cdc42 GTP-Binding Protein, Saccharomyces cerevisiae
cdc42 GTP-Binding Protein
Adaptor Proteins, Signal Transducing
rho GTP-Binding Proteins
Gene Expression Regulation, Developmental
Caenorhabditis elegans Proteins
LIM Domain Proteins
Animals, Genetically Modified
Neural Tube Defects
Molecular Sequence Data
Intracellular Signaling Peptides and Proteins
Cell Adhesion Molecules
Amino Acid Sequence
Wnt Signaling Pathway
Protein Structure, Tertiary
Schizosaccharomyces pombe Proteins
Guanine Nucleotide Exchange Factors
Protein Kinase C
Myosin Type II
Cell Surface Extensions
Zonula Occludens-1 Protein
Green Fluorescent Proteins
Cell Cycle Proteins
Saccharomyces cerevisiae Proteins
rhoA GTP-Binding Protein
Tumor Suppressor Proteins
Recombinant Fusion Proteins
rab GTP-Binding Proteins
Two-Hybrid System Techniques
Photoreceptor Cells, Invertebrate
Kidney Diseases, Cystic
Sequence Homology, Amino Acid
Junctional Adhesion Molecules
Fluorescence Recovery After Photobleaching
Compound Eye, Arthropod
Armadillo Domain Proteins
Bicyclo Compounds, Heterocyclic
rac1 GTP-Binding Protein
Myosin Type V
rac GTP-Binding Proteins
In Situ Hybridization
Guanine Nucleotide Dissociation Inhibitors
Polycystic Kidney Diseases
Fluorescent Antibody Technique
Gene Knockdown Techniques
Vesicular Transport Proteins
Hair Cells, Auditory
Glycogen Synthase Kinase 3
Organ of Corti
rap1 GTP-Binding Proteins
Cell polarization: chemotaxis gets CRACKing. (1/6230)An early stage in the establishment of cell polarity during chemotaxis of Dictyostelium dicoideum has been identified by a recent study; the new results also show that the development of cell polarity does not rely upon cytoskeletal rearrangement, and may use a spatial sensing mechanism. (+info)
Deletion analysis of the Drosophila Inscuteable protein reveals domains for cortical localization and asymmetric localization. (2/6230)The Drosophila Inscuteable protein acts as a key regulator of asymmetric cell division during the development of the nervous system  . In neuroblasts, Inscuteable localizes into an apical cortical crescent during late interphase and most of mitosis. During mitosis, Inscuteable is required for the correct apical-basal orientation of the mitotic spindle and for the asymmetric segregation of the proteins Numb   , Prospero    and Miranda   into the basal daughter cell. When Inscuteable is ectopically expressed in epidermal cells, which normally orient their mitotic spindle parallel to the embryo surface, these cells reorient their mitotic spindle and divide perpendicularly to the surface . Like the Inscuteable protein, the inscuteable RNA is asymmetrically localized . We show here that inscuteable RNA localization is not required for Inscuteable protein localization. We found that a central 364 amino acid domain - the Inscuteable asymmetry domain - was necessary and sufficient for Inscuteable localization and function. Within this domain, a separate 100 amino acid region was required for asymmetric localization along the cortex, whereas a 158 amino acid region directed localization to the cell cortex. The same 158 amino acid fragment could localize asymmetrically when coexpressed with the full-length protein, however, and could bind to Inscuteable in vitro, suggesting that this domain may be involved in the self-association of Inscuteable in vivo. (+info)
Polarized distribution of Bcr-Abl in migrating myeloid cells and co-localization of Bcr-Abl and its target proteins. (3/6230)Bcr-Abl plays a critical role in the pathogenesis of Philadelphia chromosome-positive leukemia. Although a large number of substrates and interacting proteins of Bcr-Abl have been identified, it remains unclear whether Bcr-Abl assembles multi-protein complexes and if it does where these complexes are within cells. We have investigated the localization of Bcr-Abl in 32D myeloid cells attached to the extracellular matrix. We have found that Bcr-Abl displays a polarized distribution, colocalizing with a subset of filamentous actin at trailing portions of migrating 32D cells, and localizes on the cortical F-actin and on vesicle-like structures in resting 32D cells. Deletion of the actin binding domain of Bcr-Abl (Bcr-AbI-AD) dramatically enhances the localization of Bcr-Abl on the vesicle-like structures. These distinct localization patterns of Bcr-Abl and Bcr-Abl-AD enabled us to examine the localization of Bcr-Abl substrate and interacting proteins in relation to Bcr-Abl. We found that a subset of biochemically defined target proteins of Bcr-Abl redistributed and co-localized with Bcr-Abl on F-actin and on vesicle-like structures. The co-localization of signaling proteins with Bcr-Abl at its sites of localization supports the idea that Bcr-Abl forms a multi-protein signaling complex, while the polarized distribution and vesicle-like localization of Bcr-Abl may play a role in leukemogenesis. (+info)
