Zonula Occludens-1 Protein
Zonula Occludens-2 Protein
Cell Membrane Permeability
Loop of Henle
Gene Knockdown Techniques
Gene Expression Regulation, Developmental
Fluorescent Antibody Technique, Indirect
Tissue Array Analysis
Reverse Transcriptase Polymerase Chain Reaction
Molecular Sequence Data
Kidney Tubules, Distal
Gene Expression Regulation
Carcinoma, Pancreatic Ductal
Tumor Markers, Biological
Gene Expression Profiling
Amino Acid Sequence
Fluorescent Antibody Technique
Carcinoma, Lewis Lung
Gene Expression Regulation, Neoplastic
Real-Time Polymerase Chain Reaction
Oligonucleotide Array Sequence Analysis
Cell Adhesion Molecules
Recombinant Fusion Proteins
RNA, Small Interfering
Kidney Function Tests
Ca(2+)-independent cell-adhesion activity of claudins, a family of integral membrane proteins localized at tight junctions. (1/114)In multicellular organisms, various compositionally distinct fluid compartments are established by epithelial and endothelial cellular sheets. For these cells to function as barriers, tight junctions (TJs) are considered to create a primary barrier for the diffusion of solutes through the paracellular pathway   . In ultrathin sections viewed under electron microscopy, TJs appear as a series of apparent fusions, involving the outer leaflets of plasma membranes of adjacent cells, to form the so-called kissing points of TJs, where the intercellular space is completely obliterated . Claudins are a family of 16 proteins whose members have been identified as major integral membrane proteins localized exclusively at TJs    . It remains unclear, however, whether claudins have the cell-adhesion activity that would explain the unusual intercellular adhesion at TJs. Using mouse L-fibroblast transfectants expressing various amounts of claudin-1, -2 or -3, we found that these claudins possess Ca(2+)-independent cell-adhesion activity. Using ultrathin-section electron microscopy, we observed many kissing points of TJs between adjacent transfectants. Furthermore, the cell-adhesion activity of occludin, another integral membrane protein localized at TJs   , was negligible when compared with that of claudins. Thus, claudins are responsible for TJ-specific obliteration of the intercellular space. (+info)
Clostridium perfringens enterotoxin fragment removes specific claudins from tight junction strands: Evidence for direct involvement of claudins in tight junction barrier. (2/114)Claudins, comprising a multigene family, constitute tight junction (TJ) strands. Clostridium perfringens enterotoxin (CPE), a single approximately 35-kD polypeptide, was reported to specifically bind to claudin-3/RVP1 and claudin-4/CPE-R at its COOH-terminal half. We examined the effects of the COOH-terminal half fragment of CPE (C-CPE) on TJs in L transfectants expressing claudin-1 to -4 (C1L to C4L, respectively), and in MDCK I cells expressing claudin-1 and -4. C-CPE bound to claudin-3 and -4 with high affinity, but not to claudin-1 or -2. In the presence of C-CPE, reconstituted TJ strands in C3L cells gradually disintegrated and disappeared from their cell surface. In MDCK I cells incubated with C-CPE, claudin-4 was selectively removed from TJs with its concomitant degradation. At 4 h after incubation with C-CPE, TJ strands were disintegrated, and the number of TJ strands and the complexity of their network were markedly decreased. In good agreement with the time course of these morphological changes, the TJ barrier (TER and paracellular flux) of MDCK I cells was downregulated by C-CPE in a dose-dependent manner. These findings provided evidence for the direct involvement of claudins in the barrier functions of TJs. (+info)
Manner of interaction of heterogeneous claudin species within and between tight junction strands. (3/114)In tight junctions (TJs), TJ strands are associated laterally with those of adjacent cells to form paired strands to eliminate the extracellular space. Claudin-1 and -2, integral membrane proteins of TJs, reconstitute paired TJ strands when transfected into L fibroblasts. Claudins comprise a multigene family and more than two distinct claudins are coexpressed in single cells, raising the questions of whether heterogeneous claudins form heteromeric TJ strands and whether claudins interact between each of the paired strands in a heterophilic manner. To answer these questions, we cotransfected two of claudin-1, -2, and -3 into L cells, and detected their coconcentration at cell-cell borders as elaborate networks. Immunoreplica EM confirmed that distinct claudins were coincorporated into individual TJ strands. Next, two L transfectants singly expressing claudin-1, -2, or -3 were cocultured and we found that claudin-3 strands laterally associated with claudin-1 and -2 strands to form paired strands, whereas claudin-1 strands did not interact with claudin-2 strands. We concluded that distinct species of claudins can interact within and between TJ strands, except in some combinations. This mode of assembly of claudins could increase the diversity of the structure and functions of TJ strands. (+info)
