I mutation exhibited a reduction in both cell motility and phosphorylated focal adhesion kinase expression, suggesting a defect in the focal adhesions that link the cell cytoplasm to the extracellular matrix. (lww.com)
- These structures consist of protein complexes and induce connectivity between adjacent epithelial cells, between a cell and the extracellular matrix. (pressbooks.pub)
- Plectin is recruited into hemidesmosomes, multiprotein complexes that facilitate adhesion of epithelia to the basement membrane, thereby providing linkage between the intracellular keratin filaments to the laminins of the extracellular matrix. (embl.de)
- Plectin binds to hemidesmosomes through association of its actin-binding domain with the first pair of fibronectin type III repeats and a small part of the connecting segment of the integrin-beta4 subunit, the latter (integrin-alpha6,beta4) acting as a receptor for the extracellular matrix component laminin-5. (embl.de)
- He has researched Neuromuscular junction in several fields, including Laminin, Extracellular matrix, Molecular biology and Postsynaptic potential. (research.com)
- The study incorporates disciplines such as Laminin, Extracellular matrix and Gene isoform in addition to Agrin. (research.com)
- It's composed of endothelial cells which connected by tight junctions, and together with astrocytes, pericytes, neurons and the extracellular matrix, constitute the "neurovascular unit" that is essential for proper function of the CNS. (bgu.ac.il)
- Many of these genes are involved in signaling pathways that regulate energy metabolism, cell-growth promoting and transforming activity, modulation of the cancer microenvironment and extracellular matrix components, and cellular proliferation and differentiation. (oncotarget.com)
- Background Remodeling of the extracellular matrix (ECM) regulates cell adhesion as well as signaling between cells and their microenvironment. (zfin.org)
- This protein is found in the extracellular matrix, which is the intricate lattice of proteins and other molecules that forms in the spaces between cells. (medlineplus.gov)
- Specifically, it is found in part of the extracellular matrix called the basement membrane, which is a thin, sheet-like structure that separates and supports cells in many tissues. (medlineplus.gov)
Tight junctions2
- Some examples of the major types of cell junctions: tight junctions, gap junctions, desmosomes and hemidesmosomes. (pressbooks.pub)
- Tight junctions are transmembrane proteins fused on outer plasma membrane. (pressbooks.pub)
Endothelial cells1
- The neurovascular unit, which consists of astrocytic end-feet, neurons, pericytes, and endothelial cells, plays a key role in maintaining brain homeostasis by forming the blood-brain barrier and carefully controlling local cerebral blood flow. (iospress.com)
Adhesion6
- Importantly, force transmission through a cell required coordinated modulation of cell-matrix adhesion and actomyosin contractility in the cell and its neighbors. (elsevierpure.com)
- TGF-β1 strongly enhances the expression of the gene TGFBI that encodes a cell-adhesion class, proapoptotic ECM protein called BIGH3. (scirp.org)
- Ablation of βII spectrin in myelinating glial cells disrupted the paranodal cell adhesion complex in both peripheral and CNSs, resulting in muscle weakness and sciatic nerve conduction slowing in juvenile and middle-aged mice. (jneurosci.org)
- The plectin repeat is also seen in the cell adhesion junction plaque proteins, desmoplakin, envoplakin, and bullous pemphigoid antigen. (embl.de)
- Following RNase A treatment, we detected an upregulation of carbohydrate metabolism, inositol phosphate cascade and oxidative phosphorylation, re-arrangement of cell adhesion, cell cycle control, apoptosis, and transcription. (oncotarget.com)
- Membrane palmitoylated proteins (MPPs) are a class of cell polarity-associated proteins that function in both cell-cell junction and adhesion. (amegroups.com)
Epithelial cell3
- Applying this technology to spontaneously-forming adherent epithelial cell clusters, we found that basal force fluctuations were coupled to E-cadherin localization at the level of individual cell-cell junctions. (elsevierpure.com)
- Macrophages induced a two-fold increase in BIGH3 expression and an 86% increase in renal proximal tubule epithelial cell apoptosis. (scirp.org)
- Hemidesmosomes are similar to desmosomes in terms of function, however, they attach the epithelial cell to the basement membrane rather than to an adjacent cell. (pressbooks.pub)