Changes in basement membrane thickness in the human endometrium during the luteal phase of the menstrual cycle. (4/6230)We have examined aspects of the fine structure of the basal laminae associated with the luminal and glandular epithelium and small blood vessels in the human endometrium. Four short studies are presented and reviewed. Study 1 examined biopsies from 20 fertile women taken on days after the luteinizing hormone surge (LH): LH +2, 4, 6, 8 and 10. The basal lamina (both lamina densa and lucida) increased in thickness over the period studied. Study 2 again studied the glandular epithelium and examined the effect of RU486 (a progesterone receptor blocker) administered on day LH +3 and biopsied on day LH +6. The basal laminae were found to be the same as LH +2 control group but thinner than LH +6 control. Study 3 documented increased thickness of the basal laminae between LH +6, 8 and 13 in the luminal epithelium. The within-group coefficient of variation was 16% and 27% for LH +6 and LH +13 groups but only 2 % for LH +8. Study 4 demonstrated an increase in basal lamina thickness associated with small blood vessels between LH +6 and LH +10 in normal fertile women. The basal lamina provides the interface between epithelial and mesenchymal environments; changes in its structure can alter the phenotypic expression of the epithelia. It is one of the maternal barriers that must be transgressed by the trophoblast during implantation. Together, these combined studies provide quantitative baseline structural information on the electron microscopical appearance of the basal lamina during the luteal phase of the menstrual cycle. (+info)
Myometrial zonal differentiation and uterine junctional zone hyperplasia in the non-pregnant uterus. (5/6230)Human non-gravid myometrium differentiates in response to ovarian sex steroids into a subendometrial layer or junctional zone and an outer myometrial layer. Compared to the outer myometrial layer, the junctional zone myocytes are characterized by higher cellular density and lower cytoplasmic-nuclear ratio. These structural differences allow in-vivo visualization of the myometrial zonal anatomy by T2-weighted magnetic resonance (MR) imaging. The human myometrium is also functionally polarized. Video-vaginosonography studies have shown that propagated myometrial contractions in the non-pregnant uterus originate only from the junctional zone and that the frequency and orientation of these contraction waves are dependent on the phase of the menstrual cycle. The mechanisms underlying zonal myometrial differentiation are not known, but growing evidence suggests that ovarian hormone action may be mediated through cytokines and uterotonins locally released by the basal endometrial layer and endometrio-myometrial T-lymphocytes. Irregular thickening of the junctional zone due to inordinate proliferation of the inner myometrium, junctional zone hyperplasia, is a common MR finding in women suffering from menstrual dysfunction. Preliminary data suggest that junctional zone hyperplasia is further characterized by loss of normal inner myometrial function. Although irregular thickening of the junctional zone has been associated with diffuse uterine adenomyosis, the precise relationship between subendometrial smooth muscle proliferation and myometrial invasion by endometrial glands and stroma remains to be established. (+info)
Sodium reabsorption and distribution of Na+/K+-ATPase during postischemic injury to the renal allograft. (6/6230)BACKGROUND: A loss of proximal tubule cell polarity is thought to activate tubuloglomerular feedback, thereby contributing to glomerular filtration rate depression in postischemic acute renal failure (ARF). METHODS: We used immunomicroscopy to evaluate the segmental distribution of Na+/K+-ATPase in tubules of recipients of cadaveric renal allografts. Fractional excretion (FE) of sodium and lithium was determined simultaneously. Observations were made on two occasions: one to three hours after graft reperfusion (day 0) and again on post-transplant day 7. An inulin clearance below or above 25 ml/min on day 7 was used to divide subjects into groups with sustained (N = 15) or recovering (N = 16) ARF, respectively. RESULTS: In sustained ARF, the fractional excretion of