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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Junctional adhesion molecule 3

JAM-C, junctional adhesion molecule-C, JAM-2, JAM-B, JAM-3
Tight junctions represent one mode of cell-to-cell adhesion in epithelial or endothelial cell sheets, forming continuous seals around cells and serving as a physical barrier to prevent solutes and water from passing freely through the paracellular space. The protein encoded by this immunoglobulin superfamily gene member is localized in the tight junctions between high endothelial cells. Unlike other proteins in this family, the this protein is unable to adhere to leukocyte cell lines and only forms weak homotypic interactions. The encoded protein is a member of the junctional adhesion molecule protein family and acts as a receptor for another member of this family. A mutation in an intron of this gene is associated with hemorrhagic destruction of the brain, subependymal calcification, and congenital cataracts. Alternative splicing results in multiple transcript variants.[provided by RefSeq, Apr 2011] (from NCBI)
Top mentioned proteins: JAMA, V1a, CD11b, ZO-1, CAN
Papers on JAM-C
Effect of junctional adhesion molecule-2 expression on cell growth, invasion and migration in human colorectal cancer.
Jiang et al., Beijing, China. In Int J Oncol, Feb 2016
Aberrant expression of JAM-2 is associated with cancer progression but little work has been carried out in discovering how this affects changes in cell behaviour.
Cell type-specific bipolar cell input to ganglion cells in the mouse retina.
Haverkamp et al., Frankfurt am Main, Germany. In Neuroscience, Feb 2016
To address this question we took an anatomical approach and immunolabeled retinae of two transgenic mouse lines (GFP-O and JAM-B) with markers for ribbon synapses and type 2 bipolar cells.
Cell Adhesion Molecules and Stem Cell-Niche-Interactions in the Limbal Stem Cell Niche.
Schlötzer-Schrehardt et al., Erlangen, Germany. In Stem Cells, Jan 2016
Moreover, junctional adhesion molecule JAM-C accumulating in the subepithelial limbal matrix, appeared to be involved in recruitment of immune cells, while mesenchymal stromal cells appeared to use the nephronectin receptor integrin α8 for approaching the limbal basement membrane.
Endothelial-specific deficiency of Junctional Adhesion Molecule-C promotes vessel normalisation in proliferative retinopathy.
Chavakis et al., Dresden, Germany. In Thromb Haemost, Dec 2015
Here, we examined the function of endothelial junctional adhesion molecule-C (JAM-C) in the context of ROP.
Junctional adhesion molecule B interferes with angiogenic VEGF/VEGFR2 signaling.
Garrido-Urbani et al., Genève, Switzerland. In Faseb J, Aug 2015
Using specific anti-junctional adhesion molecule (JAM)-B antibodies and Jam-b-deficient mice, we studied the role in antiangiogenesis of JAM-B.
Loss of JAM-C leads to impaired esophageal innervations and megaesophagus in mice.
Liang et al., Shanghai, China. In Dis Esophagus, Jul 2015
In this study, we reported that junctional adhesion molecule C (JAM-C) knockout mice on a C57/B6 background developed progressive megaesophagus from embryonic day (E) 15.5 onward with complete penetrance.
Leukotriene B4-Neutrophil Elastase Axis Drives Neutrophil Reverse Transendothelial Cell Migration In Vivo.
Nourshargh et al., Genève, Switzerland. In Immunity, Jul 2015
We have previously shown that neutrophils can exhibit abluminal-to-luminal migration through EC junctions within mouse cremasteric venules and that this response is elicited following reduced expression and/or functionality of the EC junctional adhesion molecule-C (JAM-C).
Curcumin prophylaxis mitigates the incidence of hypobaric hypoxia-induced altered ion channels expression and impaired tight junction proteins integrity in rat brain.