Clostridium perfringens enterotoxin binds to the second extracellular loop of claudin-3, a tight junction integral membrane protein. (4/114)Claudins (claudin-1 to -18) with four transmembrane domains and two extracellular loops constitute tight junction strands. The peptide toxin Clostridium perfringens enterotoxin (CPE) has been shown to bind to claudin-3 and -4, but not to claudin-1 or -2. We constructed claudin-1/claudin-3 chimeric molecules and found that the second extracellular loop of claudin-3 conferred CPE sensitivity on L fibroblasts. Furthermore, overlay analyses revealed that the second extracellular loop of claudin-3 specifically bound to CPE at the K(a) value of 1.0x10(8) M(-1). We concluded that the second extracellular loop is the site through which claudin-3 interacts with CPE on the cell surface. (+info)
Claudin promotes activation of pro-matrix metalloproteinase-2 mediated by membrane-type matrix metalloproteinases. (5/114)Genes associated with regulation of membrane-type matrix metalloproteinase-1 (MT1-MMP)-mediated pro-MMP-2 processing were screened in 293T cells by a newly developed expression cloning method. One of the gene products, which promoted processing of pro-MMP-2 by MT1-MMP was claudin-5, a major component of endothelial tight junctions. Expression of claudin-5 not only replaced TIMP-2 in pro-MMP-2 activation by MT1-MMP but also promoted activation of pro-MMP-2 mediated by all MT-MMPs and MT1-MMP mutants lacking the transmembrane domain (DeltaMT1-MMP). A carboxyl-terminal deletion mutant of pro-MMP-2 (proDeltaMMP-2) was processed to an intermediate form by MT1-MMP in 293T cells and was further converted to an activated form by introduction of claudin-5. In contrast to the stimulatory effect of TIMP-2 on pro-MMP-2 activation by MT1-MMP, activation of pro-MMP-2 by DeltaMT1-MMP in the presence of claudin-5 and proDeltaMMP-2 processing by MT1-MMP were both inversely repressed by expression of exogenous TIMP-2. These results suggest that TIMP-2 is not involved in cluadin-5-induced pro-MMP-2 activation by MT-MMPs. Stimulation of MT-MMP-mediated pro-MMP-2 activation was also observed with other claudin family members, claudin-1, claudin-2, and claudin-3. Amino acid substitutions or deletions in ectodomain of claudin-1 abolished stimulatory effect. Direct interaction of claudin-1 with MT1-MMP and MMP-2 was demonstrated by immunoprecipitation analysis. MT1-MMP was co-localized with claudin-1 not only at cell-cell borders, but also at other parts of the cells. TIMP-2 enhanced cell surface localization of MMP-2 mediated by MT1-MMP, and claudin-1 also stimulated it. These results suggest that claudin recruits all MT-MMPs and pro-MMP-2 on the cell surface to achieve elevated focal concentrations and, consequently, enhances activation of pro-MMP-2. (+info)
Expression of Clostridium perfringens enterotoxin receptors claudin-3 and claudin-4 in prostate cancer epithelium. (6/114)The mRNA for Rvp.1 (rat ventral prostate) increases in abundance before gland involution after androgen deprivation. Rvp.1 is homologous to CPE-R, the high-affinity intestinal epithelial receptor for Clostridium perfringens enterotoxin (CPE), and is sufficient to mediate CPE binding and trigger subsequent toxin-mediated cytolysis. Rvp.1 (claudin-3) and CPE-R (claudin-4) are members of a larger family of transmembrane tissue-specific claudin proteins that are essential components of intercellular tight junction structures regulating paracellular ion flux. However, claudin-3 and claudin-4 are the only family members capable of mediating CPE binding and cytolysis. The present study was designed to study the expression of claudin-3 and claudin-4 in human prostate tissue as potential targets for CPE toxin-mediated therapy for prostate cancer. On human multiple-tissue Northern blot analysis, mRNAs for both claudin-3 and claudin-4 were expressed at high levels in prostate tissue. In normal prostate tissue, expression of claudin-3 was localized exclusively within acinar epithelial cells by in situ mRNA hybridization. Compared with expression within prostate epithelial cells in surrounding normal glandular tissue, expression of claudin-3 mRNA remained high in the epithelium of prostate adenocarcinoma (10 of 10) and prostatic intraepithelial neoplasia (five of five). Prostate adenocarcinoma cells metastatic to bone were obtained from a patient with disease progression during antiandrogen therapy. These metastatic cells were prostate-specific antigen-positive by immunohistochemical staining and also expressed functional CPE receptors as measured by sensitivity to CPE-induced cell lysis. The persistent high level of claudin-3 expression in prostate adenocarcinoma and functional cytotoxicity of CPE in metastatic androgen-independent prostate adenocarcinoma suggests a new potential therapeutic strategy for prostate cancer. (+info)