Cytoplasm1
- Gap junctions connect the cytoplasm of two cells and allow for the passage of molecules freely between cells. (pressbooks.pub)
Neurons1
- They have been observed in the nucleus and cytosol of somatic cells, neurons, and germ cells and are implicated in a variety of different functions. (rupress.org)
Proteins8
- Further, the vast majority of somatic cell mutations occur in unused areas of DNA, and should not change cell behavior via altered or missing proteins. (fightaging.org)
- Covers exciting breakthroughs such as SMC motor proteins actively organizing chromosomal DNA, TOR kinases regulating metabolism, new types of immunotherapy for cancer treatment, mechanisms regulating fast axonal transport and their relation to neurodegenerative diseases, how completion of DNA replication sets the time for cells to enter mitosis, how a cascade of signals specifies the site of cell division, and newly understood pathways of normal and pathological cell death. (books-express.ro)
- Integral membrane proteins are those proteins that are a part of the cell membrane structure. (ukessays.com)
- These fibrous proteins present may span the entire length of the cell membrane. (ukessays.com)
- Some of the proteins of the cell membrane may also enter the cell. (ukessays.com)
- Furthermore, other integral proteins serve as channel proteins as well to aid in selective transport of ions in and out of the cell. (ukessays.com)
- These structures include globular proteins, which are peripherally placed and are only at times associated with the cell. (ukessays.com)
- It is concluded that dermal application of a contact allergen, as exemplified by OX and HCA, may induce cell proliferation in the neighboring lymph nodes and spleen indicative of hapten and/or haptenated proteins diffusing through the skin to periph- eral nodes and the blood to produce systemic sensitization. (cdc.gov)
Biology11
- Reader-friendly Cell Biology, 4th Edition, provides a concise but comprehensive foundation for students entering research or health care career paths. (books-express.ro)
- Knowledge of cell biology has led to new treatments for cancer, heart failure, cystic fibrosis, and many other diseases. (books-express.ro)
- His primary areas of study are Cell biology, Agrin, Neuromuscular junction, mTORC1 and Internal medicine. (research.com)
- Markus A. Rüegg interconnects Receptor and Cellular differentiation in the investigation of issues within Cell biology. (research.com)
- Markus A. Rüegg mainly focuses on Cell biology, mTORC1, mTORC2, Skeletal muscle and Internal medicine. (research.com)
- His Cell biology study incorporates themes from Receptor, Neuromuscular junction, Cellular differentiation and Downregulation and upregulation. (research.com)
- Markus A. Rüegg mainly investigates mTORC1, Cell biology, mTORC2, PI3K/AKT/mTOR pathway and Internal medicine. (research.com)
- His Cell biology research incorporates elements of Biochemistry, Cell growth and Cellular differentiation. (research.com)
- The study of cell is one of the vital parts of biology. (isrgrajan.com)
- It offers an amazing way to learn fundamental cell biology by providing study guides, flashcards and random practice tests. (isrgrajan.com)
- It is an app good for college students or anyone who already has a basic level of idea of Cell Biology. (isrgrajan.com)
Expression2
- He has included themes like Motor neuron, Gene expression, Anatomy and Agrin in his Neuromuscular junction study. (research.com)
- MPP7 expression was associated with multiple types of immune cells and correlated with the enrichment of these cells. (amegroups.com)
Tissue7
- Force transduction at cell-cell adhesions regulates tissue development, maintenance and adaptation. (elsevierpure.com)
- Daughter somatic cells resulting from mutated cells also bear these mutations, and so a pattern of differently mutated somatic cell populations spreads throughout a tissue over years and decades. (fightaging.org)
- With regard to changes that do affect cell function and then spread from stem cells into a sizable fraction of cells in a tissue, evidence is sparse when it comes to clear connections between this somatic mosaicism and specific issues in aging, however. (fightaging.org)
- Cell junctions are the contact points between plasma membrane and tissue cells. (pressbooks.pub)
- Pulp tissue was collected from permanent third molars and digested and then the cells were seeded onto plates containing HDMEM medium. (bvsalud.org)