sodium (FENa) was 40 +/- 6% and 11 +/- 5%, and the fractional excretion of lithium (FELi) was 76 +/- 5% and 70 +/- 2% on days 0 and 7, respectively. Corresponding findings in recovering ARF were 28 +/- 2% and 6 +/- 2% for the FENa and 77 +/- 4% and 55 +/- 3% (P < 0.05 vs. sustained) for FELi. Na+/K+-ATPase distribution in both groups was mainly basolateral in distal straight and convoluted tubule segments and collecting ducts. However, Na+/K+-ATPase was poorly retained in the basolateral membrane of proximal convoluted and straight tubule segments in sustained and recovering ARF on both days 0 and 7. CONCLUSIONS: We conclude that loss of proximal tubule cell polarity for Na+/K+-ATPase distribution is associated with enhanced delivery of filtered Na+ to the macula densa for seven days after allograft reperfusion. Whether an ensuing activation of tubuloglomerular feedback is an important cause of glomerular filtration rate depression in this form of ARF remains to be determined. (+info)
Coupling assembly of the E-cadherin/beta-catenin complex to efficient endoplasmic reticulum exit and basal-lateral membrane targeting of E-cadherin in polarized MDCK cells. (7/6230)The E-cadherin/catenin complex regulates Ca++-dependent cell-cell adhesion and is localized to the basal-lateral membrane of polarized epithelial cells. Little is known about mechanisms of complex assembly or intracellular trafficking, or how these processes might ultimately regulate adhesion functions of the complex at the cell surface. The cytoplasmic domain of E-cadherin contains two putative basal-lateral sorting motifs, which are homologous to sorting signals in the low density lipoprotein receptor, but an alanine scan across tyrosine residues in these motifs did not affect the fidelity of newly synthesized E-cadherin delivery to the basal-lateral membrane of MDCK cells. Nevertheless, sorting signals are located in the cytoplasmic domain since a chimeric protein (GP2CAD1), comprising the extracellular domain of GP2 (an apical membrane protein) and the transmembrane and cytoplasmic domains of E-cadherin, was efficiently and specifically delivered to the basal-lateral membrane. Systematic deletion and recombination of specific regions of the cytoplasmic domain of GP2CAD1 resulted in delivery of <10% of these newly synthesized proteins to both apical and basal-lateral membrane domains. Significantly, >90% of each mutant protein was retained in the ER. None of these mutants formed a strong interaction with beta-catenin, which normally occurs shortly after E-cadherin synthesis. In addition, a simple deletion mutation of E-cadherin that lacks beta-catenin binding is also localized intracellularly. Thus, beta-catenin binding to the whole cytoplasmic domain of E-cadherin correlates with efficient and targeted delivery of E-cadherin to the lateral plasma membrane. In this capacity, we suggest that beta-catenin acts as a chauffeur, to facilitate transport of E-cadherin out of the ER and the plasma membrane. (+info)
Identification and characterization of genes required for hyphal morphogenesis in the filamentous fungus Aspergillus nidulans. (8/6230)In the filamentous fungus Aspergillus nidulans, germination of an asexual conidiospore results in the formation of a hyphal cell. A key feature of spore germination is the switch from isotropic spore expansion to polarized apical growth. Here, temperature-sensitive mutations are used to characterize the roles of five genes (sepA, hypA, podB-podD) in the establishment and maintenance of hyphal polarity. Evidence that suggests that the hypA, podB, and sepA genes are required for multiple aspects of hyphal morphogenesis is presented. Notably, podB and sepA are needed for organization of the cytoskeleton at sites of polarized growth. In contrast, podC and podD encode proteins that appear to be specifically required for the establishment of hyphal polarity during spore germination. The role of sepA and the pod genes in controlling the spatial pattern of polarized morphogenesis in germinating spores is also described. Results obtained from these experiments indicate that the normal pattern of germ-tube emergence is dependent upon the integrity of the actin cytoskeleton. (+info)
There are several types of NTDs, including:
1. Anencephaly: A severe form of NTD where a large portion of the neural tube does not develop, resulting in the absence of a major part of the brain and skull.
2. Spina Bifida: A type of NTD where the spine does not close properly, leading to varying degrees of neurological damage and physical disability.