The renal segmental distribution of claudins changes with development. (7/114)BACKGROUND: Permeability properties of mammalian nephron are tuned during postnatal maturation. The transepithelial electrical resistance (TER) and complexity of tight junctions (TJs) vary along the different tubular segments, suggesting that the molecules constituting this structure change. We studied the differential expression of occludin and several claudins in isolated renal tubules from newborn and adult rabbits. METHODS: Isolated renal tubules from newborn and adult rabbits were processed for occludin, claudin-1 and claudin-2 immunofluorescence, and Western blot detection of claudin-1 and -2. Claudin-5 was detected in whole kidney frozen sections. RT-PCR from isolated tubules was performed for claudins-1 to -8. RESULTS: Immunofluorescence revealed that occludin, claudin-1 and -2 were present at the cell boundaries at the neonatal stage of development. Claudin-1 was detected in the tighter segments of the nephron (distal and collecting duct), while claudin-2 was found in the leaky portions (proximal). Claudin 5 was found in the kidney vasculature. PCR amplification revealed the presence of claudins-1 to -4 in tubules of newborns. In adults, claudins-1, -2 and -4 were present in proximal, Henle's loop and collecting segments; claudin-3 was in proximal and collecting tubules, while claudins-5 and -6 were absent from all tubular portions. Claudin-7 was restricted to proximal tubules, while claudin-8 was present in proximal and Henle's segments. CONCLUSIONS: The pattern of occludin distribution is present from the neonatal age. Claudins-7 and -8 are up-regulated after birth. Each tubular segment expresses a peculiar set of claudins that might be responsible for the permeability properties of their TJs. (+info)
Claudin localization in cilia of the retinal pigment epithelium. (8/114)Using immunocytochemistry and confocal microscopy we demonstrate that claudin-immunoreactivity is a novel marker for retinal pigment epithelial cilia. Claudin-immunoreactivity obtained by polyclonal anti-claudin 1 antibody, which could crossreact with claudin 3, was colocalized with acetylated tubulin-immunoreactivity in cultured human retinal pigment epithelial cells. Claudin-immunoreactivity associated with the retinal pigment epithelium (RPE) cilia was more intense than was claudin-immunoreactivity in the junctional complex. Approximately two-thirds of the RPE cells in the rat contain cilia that are immunoreactive with acetylated tubulin on postnatal day 1, and a significant portion of these cilia label with the anti-claudin 1 antibody. Cilia decrease in frequency over subsequent postnatal days, and are absent by postnatal day 30. As RPE cilia decrease in number during postnatal rat development, claudin-immunoreactivity is lost earlier than acetylated tubulin, suggesting that the loss of claudin may initiate RPE cilium degeneration. Claudin-immunoreactivity was not evident in cilia of photoreceptor cells, epithelia of nasal mucosa, small intestine, or colon, suggesting that claudin may be a unique molecule in RPE cilia. These data suggest that cilia of the RPE, unlike cilia on other cell types, contain claudin, and that this molecule may play an important and specific role in the function and/or maintenance of RPE cilia. (+info)
Treatment for hypercalciuria typically involves addressing the underlying cause of the condition. In some cases, this may involve medication to lower calcium levels or surgery to remove any kidney stones or tumors that may be contributing to the condition. It is important for individuals with hypercalciuria to work closely with their healthcare provider to develop a personalized treatment plan and monitor their calcium levels regularly.
If you suspect you may have hypercalciuria, it is important to speak with your healthcare provider as soon as possible. They can perform tests to confirm the diagnosis and recommend appropriate treatment. With proper treatment, it is possible to manage hypercalciuria and prevent any complications.