- The cells isolated from dental pulp exhibited characteristics compatible with those expected for mesenchymal stem cells (MSCs) and are good candidates for cell therapy applications and tissue bioengineering. (bvsalud.org)
- Pulp stem cells (PSCs) are able to form ectopic dentin in vitro and in vivo and also to generate a dentine-pulp complex composed of a mineralized matrix, with dentinal tubules that are aligned and fi lled with odontoblastic prolongations, containing vascularized pulp tissue, in a similar arrangement to that observed in natural dental structures (3,6). (bvsalud.org)
Cytoskeleton3
- βII spectrin is expressed in diverse cells and is an essential part of the submembranous cytoskeleton. (jneurosci.org)
- These findings demonstrate that a spectrin-based cytoskeleton in myelinating glia contributes to formation and maintenance of paranodal junctions. (jneurosci.org)
- We found that a submembranous spectrin cytoskeleton is highly enriched at paranodes in Schwann cells. (jneurosci.org)
Receptor1
- Identification of novel driver mutations of the discoidin domain receptor 2 (DDR2) gene in squamous cell lung cancer of Chinese patients. (cdc.gov)
MEMBRANE9
- A cell is the basic unit of life, and the cell membrane is an important structure present in all cells, irrespective of whether they are plant cells or animal cells. (ukessays.com)
- Cell membrane functions include maintaining the boundaries of the cells, thus supporting the contents of the cell, maintaining proper cell to cell contact, regulating the entry and exit of molecules in and out of the cell, etc. (ukessays.com)
- Thus, to understand how the cell membrane manages to carry out this procedure, one needs to understand the cell membrane structure. (ukessays.com)
- Given below are the various components that comprise the structure of the cell membrane according to the Fluid Mosaic model. (ukessays.com)
- The first layer of cell membrane consists of a phosphid bilayer. (ukessays.com)
- Certain other elements may also be present along the length of the cell membrane, depending on the location and needs of the cell. (ukessays.com)
- These cholesterol molecules also stabilize the membrane and provide the cell with a 'cushion effect', which prevents it from suffering any major injuries due to trauma and impact forces. (ukessays.com)
- Cell membrane is the outer covering of a cell, which keep the ingredients of a cell intact. (ukessays.com)
- Desmosomes and hemidesmosomes allow for strong attachment between cells or to a basement membrane. (pressbooks.pub)
Metalloproteinase2
- Results We show that laminin polymerization indirectly promotes Fn downregulation at the MTJ, via a matrix metalloproteinase 11 (Mmp11)-dependent mechanism. (zfin.org)
- A functional polymorphism in the matrix metalloproteinase-2 gene promoter (-1306C/T) is associated with risk of development but not metastasis of gastric cardia adenocarcinoma. (cdc.gov)
Adhesions2
- These data provide insights into mechanisms that could control mechanical stress homeostasis in dynamic epithelial tissues, and highlight our methods as a resource for the study of mechanotransduction in cell-cell adhesions [corrected]. (elsevierpure.com)
- Phosphorylation of CAP was not necessary for its localization to focal adhesions and stress fibers, but Tyr326Phe substitution alters the function of CAP during cell spreading. (biomedcentral.com)
Renal cell carc2
- Metastasis is a major negative prognostic marker in clear cell renal cell carcinoma (ccRCC). (amegroups.com)
- Evidence-based recommendations on lenvatinib (Kisplyx) with pembrolizumab (Keytruda) for untreated advanced renal cell carcinoma in adults. (bvsalud.org)
Somatic cells1
- Otherwise, one must accept that near all mutations (a) affect few cells, as somatic cells are limited in their ability to replicate, and (b) occur in cells that will be destroyed on some timescale, as they hit the Hayflick limit. (fightaging.org)
Metabolism3
- Tumor development is accompanied by a variety of disorders, such as fast unlimited proliferation, resistance to tumor suppressors, loss of the initial differentiation, cell death resistance, replicative immortality, reprogramming of energy metabolism, evasion from immune surveillance, induction of angiogenesis, infiltrated growth and dissemination [ 1 ]. (oncotarget.com)
- 5-HT interacts with its receptors, which alters cell metabolism and influences several stages of organogenesis 7 . (bvsalud.org)