3. Encephalocele: A type of NTD where the brain or meninges protrude through a opening in the skull.
4. Meningomyelocele: A type of NTD where the spinal cord and meninges protrude through a opening in the back.
Causes and risk factors:
1. Genetic mutations: Some NTDs can be caused by genetic mutations that affect the development of the neural tube.
2. Environmental factors: Exposure to certain chemicals, such as folic acid deficiency, has been linked to an increased risk of NTDs.
3. Maternal health: Women with certain medical conditions, such as diabetes or obesity, are at a higher risk of having a child with NTDs.
Symptoms and diagnosis:
1. Anencephaly: Severely underdeveloped brain, absence of skull, and often death shortly after birth.
2. Spina Bifida: Difficulty walking, weakness or paralysis in the legs, bladder and bowel problems, and intellectual disability.
3. Encephalocele: Protrusion of brain or meninges through a opening in the skull, which can cause developmental delays, seizures, and intellectual disability.
4. Meningomyelocele: Protrusion of spinal cord and meninges through a opening in the back, which can cause weakness or paralysis in the legs, bladder and bowel problems, and intellectual disability.
Treatment and management:
1. Surgery: Depending on the type and severity of the NTD, surgery may be necessary to close the opening in the skull or back, or to release compressed tissue.
2. Physical therapy: To help improve mobility and strength in affected limbs.
3. Occupational therapy: To help with daily activities and fine motor skills.
4. Speech therapy: To help with communication and language development.
5. Medications: To manage seizures, pain, and other symptoms.
6. Nutritional support: To ensure adequate nutrition and growth.
7. Supportive care: To help manage the physical and emotional challenges of living with an NTD.
1. Folic acid supplements: Taking a daily folic acid supplement during pregnancy can help prevent NTDs.
2. Good nutrition: Eating a balanced diet that includes foods rich in folate, such as leafy greens, citrus fruits, and beans, can help prevent NTDs.
3. Avoiding alcohol and tobacco: Both alcohol and tobacco use have been linked to an increased risk of NTDs.
4. Getting regular prenatal care: Regular check-ups with a healthcare provider during pregnancy can help identify potential problems early on and reduce the risk of NTDs.
5. Avoiding infections: Infections such as rubella (German measles) can increase the risk of NTDs, so it's important to avoid exposure to these infections during pregnancy.
It's important to note that not all NTDs can be prevented, and some may be caused by genetic factors or other causes that are not yet fully understood. However, taking steps to maintain good health and getting regular prenatal care can help reduce the risk of NTDs and improve outcomes for babies born with these conditions.
There are several types of kidney diseases that are classified as cystic, including:
1. Autosomal dominant polycystic kidney disease (ADPKD): This is the most common form of cystic kidney disease and is caused by a genetic mutation. It is characterized by the growth of numerous cysts in both kidneys, which can lead to kidney damage and failure.
2. Autosomal recessive polycystic kidney disease (ARPKD): This is a rare form of cystic kidney disease that is also caused by a genetic mutation. It is characterized by the growth of numerous cysts in both kidneys, as well as other organs such as the liver and pancreas.
3. Cystinosis: This is a rare genetic disorder that causes the accumulation of cystine crystals in the kidneys and other organs. It can lead to the formation of cysts and damage to the kidneys.
4. Medullary cystic kidney disease (MCKD): This is a rare genetic disorder that affects the medulla, the innermost layer of the kidney. It is characterized by the growth of cysts in the medulla, which can lead to kidney damage and failure.
5. Other rare forms of cystic kidney disease: There are several other rare forms of cystic kidney disease that can be caused by genetic mutations or other factors. These include hereditary cystic papillary necrosis, familial juvenile nephropathy, and others.
The symptoms of kidney diseases, cystic can vary depending on the specific type of disease and the severity of the condition. Common symptoms include:
* High blood pressure
* Proteinuria (excess protein in the urine)
* Hematuria (blood in the urine)
* Decreased kidney function
* Abdominal pain
* Weight loss
* Swelling in the legs and ankles
If you suspect that you or your child may have a cystic kidney disease, it is important to seek medical attention as soon as possible. A healthcare provider can perform a physical examination, take a medical history, and order diagnostic tests such as urinalysis, blood tests, and imaging studies (such as ultrasound or CT scans) to determine the cause of the symptoms.