The main symptoms of Gitelman syndrome include:
* Muscle weakness and paralysis that can be triggered by changes in potassium levels, stress, or certain medications
* Muscle cramps and twitching
* Fatigue and malaise
* Abnormal heart rhythms (arrhythmias)
* Low blood pressure
Gitelman syndrome can be diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment typically involves managing symptoms with medications such as potassium supplements, salt substitutes, and medications to regulate heart rhythm and blood pressure. In some cases, a gluten-free diet may be recommended.
Gitelman syndrome is an autosomal recessive disorder, meaning that an individual must inherit two copies of the mutated gene (one from each parent) to develop the condition. The prevalence of Gitelman syndrome is estimated to be around 1 in 20,000 to 1 in 40,000 individuals worldwide.
Overall, Gitelman syndrome is a rare and complex disorder that requires careful management by a multidisciplinary team of healthcare professionals. With appropriate treatment and lifestyle modifications, individuals with Gitelman syndrome can lead relatively normal lives.
Symptoms of nephrocalcinosis may include nausea, vomiting, abdominal pain, frequent urination, and blood in the urine. Diagnosis is typically made through imaging tests such as X-rays, CT scans, or ultrasound, and blood tests to determine calcium levels and kidney function.
Treatment for nephrocalcinosis depends on the underlying cause of the condition and may include medications to lower calcium levels, dietary changes to reduce calcium intake, and in severe cases, dialysis or kidney transplantation may be necessary. It is important to seek medical attention if symptoms persist or worsen over time, as early detection and treatment can help prevent long-term damage to the kidneys.
Examples and Observations:
Oxyphil adenomas are rare in the small bowel (less than 1% of all small intestinal tumors) but are more common in the duodenum and proximal jejunum. They usually manifest as multiple, submucosal nodules that can vary in size from a few millimeters to several centimeters in diameter. 
The presence of oxyphil adenomas in the stomach is rare (less than 1% of all gastric tumors) and most often occurs as multiple, small, submucosal nodules. However, larger adenomas may also be present. 
Synonyms: oxyphil cell adenoma; oxyphil cell tumor; oxyphil polyp. 
* Oxyphil adenomas are often associated with familial adenomatous polyposis (FAP) and Turcot syndrome. 
 Dorland's Medical Dictionary for Health Care Professionals. © 2008 Saunders, an imprint of Elsevier Inc. All rights reserved. Used with permission.
 Oxyphil Adenoma. The Merck Manual of Diagnosis and Therapy, Professional Edition. © 2015 Merck Sharp & Dohme Corp., a subsidiary of Merck & Co., Inc. All rights reserved. Used with permission.
 Oxyphil Adenoma. Gastrointestinal Tumors: benign and malignant tumors of the digestive system, including colorectal cancer, stomach cancer, pancreatic cancer, liver cancer, biliary tract cancer, and soft tissue sarcomas. © 2015 Springer International Publishing Switzerland. All rights reserved. Used with permission.
There are three main types of hearing loss: conductive, sensorineural, and mixed. Conductive hearing loss occurs when there is a problem with the middle ear and its ability to transmit sound waves to the inner ear. Sensorineural hearing loss occurs when there is damage to the inner ear or the auditory nerve, which can lead to permanent hearing loss. Mixed hearing loss is a combination of conductive and sensorineural hearing loss.
Symptoms of hearing loss may include difficulty hearing speech, especially in noisy environments, muffled or distorted sound, ringing or buzzing in the ears (tinnitus), and difficulty hearing high-pitched sounds. If you suspect you have hearing loss, it is important to seek medical advice as soon as possible, as early treatment can help improve communication and quality of life.
Hearing loss is diagnosed through a series of tests, including an audiometric test, which measures the softest sounds that can be heard at different frequencies. Treatment options for hearing loss include hearing aids, cochlear implants, and other assistive devices, as well as counseling and support to help manage the condition and improve communication skills.
Overall, hearing loss is a common condition that can have a significant impact on daily life. If you suspect you or someone you know may be experiencing hearing loss, it is important to seek medical advice as soon as possible to address any underlying issues and improve communication and quality of life.
The carcinogenesis process of PDAC usually starts with the accumulation of genetic mutations in the pancreatic duct cells, which progressively leads to the formation of a premalignant lesion called PanIN (pancreatic intraepithelial neoplasia). Over time, these lesions can develop into invasive adenocarcinoma, which is PDAC.
