N-cadherin Monoclonal Antibody (3B9) - Citations

N-cadherin Monoclonal Antibody (3B9) - Citations

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Citations & References
Abstract
rpS6 regulates blood-testis barrier dynamics through Akt-mediated effects on MMP-9.
AuthorsMok KW, Mruk DD, Cheng CY,
Journal
PubMed ID25217631
'Mammalian target of rapamycin complex 1 (mTORC1) is an emerging regulator of blood-tissue barriers that utilizes ribosomal protein S6 (rpS6) as the downstream signaling molecule. To explore the role of rpS6 in blood-testis barrier (BTB) function, a constitutively active quadruple rpS6 phosphomimetic mutant was constructed in mammalian expression vector and ... More
Blood-testis barrier dynamics are regulated by testosterone and cytokines via their differential effects on the kinetics of protein endocytosis and recycling in Sertoli cells.
AuthorsYan HH, Mruk DD, Lee WM, Cheng CY,
JournalFASEB J
PubMed ID18192323
During spermatogenesis in the mammalian testis, preleptotene/leptotene spermatocytes differentiate from type B spermatogonia and traverse the blood-testis barrier (BTB) at stage VIII of the seminiferous epithelial cycle for further development. This timely movement of germ cells involves extensive junction restructuring at the BTB. Previous studies have shown that these events ... More
Monoclonal antibody targeting of N-cadherin inhibits prostate cancer growth, metastasis and castration resistance.
AuthorsTanaka H, Kono E, Tran CP, Miyazaki H, Yamashiro J, Shimomura T, Fazli L, Wada R, Huang J, Vessella RL, An J, Horvath S, Gleave M, Rettig MB, Wainberg ZA, Reiter RE,
JournalNat Med
PubMed ID21057494
The transition from androgen-dependent to castration-resistant prostate cancer (CRPC) is a lethal event of uncertain molecular etiology. Comparing gene expression in isogenic androgen-dependent and CRPC xenografts, we found a reproducible increase in N-cadherin expression, which was also elevated in primary and metastatic tumors of individuals with CRPC. Ectopic expression of ... More
Gene expression in thyroid autonomous adenomas provides insight into their physiopathology.
AuthorsWattel S, Mircescu H, Venet D, Burniat A, Franc B, Frank S, Andry G, Van Sande J, Rocmans P, Dumont JE, Detours V, Maenhaut C,
JournalOncogene
PubMed ID16027733
The purpose of this study was to use the microarray technology to define expression profiles characteristic of thyroid autonomous adenomas and relate these findings to physiological mechanisms. Experiments were performed on a series of separated adenomas and their normal counterparts on Micromax cDNA microarrays covering 2400 genes (analysis I), and ... More
N-cadherin acts upstream of VE-cadherin in controlling vascular morphogenesis.
AuthorsLuo Y, Radice GL,
JournalJ Cell Biol
PubMed ID15809310
Endothelial cells express two classic cadherins, VE-cadherin and N-cadherin. The importance of VE-cadherin in vascular development is well known; however, the function of N-cadherin in endothelial cells remains poorly understood. Contrary to previous studies, we found that N-cadherin localizes to endothelial cell-cell junctions in addition to its well-known diffusive membrane ... More
The differential expression of N-cadherin and E-cadherin distinguishes pleural mesotheliomas from lung adenocarcinomas.
AuthorsPeralta Soler A, Knudsen KA, Jaurand MC, Johnson KR, Wheelock MJ, Klein-Szanto AJ, Salazar H,
JournalHum Pathol
PubMed ID8522310
Malignant mesotheliomas are highly aggressive tumors that develop most frequently in the pleura of patients chronically exposed to asbestos. The distinction between malignant mesotheliomas and tumors of epithelial origin, particularly peripheral lung adenocarcinoma, can be difficult despite the use of immunocytochemical markers and other diagnostic tools. During embryonic development the ... More
VEGF-mediated angiogenesis links EMT-induced cancer stemness to tumor initiation.
AuthorsFantozzi A, Gruber DC, Pisarsky L, Heck C, Kunita A, Yilmaz M, Meyer-Schaller N, Cornille K, Hopfer U, Bentires-Alj M, Christofori G,
Journal
PubMed ID24413534
An epithelial-mesenchymal transition (EMT) underlies malignant tumor progression and metastatic spread by enabling cancer cells to depart from the primary tumor, invade surrounding tissue, and disseminate to distant organs. EMT also enriches for cancer stem cells (CSC) and increases the capacity of cancer cells to initiate and propagate tumors upon ... More
Loss of Cadherin-Binding Proteins ß-Catenin and Plakoglobin in the Heart Leads to Gap Junction Remodeling and Arrhythmogenesis.
AuthorsSwope D, Cheng L, Gao E, Li J, Radice GL,
JournalMol Cell Biol
PubMed ID22252313
Arrhythmic right ventricular cardiomyopathy (ARVC) is a hereditary heart muscle disease that causes sudden cardiac death (SCD) in young people. Almost half of ARVC patients have a mutation in genes encoding cell adhesion proteins of the desmosome, including plakoglobin (JUP). We previously reported that cardiac tissue-specific plakoglobin (PG) knockout (PG ... More
Cadherin-11 contributes to pulmonary fibrosis: potential role in TGF-ß production and epithelial to mesenchymal transition.
AuthorsSchneider DJ, Wu M, Le TT, Cho SH, Brenner MB, Blackburn MR, Agarwal SK,
JournalFASEB J
PubMed ID21990376
Pulmonary fibrosis, characterized by excess deposition of extracellular matrix by myofibroblasts, is a serious component of chronic lung diseases. Cadherin-11 (CDH11) is increased in wound healing and fibrotic skin. We hypothesized that CDH11 is increased in pulmonary fibrosis and contributes its development. CDH11 expression was assessed in lung tissue from ... More
Connexin43 associated with an N-cadherin-containing multiprotein complex is required for gap junction formation in NIH3T3 cells.
AuthorsWei CJ, Francis R, Xu X, Lo CW,
JournalJ Biol Chem
PubMed ID15741167
Previous studies have indicated an intimate linkage between gap junction and adherens junction formation. It was suggested this could reflect the close membrane-membrane apposition required for junction formation. In NIH3T3 cells, we observed the colocalization of connexin43 (Cx43alpha1) gap junction protein with N-cadherin, p120, and other N-cadherin-associated proteins at regions ... More
Temporal and spatial localization of nectin-1 and l-afadin during synaptogenesis in hippocampal neurons.
AuthorsLim ST, Lim KC, Giuliano RE, Federoff HJ
JournalJ Comp Neurol
PubMed ID18181141
Nectins are cell adhesion molecules that, together with the intracellular binding partner afadin, mediate adhesion and signaling at a variety of intercellular junctions. In this work we studied the distribution of nectin-1 and afadin during hippocampal synapse formation using cultured primary hippocampal neurons. Nectin-1 and afadin cluster at developing synapses ... More