Treatment for cystic kidney disease will depend on the specific type of disease and the severity of the condition. Treatment options may include:
* Medications to control high blood pressure and proteinuria
* Medications to slow the progression of kidney damage
* Dialysis or kidney transplantation in advanced cases
* Cyst aspiration or surgical removal of cysts in some cases
It is important to note that there is no cure for cystic kidney disease, and the best treatment approach is to slow the progression of the disease and manage its symptoms. Early detection and aggressive management can help improve quality of life and delay the need for dialysis or transplantation.
In addition to medical treatment, there are some lifestyle modifications that may be helpful in managing cystic kidney disease. These include:
* Maintaining a healthy diet with low salt and protein intake
* Staying hydrated by drinking plenty of water
* Engaging in regular physical activity
* Avoiding harmful substances such as tobacco and alcohol
* Monitoring blood pressure and weight regularly
It is important to note that cystic kidney disease can be a serious condition, and it is important to work closely with a healthcare provider to manage the disease and slow its progression. With appropriate treatment and lifestyle modifications, many people with cystic kidney disease are able to lead active and fulfilling lives.
There are two main types of PKD: autosomal dominant polycystic kidney disease (ADPKD) and autosomal recessive polycystic kidney disease (ARPKD). ADPKD is the most common form of PKD and accounts for about 90% of all cases. It is caused by mutations in the PKD1 or PKD2 genes, which are inherited from one's parents. ARPKD is less common and is caused by mutations in the PKHD1 gene.
The symptoms of PKD can vary depending on the severity of the disease and the age of onset. Common symptoms include high blood pressure, back pain, kidney stones, urinary tract infections, and frequent urination. As the cysts grow, they can also cause complications such as kidney damage, anemia, and electrolyte imbalances.
PKD is typically diagnosed through a combination of imaging tests such as ultrasound, CT scans, and MRI, as well as genetic testing to identify the presence of the disease-causing mutations. There is no cure for PKD, but treatment options are available to manage the symptoms and slow the progression of the disease. These may include medications to control high blood pressure, pain management, and dialysis in advanced cases.
In conclusion, polycystic kidney disease (PKD) is a genetic disorder that affects the kidneys and can lead to chronic kidney disease and eventually kidney failure. It is important to be aware of the symptoms and risk factors for PKD, as well as to seek medical attention if they are present, in order to receive proper diagnosis and treatment.
Prickle planar cell polarity protein 2
Wd repeat containing planar cell polarity effector
Segment polarity gene
David G. Drubin
Symmetry breaking and cortical rotation
List of Vanderbilt University people
Madin-Darby canine kidney cells
Primordial germ cell migration
Collapsin response mediator protein family
Anomalous photovoltaic effect
Lisa L. Cunningham
AmotL2 disrupts apical-basal cell polarity and promotes tumour invasion | Nature Communications
WIF-B cells: an in vitro model for studies of hepatocyte polarity. | Journal of Cell Biology | Rockefeller University Press
Analysis of spontaneous emergence of cell polarity with delayed negative feedback - CityU Scholars | A Research Hub of...
Hello world! - Rho-kinase regulate the cell Polarity
Guiding self-organized pattern formation in cell polarity establishment
T cell receptor reversed polarity recognition of a self-antigen major histocompatibility complex. | Nat Immunol;16(11): 1153...
Cell polarity in the protist-to-animal transition - Institut Pasteur
STAT1-induced ASPP2 transcription identifies a link between neuroinflammation, cell polarity, and tumor suppression - Ludwig...
Loss of Endothelium-Derived Wnt5a Is Associated With Reduced Pericyte Recruitment and Small Vessel Loss in Pulmonary Arterial...
A Density-Dependent Switch Drives Stochastic Clustering and Polarization of Signaling Molecules | PLOS Computational Biology
Human Parainfluenza Viruses (HPIV) and Other Parainfluenza Viruses: Background, Pathophysiology, Etiology
MedlinePlus: Genes: C
Human Parainfluenza Viruses (HPIV) and Other Parainfluenza Viruses: Background, Pathophysiology, Etiology
Cold Spring Harbor Lab Press Developmental Biology
Cold Spring Harbor Lab Press Developmental Biology
Replication and Shedding of MERS-CoV in Upper Respiratory Tract of Inoculated Dromedary Camels - Volume 20, Number 12-December...