The main risk factor for developing PDAC is smoking, but other factors such as obesity, diabetes, and family history of pancreatic cancer also contribute to the development of the disease. Symptoms of PDAC are often non-specific and late-stage, which makes early diagnosis challenging.
The treatment options for PDAC are limited, and the prognosis is generally poor. Surgery is the only potentially curative treatment, but only a small percentage of patients are eligible for surgical resection due to the locally advanced nature of the disease at the time of diagnosis. Chemotherapy, radiation therapy, and targeted therapies are used to palliate symptoms and improve survival in non-surgical cases.
PDAC is an aggressive and lethal cancer, and there is a need for better diagnostic tools and more effective treatment strategies to improve patient outcomes.
The tumor cells are typically small, uniform, and well-differentiated, with a distinct cell border and a central nucleus. The tumor cells are often arranged in a glandular or tubular pattern, which is characteristic of this type of cancer.
Carcinoma, Lewis lung usually affects older adults, with the median age at diagnosis being around 60 years. Men are slightly more likely to be affected than women. The main risk factor for developing this type of cancer is smoking, although it can also occur in people who have never smoked.
The symptoms of Carcinoma, Lewis lung can vary depending on the location and size of the tumor, but they may include:
* Chest pain or discomfort
* Coughing up blood
* Shortness of breath
* Weight loss
If you suspect you may have Carcinoma, Lewis lung or are experiencing any of these symptoms, it is important to consult a healthcare professional for an accurate diagnosis and appropriate treatment.
The post Definition of 'Carcinoma, Lewis Lung' in the medical field appeared first on Healthy Life Tips.
There are different types of Breast Neoplasms such as:
1. Fibroadenomas: These are benign tumors that are made up of glandular and fibrous tissues. They are usually small and round, with a smooth surface, and can be moved easily under the skin.
2. Cysts: These are fluid-filled sacs that can develop in both breast tissue and milk ducts. They are usually benign and can disappear on their own or be drained surgically.
3. Ductal Carcinoma In Situ (DCIS): This is a precancerous condition where abnormal cells grow inside the milk ducts. If left untreated, it can progress to invasive breast cancer.
4. Invasive Ductal Carcinoma (IDC): This is the most common type of breast cancer and starts in the milk ducts but grows out of them and invades surrounding tissue.
5. Invasive Lobular Carcinoma (ILC): It originates in the milk-producing glands (lobules) and grows out of them, invading nearby tissue.
Breast Neoplasms can cause various symptoms such as a lump or thickening in the breast or underarm area, skin changes like redness or dimpling, change in size or shape of one or both breasts, discharge from the nipple, and changes in the texture or color of the skin.
Treatment options for Breast Neoplasms may include surgery such as lumpectomy, mastectomy, or breast-conserving surgery, radiation therapy which uses high-energy beams to kill cancer cells, chemotherapy using drugs to kill cancer cells, targeted therapy which uses drugs or other substances to identify and attack cancer cells while minimizing harm to normal cells, hormone therapy, immunotherapy, and clinical trials.
It is important to note that not all Breast Neoplasms are cancerous; some are benign (non-cancerous) tumors that do not spread or grow.
Pancreatic adenocarcinoma is the most common type of malignant pancreatic neoplasm and accounts for approximately 85% of all pancreatic cancers. It originates in the glandular tissue of the pancreas and has a poor prognosis, with a five-year survival rate of less than 10%.
Pancreatic neuroendocrine tumors (PNETs) are less common but more treatable than pancreatic adenocarcinoma. These tumors originate in the hormone-producing cells of the pancreas and can produce excess hormones that cause a variety of symptoms, such as diabetes or high blood sugar. PNETs are classified into two main types: functional and non-functional. Functional PNETs produce excess hormones and are more aggressive than non-functional tumors.
Other rare types of pancreatic neoplasms include acinar cell carcinoma, ampullary cancer, and oncocytic pancreatic neuroendocrine tumors. These tumors are less common than pancreatic adenocarcinoma and PNETs but can be equally aggressive and difficult to treat.