- Glucose measurements are used in the diagnosis and treatment of pancreatic islet cell carcinoma and of carbohydrate metabolism disorders, including diabetes mellitus, neonatal hypoglycemia, and idiopathic hypoglycemia. (cdc.gov)
Alters1
- A reduced amount of functional perlecan at the neuromuscular junction likely alters the balance of other molecules that signal when muscles should contract and when they should relax. (medlineplus.gov)
STRUCTURES1
- Major new themes in the 4th edition include the roles of intrinsically disordered polypeptides and phase separation in cellular functions, the influence of new molecular structures on understanding mechanisms, and the impact of exciting new methods¿from single cell RNA sequencing to second generation super resolution fluorescence microscopy¿on advancing our understanding. (books-express.ro)
Proliferation3
- Serotonergic neurotransmission modulates cell proliferation in several tissues, but is involved mainly in the morphogenesis of the craniofacial region 8 . (bvsalud.org)
- Extensive renovation of the epithelium, cell proliferation, apoptosis and changes in the shape and positioning of cell groups are determined by morphogenetic gradients that play critical roles during the morphogenesis of teeth 13 . (bvsalud.org)
- Cell proliferation in proper axillary and renal nodes, as well as in the spleen was also assessed. (cdc.gov)
Apoptosis1
- Even with modern therapeutic interventions, dysregulated cell signaling, changes in ECM turnover, and apoptosis promote kidney damage and end-stage renal disease, highlighting a need for a more complete understanding of the mechanisms underlying diabetic nephropathy. (scirp.org)
Morphology1
- The objective of this study is to isolate and characterize stem cells from the pulp of permanent third molars and analyze the cells obtained in terms of their morphology and chondrogenic, osteogenic and adipogenic cell differentiation. (bvsalud.org)
Metalloproteinases1
- Polymorphisms in matrix metalloproteinases 2, 3, and 8 increase recurrence and mortality risk by regulating enzyme activity in gastric adenocarcinoma. (cdc.gov)
Molecules4
- Thus, the phosphate lipid bilayer is one of the main factors responsible for regulating the entry and exit of molecules in and out of the cell. (ukessays.com)
- These molecules have important functions, as they serve as receptors for the cell. (ukessays.com)
- These kind of protein molecules act as carriers for active transport of substances in and out of the cell. (ukessays.com)
- The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. (oncotarget.com)
Molecular1
- Clear, readable explanations provide a concise story about how cells function at the molecular level. (books-express.ro)
Gene1
- which means both copies of the gene in each cell have mutations. (medlineplus.gov)
Mutations2
- Clonal hematopoiesis (CH), where hematopoietic stem and progenitor cell (HSPC) clones and their progeny expand in the circulating blood cell population, occurs following the acquisition of somatic driver mutations. (fightaging.org)
- Individuals diagnosed with clonal hematopoiesis of indeterminate potential (CHIP) carry somatic mutations in hematological malignancy-associated driver genes, historically at or above a variant allele frequency of 2%, but do not exhibit abnormal blood cell counts or any other symptoms of hematologic disease. (fightaging.org)
Cellular2
- We developed computational and experimental approaches to quantify, with both sub-cellular and multi-cellular resolution, the dynamics of force transmission in cell clusters. (elsevierpure.com)
- At the multi-cellular scale, cell-cell force exchange depended on the cell position within a cluster, and was adaptive to reconfigurations due to cell divisions or positional rearrangements. (elsevierpure.com)
Germ2
- Paternal Occupational Exposure to Heavy Metals and Welding Fumes and Testicular Germ Cell Tumours in Sons in France. (who.int)
- Parental occupational exposures in wood-related jobs and risk of testicular germ cell tumours in offspring in NORD-TEST a registry-based case-control study in Finland, Norway, and Sweden. (who.int)
Differentiation3
- To characterize pulp stem cells and evaluate their capacity for expansion and differentiation in vitro . (bvsalud.org)
- It was observed that the pulp stem cells exhibited the capacity to adhere to plastic and a high rate of expansion and, after detection with specifi c stains, it was shown that the cells were capable of differentiation into osteoblasts and chondroblasts, but not into adipocytes. (bvsalud.org)