2018 Cellular and Molecular Fungal Biology Conference GRC
Rubén G. Contreras | IntechOpen
Vauthey Research Group - Group Members
Combined Deletion of Vhl and Kif3a Accelerates Renal Cyst Fo... : Journal of the American Society of Nephrology
Vascular plant - New World Encyclopedia
Chiral cell sliding drives left-right asymmetric organ twisting | eLife
Local Wnt signalling in the asymmetric migrating vertebrate cells | Lékařská fakulta Masarykovy univerzity | MED MUNI
SOLVED: Ge 900 MHz cordless phone set on rotary dialing - Fixya
Chromosome 6 - wikidoc
NAVBO Newsletter - Don't Miss Today's Journal Club
Table of Contents - February 22, 2017, 37 (8) | Journal of Neuroscience
24/365 solar cell output theory and experiments
Microorganisms | Free Full-Text | Preclinical Evidence for the Role of Botulinum Neurotoxin A (BoNT/A) in the Treatment of...
Planar cell polarity pa2
- We have shown that activation of the Wnt/planar cell polarity pathway is required for pericyte recruitment, but whether production and release of specific Wnt ligands by PMVECs are responsible for Wnt/planar cell polarity activation in pericytes is unknown. (nih.gov)
- Wnt signalling is known to generate cellular asymmetry via Wnt/planar cell polarity pathway (Wnt/PCP). (muni.cz)
- Four apical PM proteins were concentrated in the BC membrane of WIF-B cells. (rupress.org)
- We quantified the strength of two feedback systems that operate during polarity establishment, feedback between polarity proteins and the actomyosin cortex, and mutual antagonism amongst polarity proteins. (figshare.com)
- By coupling a mass-conserved Turing-like reaction-diffusion system for polarity proteins to an active gel description of the actomyosin cortex, we reveal a transition point beyond which feedback ensures self-organized polarization even when cues are removed. (figshare.com)
- Finally, the bulk of "polarity proteins" as well as specialized adhesion complexes evolved in the metazoan stem-line, in concert with the newly evolved intercellular junctional belts. (archives-ouvertes.fr)
- After treatment with epidermal growth factor or ouabain, epithelial dog kidney MDCK cells undergo a drastic remodeling that includes changes in the transcription, translation, localization, and degradation of cell junction proteins. (intechopen.com)
- Wnt/PCP acts locally (i) to orient membrane polarity and asymmetric establishment of intercellular junctions via conserved set of PCP proteins most specifically represented by Vangl and Prickle, and (ii) to asymmetrically rearrange cytoskeletal structures via downstream effectors of Dishevelled (Dvl). (muni.cz)
- The human leukocyte antigen lies on chromosome 6, with the exception of the gene for β2-microglobulin (which is located on chromosome 15 ), and encodes cell-surface antigen -presenting proteins among other functions. (wikidoc.org)
- Polarized cells must direct proteins from the Golgi apparatus to the appropriate domain since tight junctions prevent proteins from diffusing between the two domains. (bvsalud.org)
- The formation of three-dimensional (3D) epithelial structures in organs such as the breast, prostate and colon is dependent on the establishment of cell polarity. (nature.com)
- Epithelial cells display a marked apico-basal polarity, which is highly conserved across the animal kingdom, both in terms of morphology and of molecular regulators. (archives-ouvertes.fr)
- Although the last eukaryotic common ancestor almost certainly possessed a simple form of apico-basal polarity (marked by the presence of one or several flagella at a single cellular pole), comparative genomics and evolutionary cell biology reveal that the polarity regulators of animal epithelial cells have a surprisingly complex and stepwise evolutionary history. (archives-ouvertes.fr)
- We suggest that the "polarity network" that polarized animal epithelial cells evolved by integration of initially independent cellular modules that evolved at distinct steps of our evolutionary ancestry. (archives-ouvertes.fr)
- Epithelial cells develop tight junctions (TJs) and cell polarity. (intechopen.com)
- Using live-imaging analysis and a three-dimensional vertex model, we identified 'cell sliding,' a novel mechanism driving epithelial morphogenesis, in which cells directionally change their position relative to their subjacent (posterior) neighbors by sliding in one direction. (elifesciences.org)
- In Drosophila embryonic hindgut, an initial left-right (LR) asymmetry of the cell shape (cell chirality in three dimensions), which occurs intrinsically before tissue deformation, is converted through LR asymmetric cell sliding into a directional axial twisting of the epithelial tube. (elifesciences.org)
- Cell sliding may also be involved in other cases of LR-polarized epithelial morphogenesis. (elifesciences.org)