Vijayalakshmi et al., Delhi, India. In J Neuroinflammation, 2014
Transvascular leakage, expression of transcriptional factors (nuclear factor-kappa B (NF-κB) and hypoxia inducible factor 1 alpha (Hif-1α) and also the genes regulated by these transcriptional factors, sodium potassium-adenosine triphosphatase (Na(+)/K(+)-ATPase) and endothelial sodium channel (ENaC) levels and brain tight junction (TJ) proteins like ZO-1, junctional adhesion molecule C (JAMC), claudin 4 and claudin 5 levels were determined in the brain of rats under hypoxia by Western blotting, electro mobility shift assay, ELISA, immunohistochemistry, and histopathology along with haematological parameters.
Analysis of tumour- and stroma-supplied proteolytic networks reveals a brain-metastasis-promoting role for cathepsin S.
Joyce et al., New York City, United States. In Nat Cell Biol, 2014
Cathepsin S specifically mediates blood-brain barrier transmigration through proteolytic processing of the junctional adhesion molecule, JAM-B.
JAM-related proteins in mucosal homeostasis and inflammation.
Parkos et al., Atlanta, United States. In Semin Immunopathol, 2014
JAM family encompasses three classical members (JAM-A, JAM-B, and JAM-C) and related molecules including JAM4, JAM-like protein, Coxsackie and adenovirus receptor (CAR), CAR-like membrane protein and endothelial cell-selective adhesion molecule.
A four-gene methylation marker panel as triage test in high-risk human papillomavirus positive patients.
Wisman et al., Groningen, Netherlands. In Int J Cancer, 2012
Data suggest that the four-gene methylation panel might provide an alternative triage test after primary high-risk papillomavirus (hr-HPV) testing.
JAM-C is an apical surface marker for neural stem cells.
Schwamborn et al., Münster, Germany. In Stem Cells Dev, 2012
Results indicate that in vivo JAM-C shows enrichment at the apical surface and therefore is asymmetrically distributed during cell divisions.
Schwann cell-specific JAM-C-deficient mice reveal novel expression and functions for JAM-C in peripheral nerves.
Nourshargh et al., London, United Kingdom. In Faseb J, 2012
Data indicate deletion of JAM-C in deletion of JAM-C in Schwann cells (SCs) (JAM-C SC KO) mice showed electrophysiological defects, muscular weakness, and hypersensitivity to mechanical stimuli.
JAM-B regulates maintenance of hematopoietic stem cells in the bone marrow.
Aurrand-Lions et al., Marseille, France. In Blood, 2011
JAM-B is an active player in the maintenance of the bone marrow stromal microenvironment.
The junctional adhesion molecule JAM-C regulates polarized transendothelial migration of neutrophils in vivo.
Nourshargh et al., London, United Kingdom. In Nat Immunol, 2011
Endothelial cell JAM-C has a key role in supporting luminal-to-abluminal migration of neutrophils in vivo, suggsting that reverse transepithial cell migration of neutrophils can contribute to the dissemination of systemic inflammation.
Tumour angiogenesis is reduced in the Tc1 mouse model of Down's syndrome.
Hodivala-Dilke et al., London, United Kingdom. In Nature, 2010
Examination of the genes on the segment of Hsa21 in Tc1 mice identified putative anti-angiogenic genes (ADAMTS1and ERG) and novel endothelial cell-specific genes, never previously shown to be involved in angiogenesis (JAM-B and PTTG1IP), that, when overexpressed, are responsible for inhibiting angiogenic responses to VEGF.
Molecular identification of a retinal cell type that responds to upward motion.
Sanes et al., Cambridge, United States. In Nature, 2008
JAM-B identifies a unique population of RGCs in which structure corresponds remarkably to function
Ectoplasmic specialization: a friend or a foe of spermatogenesis?
Cheng et al., New York City, United States. In Bioessays, 2007
Furthermore, JAM-C and CAR, two tight junction integral membrane proteins, are also components of apical ES involving in spermatid orientation.
Junctional adhesion molecule 1 (JAM-1).
Eckfeld et al., Newark, United States. In J Biol Regul Homeost Agents, 2003
Two proteins with structural and sequence similarities to JAM-1, named JAM-2 and JAM-3, have been identified more recently.
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