- Stem cells are cells with a low degree of differentiation that have the capacity to reproduce and can generate differentiated cells of several different types of tissues (1). (bvsalud.org)
Adenocarcinoma2
- Genetic polymorphisms at TIMP3 are associated with survival of adenocarcinoma of the gastroesophageal junction. (cdc.gov)
- Next Evidence-based recommendations on nivolumab (Opdivo) with platinum- and fluoropyrimidine-based chemotherapy for untreated HER2-negative advanced gastric, gastro-oesophageal junction or oesophageal adenocarcinoma in adults. (bvsalud.org)
Function5
- The objective of this study was to evaluate the diagnostic biomarkers of pediatric sepsis and the function of immune cell infiltration in the development of this illness. (bvsalud.org)
- Our findings suggest that coordinated action of Src and Abl might regulate the function of CAP and reveal a functional role especially for the Src-mediated Tyr phosphorylation of CAP in cell spreading. (biomedcentral.com)
- These junctions contribute to node formation and maintenance and are essential for proper nervous system function. (jneurosci.org)
- All of these cover the structure and function of a particular cell. (isrgrajan.com)
- One such shift involves the replacement of Fibronectin (Fn)-rich matrix, which is essential for both somite and early muscle development, with laminin-rich matrix essential for normal function of the myotome. (zfin.org)
Skeletal2
- His mTORC1 research integrates issues from Sirolimus, Endocrinology, Internal medicine, Skeletal muscle and Cell growth. (research.com)
- One excellent paradigm in which to study ECM remodeling in vivo is morphogenesis of the myotendinous junction (MTJ) during zebrafish skeletal muscle development. (zfin.org)
Infiltration1
- The Tumor Immune Estimation Resource (TIMER) database was used to investigate the correlation between MPP7 and the infiltration patterns of immune cells. (amegroups.com)
Nodes1
- SIGNIFICANCE STATEMENT Myelinating glia form paranodal axoglial junctions that flank both sides of the nodes of Ranvier. (jneurosci.org)
Stem2
- Somatic mosaicism arises from random mutational damage to stem cells and progenitor cells. (fightaging.org)
- His study in mTORC2 is interdisciplinary in nature, drawing from both Regulator, Embryonic stem cell and Stem cell. (research.com)
Peripheral1
- Flanking each node, paranodal junctions (paranodes) are formed between axons and Schwann cells in the peripheral nervous system (PNS) or oligodendrocytes in the CNS. (jneurosci.org)
Lipid1
- Thus, citric acid cycle intermedi- ates are not used for adenosine triphosphate (ATP) production and are shuttled out of the mitochondria, providing precursors for nucleotide, amino acid, and lipid synthesis path- ways for the dividing cell [13]. (who.int)
Cancer2
- Taken together, our data suggest that the antitumor activity and decreased invasion potential of tumor cells caused by RNase A are associated with enhanced energy cascade functioning, rearrangement of cancer-related events regulating cell growth and dissemination, and attenuation of signaling pathways having tumor-promoting activity. (oncotarget.com)
- In the USA, obesity has recent- obesity is associated with progres- aberrations of cancer cells, summa- ly surpassed tobacco use as the sion but not incidence [9]. (who.int)
Contribute1
- Paranodal junctions contribute to both node assembly and maintenance. (jneurosci.org)
Therapeutic1
- A increasing number of studies have proved that blocking the PD-1/PD-L1 signaling pathway and restoring the immune killing inhibition of T cells can produce better therapeutic effects on tumors and chronic infectious diseases. (bvsalud.org)
Immune1
- In addition, the inflammatory and immune status of pediatric sepsis was assessed using cell-type identification by estimating relative subsets of RNA transcripts (CIBERSORT). (bvsalud.org)
Synapse1
- Within one scientific family, he focuses on topics pertaining to Postsynaptic potential under Neuromuscular junction, and may sometimes address concerns connected to Synapse. (research.com)
Acute1
- Temporal changes of the incidence of childhood B-cell precursor acute lymphoblastic leukaemia in Germany during the COVID-19 pandemic. (who.int)
Fundamental1
- It is a common fact that cells are the fundamental building blocks of life. (ukessays.com)
Signals1
- which is the area between the ends of nerve cells and muscle cells where signals are relayed to trigger muscle contraction. (medlineplus.gov)