- This process is best described on stable phenotypes of epithelial cells. (muni.cz)
- The ability of glomerular epithelial cells, podocytes, to form foot processes with unique intercellular slit diaphragms (SD) reflects a special organization with possible direct consequences for glomerular filtration. (lww.com)
- c-Fos/hypoxia-induced p60 AmotL2 interacts with the Crb3 and Par3 polarity complexes retaining them in large vesicles and preventing them from reaching the apical membrane. (nature.com)
- The establishment and the maintenance of apical-basal cell polarity and eventually the depolarization of a cell is a complex process controlled by a set of core protein complexes. (nature.com)
- The ternary complexes revealed a 180° polarity reversal compared to all other TCR- peptide -MHC complex structures. (bvsalud.org)
- With the recent molecular findings, the podocyte is emerging as a key cell type involved in glomerular damage, but protein complexes involved remain poorly understood. (lww.com)
- Currently, either conventional cancer therapies or modern immunotherapies are non-tumor-targeted therapeutic approaches that cannot accurately distinguish malignant cells from healthy ones, giving rise to multiple undesired side effects. (bvsalud.org)
- Recent advances in nanotechnology, accompanied by our growing understanding of cancer biology and nano-bio interactions, have led to the development of a series of nanocarriers, which aim to improve the therapeutic efficacy while reducing off-target toxicity of the encapsulated anticancer agents through tumor tissue-, cell-, or organelle-specific targeting. (bvsalud.org)
- This Review outlines current and prospective strategies in the design of tumor tissue-, cell-, and organelle-targeted cancer nanomedicines, and highlights the latest progress in hierarchical targeting technologies that can dynamically integrate these three different stages of static tumor targeting to maximize therapeutic outcomes. (bvsalud.org)
- These data provide a molecular mechanism how hypoxic stress deregulates cell polarity during tumour progression. (nature.com)
- Patterns in cells and tissues however often do not form spontaneously, but are under control of upstream pathways that provide molecular guiding cues. (figshare.com)
- Previous studies have shown that hydrophobicity, polarity, molecular volume and hydrogen bonding capability of chemicals are among the most important characteristics to be used for predicting permeability. (cdc.gov)
- A signature feature of the animal kingdom is the presence of epithelia: sheets of polarized cells that both insulate the organism from its environment and mediate interactions with it. (archives-ouvertes.fr)
- EGF is regarded as the main protector against injuries in epithelia, and ouabain is a hormone that regulates blood pressure, natriuresis, cell survival, and cell adhesion. (intechopen.com)
- Here, however, we review the activity of Wnt signalling in migratory cells which experience the extensive rearrangements of cytoskeleton and consequently dynamic asymmetry, making the localised effects of Wnt signalling easier to distinguish. (muni.cz)
- Department of Cell Biology and Anatomy, Johns Hopkins School of Medicine, Baltimore, Maryland 21205. (rupress.org)
- Reduced pericyte coverage of pulmonary microvessels is a pathological feature of PAH and is caused partly by the inability of pericytes to respond to signaling cues from neighboring pulmonary microvascular endothelial cells (PMVECs). (nih.gov)
- Despite extensive knowledge regarding the formation and maintenance of polarity, the mechanisms that deregulate polarity in metastasizing cells remain to be fully characterized. (nature.com)
- Due to its known involvement in the synaptic organization, maintenance of cell shape and polarity in nerve cells, together with its demonstrated interactions with α-actinin-4, densin may share the same functions in podocytes by associating with the nephrin interacting protein complex at the slit diaphragm. (lww.com)
- Central to adaptive immunity is the interaction between the αß T cell receptor (TCR) and peptide presented by the major histocompatibility complex (MHC) molecule. (bvsalud.org)
- We report the structures of two TCRs, derived from human induced T regulatory (iT(reg)) cells , complexed to an MHC class II molecule presenting a proinsulin -derived peptide . (bvsalud.org)
- This type of chemical derivatization results in loss of ionic charge and reduced polarity making each mercury species molecule volatile so that it can escape the liquid phase and accumulate in the gaseous phase ("headspace") directly above the sample. (cdc.gov)
- The resulting loss of polarity potentiates the response to invasive cues in vitro and in vivo in mice. (nature.com)