The symptoms of pancreatic neoplasms vary depending on the type and location of the tumor, but they often include abdominal pain, weight loss, jaundice, and fatigue. Diagnosis is typically made through a combination of imaging tests such as CT scans, endoscopic ultrasound, and biopsy. Treatment options for pancreatic neoplasms depend on the type and stage of the tumor but may include surgery, chemotherapy, radiation therapy, or a combination of these.
Prognosis for patients with pancreatic neoplasms is generally poor, especially for those with advanced stages of disease. However, early detection and treatment can improve survival rates. Research into the causes and mechanisms of pancreatic neoplasms is ongoing, with a focus on developing new and more effective treatments for these devastating diseases.
Transverse aeolian ridges
List of possible impact structures on Earth
Neonatal ichthyosis-sclerosing cholangitis syndrome
Rubielos de la Cérida impact structure
Medullary thymic epithelial cells
Cortical thymic epithelial cells
Blood-Spinal Cord Barrier
The Stalinist Legacy
Breast cancer classification
Protein inhibitor of activated STAT
Arnaud de Cervole
Microbial symbiosis and immunity
The effect of AAV-mediated downregulation of Claudin-3 on the development of mouse retinal vasculature. | Exp Eye Res;213:...
Interaction between Epithelial Sodium Channel γ-Subunit and Claudin-8 Modulates Paracellular Sodium Permeability in Renal...
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- Lipopolysaccharide (LPS), one of the most important inflammatory factors will downregulate specific TJ proteins including Occludin and Claudin-1 and impair integrity of the epithelial barrier. (biomedcentral.com)
- Immunofluorescent quantification and/or RT-qPCR showed that DEP exposure increases claudin-3, occludin, zona occludens (ZO)-1, matrix metalloproteinase (MMP)-9, and toll-like receptor (TLR)-4, and decreases tumor necrosis factor (TNF)-α and interleukin (IL)-10 expression compared to CON. (nih.gov)
- In conclusion, our research demonstrated that betaine attenuated LPS-induced downregulation of Occludin and Claudin-1 and restored the intestinal barrier function. (biomedcentral.com)
- The protein levels of Claudin-3 , VEGF-A and B cell lymphoma 2 (Bcl-2) were evaluated by Western blot at P7, P10 and P14. (bvsalud.org)
- The immunofluorescent images consistently revealed that LPS induced the disruption of TJ protein Claudin-1 and reduced its expression while betaine could reverse these alterations. (biomedcentral.com)
- A ubiquitously-expressed claudin subtype that acts as a general barrier-forming protein in TIGHT JUNCTIONS . (nih.gov)
- Description: Claudin-18 is a protein that in humans is encoded by the CLDN18 gene. (resourcerecovery.be)
- The effect of AAV-mediated downregulation of Claudin-3 on the development of mouse retinal vasculature. (bvsalud.org)
- The AAV-mediated downregulation of Claudin-3 at P3 impeded the development of retinal deep vascularization of P10 mouse , but without effect on the development of the retinal superficial plexus. (bvsalud.org)
- These results suggested that the downregulation of Claudin-3 induced RGC apoptosis and impeded the mouse retinal vascular development by downregulating the levels of VEGF-A and Bcl-2. (bvsalud.org)
- Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Human Claudin 18 (CLDN18) in tissue homogenates, cell lysates and other biological fluids. (resourcerecovery.be)
- Description: Enzyme-linked immunosorbent assay based on the Double-antibody Sandwich method for detection of Human Claudin 18 (CLDN18) in samples from tissue homogenates, cell lysates and other biological fluids with no significant corss-reactivity with analogues from other species. (resourcerecovery.be)
- 14(3): 291-296, 2023 Mar 09. (bvsalud.org)
- Immunofluorescent staining was performed to detect the expression and localization of Claudin-3 in the mouse retina . (bvsalud.org)
- Intravitreal injection of a recombinant adeno-associated virus (AAV) expressing a short hairpin RNA targeting Claudin-3 mRNA was performed to down-regulate Claudin-3 expression in retina in neonatal (Postnatal Day 3, P3) C57BL/6J mice . (bvsalud.org)
- Claudin-3 knockdown increased RGC apoptosis and reduced the expression of VEGF-A and Bcl-2 in the retinas. (bvsalud.org)
- Elevated expression of claudin-3 is found in a variety of tumor cell types, suggesting its role as a therapeutic target for specific ANTINEOPLASTIC AGENTS . (nih.gov)