- Through the Turing stability analysis, we identify the parameter conditions, including the range of the time delay constant, for achieving cell polarization without any inhomogeneous spatial cues. (edu.hk)
- The virus was propagated in Vero E6 cells cultured in Dulbecco modified Eagle medium (Invitrogen, Carlsbad, CA, USA) supplemented with 2% fetal bovine serum, 2 mmol/L glutamine, 50 U/mL penicillin, and 50 μg/mL streptomycin. (cdc.gov)
- Fetal damage occurs through destruction of cells, as well as disruption of cell division. (cdc.gov)
- which may render the genetic mate doses of NDMA is the kidney, but a Transplacental carcinogenesis rial of fetal cells highly accessible to much lower incidence of tumours is stu dies with ENU in nonhuman pri carcinogens. (who.int)
- Cell polarity is often lost in advanced tumours correlating with acquisition of invasive and malignant properties. (nature.com)
- Thus TCRs are not 'hardwired' to interact with MHC molecules in a stereotypic manner to elicit a T cell signal, a finding that fundamentally challenges our understanding of TCR recognition. (bvsalud.org)
- Recent studies proposed that delayed negative feedback may be important for maintaining the robustness of cell polarization and the observed oscillating behavior of signaling cluster. (edu.hk)
- The results suggest that a previously unidentified type of cell behavior called 'cell sliding' is responsible for twisting the hindgut. (elifesciences.org)
- T cell receptor reversed polarity recognition of a self-antigen major histocompatibility complex. (bvsalud.org)
- Then, we reviewed the role of Wnt signalling in models of mesenchymal migration including neural crest, melanoma, and breast cancer cells. (muni.cz)
- Digenic variants of planar cell polarity genes in human neural tube defect patients. (cdc.gov)
- Rare copy number variations of planar cell polarity genes are associated with human neural tube defects. (cdc.gov)
- We further show that hypoxic stress results in activation of c-Fos-dependent expression of AmotL2 leading to loss of polarity. (nature.com)
- Cell polarity refers to spatial differences in the shape and structure of cells, which leads to the generation of diverse cell types playing different roles in biological processes. (edu.hk)
- During twisting, the cells in the hindgut also change shape. (elifesciences.org)
- It was not known how this shape change and other behaviors of the cells cause the hindgut to twist. (elifesciences.org)
- Sliding is triggered by the cells in the hindgut taking on a more symmetrical shape. (elifesciences.org)
- Cell sliding may prove to be a common way to shape organs, many of which feature non-symmetrical twisted tubes of cells. (elifesciences.org)
- In a Drosophila inversion mutant showing inverted cell chirality and hindgut rotation, cell sliding occurs in the opposite direction to that in wild-type. (elifesciences.org)
- The evolution of this vascular tissue allowed for an early dominance of these plants on land (first appearing 430 million years ago, during the Silurian period), giving them the ability to transport water and dissolved minerals through specialized strands of elongated cells that run from the plant root to the tips of the leaves . (newworldencyclopedia.org)
- In the future, learning how to control cell sliding could help researchers to create organs and biological structures in the laboratory that could be used in organ transplants and regenerative medicine. (elifesciences.org)
- Initially, the hindgut is a simple tube of cells. (elifesciences.org)
- Is the Subject Area "Cell membranes" applicable to this article? (plos.org)
- In this paper, we formulate the cell polarization system as a non-local reaction diffusion equation with positive and delayed negative feedback loops. (edu.hk)
- Liu, Y & Lo, W-C 2019, ' Analysis of spontaneous emergence of cell polarity with delayed negative feedback ', Mathematical Biosciences and Engineering , vol. 16, no. 3, pp. 1392-1413. (edu.hk)
- Early vascular plants only developed by primary growth , in which the plants grew through cell division of the plant body. (newworldencyclopedia.org)
- Secondary growth developed early (the Devonian period, 380 million years ago) in the evolution of vascular plants, which allowed for cell division to take place in the active regions of the plant's periphery. (newworldencyclopedia.org)
- Many organs arise from simple sheets and tubes of cells. (elifesciences.org)
- The viruses attach to the host cells through hemagglutinin, which specifically combines with neuraminic acid receptors in the host cells. (medscape.com)
- Nous avons examiné 132 agents de santé à la recherche d'ADN du virus de l'hépatite B (VHB) au moyen de l'amplification en chaîne par polymérase (PCR) nichée et de l'anticorps du virus de l'hépatite C (anti-VHC) par la méthode ELISA. (who.int)