- Differential Claudin 3 and EGFR Expression Predicts BRCA1 Mutation in Triple-Negative Breast Cancer. (cdc.gov)
- Association of Cytokeratin 5 and Claudin 3 expression with BRCA1 and BRCA2 germline mutations in women with early breast cancer. (cdc.gov)
- However, we and others have shown that many common epithelial neoplasms can be easily analyzed by FC [ 3,4,5,6 ]. (karger.com)
- Epub 2020 Apr 3. (nih.gov)
- Description: A competitive ELISA for quantitative measurement of Human Claudin 18(CLDN18) in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. (resourcerecovery.be)
- Claudin-3 has been found to be required for the normal development of the neural retina and its vessels in zebrafish in our recent study. (bvsalud.org)
- Brain metastases have been found to occur in 10-16% of surviving individuals with advanced BC and as high as 30% in autopsy series [ 3 ]. (hindawi.com)
- CAR-T cell therapy (Kymriah), approved by the Food and Drug Administration (FDA) to treat B-cell acute lymphoblastic leukemia (ALL) in 2017, was the world's first approved CAR-T product ( 3 ). (spandidos-publications.com)
- A simple 3-color flow cytometric panel can provide a high sensitivity and specificity compared to cytomorphology. (karger.com)
- To investigate whether transcellular sodium transport controls tight-junction composition and paracellular permeability via modulating expression of the transmembrane protein claudin-8, we used cultured mouse cortical collecting duct cells to see how overexpression or silencing of epithelial sodium channel (ENaC) subunits and claudin-8 affect paracellular permeability. (nih.gov)
- 3. Indomethacin induces increase in gastric epithelial tight junction permeability via redistribution of occludin and activation of p38 MAPK in MKN-28 Cells. (nih.gov)
- 4. Oxidative stress induces gastric epithelial permeability through claudin-3. (nih.gov)
- 15. Extracellular Mg(2+) regulates the tight junctional localization of claudin-16 mediated by ERK-dependent phosphorylation. (nih.gov)
- Recent evidence suggests that certain alternate growth factor pathways, such as fibroblast growth factor receptor 1, HER1, phosphoinositide-3-kinase catalytic alpha polypeptide, and Src, may contribute to the higher proliferation and poorer prognosis of the luminal B subtype. (medscape.com)
- Caspase 3 activation occasionally involved olfactory nerve bundles that synapse in the olfactory bulb (OB). (cdc.gov)
- Flavoring s-related lung disease is a potentially disabling disease of food industry workers associated with exposure to the a-diketone butter flavoring , diacetyl (2,3-butanedione). (cdc.gov)
- To investigate delayed toxicity, additional rats inhaled 318 (range, 317.9-318.9) ppm 2,3- pentanedione for 6 hours and were sacrificed 0 to 2, 12 to 14, or 18 to 20 hours after exposure. (cdc.gov)
- The hormone receptor-negative subtypes comprise the HER2-enriched, claudin-low, and basal-like subtypes. (medscape.com)
- Understanding of the pathogenesis of human cate in a physiologically relevant 3-dimensional (3-D), organoid model of human small intestinal epithelium. (cdc.gov)
- We present cultured in the RWV bioreactors, with the rotation speed the results of our first attempts to infect a physiologically adjusted to maintain the cell aggregates in suspension dur- relevant 3-D small intestinal epithelium model (INT-407) ing the entire culture duration (18-20 rotations/min ini- with genogroup I and II human noroviruses. (cdc.gov)
- We show that noroviruses can infect and replicate in a 3-dimensional (3-D), organoid model of human small intestinal epithelium. (cdc.gov)
- We present the results of our first attempts to infect a physiologically relevant 3-D small intestinal epithelium model (INT-407) with genogroup I and II human noroviruses. (cdc.gov)
- Representative models of differentiated human intes- transmission are ingestion of contaminated food and water tinal epithelium can be established by growing cells in 3 and person-to-person contact ( 5 ). (cdc.gov)
- Cells grown on porous collage-coated beads under fluid shear conditions in rotating wall vessel bioreactors differentiate into 3-D architectures resembling both the morphologic and physiologic function of in vivo tissues. (cdc.gov)
- Representative models of differentiated human intestinal epithelium can be established by growing cells in 3 dimensions (3-D) on collagen-I-coated porous microcarrier beads in rotating-wall vessel (RWV) bioreactors that model the physiologic fluid-shear environment in their respective organs ( 21 - 24 ). (cdc.gov)