Rat Anti-JAM3 Recombinant Antibody (19H36) (CBMAB-0072-WJ)

junctional adhesion molecule 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. Diseases associated with JAM3 include Hemorrhagic Destruction Of The Brain, Subependymal Calcification, And Cataracts and Pseudo-Torch Syndrome 1. Among its related pathways are Response to elevated platelet cytosolic Ca2+ and Blood-Brain Barrier and Immune Cell Transmigration: VCAM-1/CD106 Signaling Pathways. An important paralog of this gene is JAM2.

JAM3; junctional adhesion molecule 3; junctional adhesion molecule C; JAM C; JAMC; JAM-2; JAM-3; JAM-C; FLJ14529

Junctional adhesion protein that mediates heterotypic cell-cell interactions with its cognate receptor JAM2 to regulate different cellular processes (PubMed:11590146, PubMed:11823489).
Plays a role in homing and mobilization of hematopoietic stem and progenitor cells within the bone marrow. At the surface of bone marrow stromal cells, it contributes to the retention of the hematopoietic stem and progenitor cells expressing JAM3 (PubMed:11590146, PubMed:24357068).
Plays a central role in leukocytes extravasation by facilitating transmigration through the endothelium (By similarity).
Plays a role in spermatogenesis where JAM2 and JAM3, which are respectively expressed by Sertoli and germ cells, mediate an interaction between both cell types and play an essential role in the anchorage of germ cells onto Sertoli cells and the assembly of cell polarity complexes during spermatid differentiation (By similarity).
Also functions as a counter-receptor for ITGAM, mediating leukocyte-platelet interactions and is involved in the regulation of transepithelial migration of polymorphonuclear neutrophils (PMN) (PubMed:12208882, PubMed:15194813).
Plays a role in angiogenesis (PubMed:23255084).
Plays a role in the regulation of cell migration (Probable). During myogenesis, it is involved in myocyte fusion (By similarity).
Soluble form of JAM-C
Promotes chemotaxis of vascular endothelial cells and stimulates angiogenesis.

Adaptive immune responseIEA:Ensembl
Adherens junction assemblyManual Assertion Based On ExperimentIMP:ARUK-UCL
AngiogenesisManual Assertion Based On ExperimentIDA:UniProtKB
Apical protein localizationManual Assertion Based On ExperimentIMP:ARUK-UCL
Cell-cell adhesionManual Assertion Based On ExperimentIDA:ARUK-UCL
Cell-matrix adhesionIEA:Ensembl
Establishment of cell polarityIEA:Ensembl
Granulocyte migrationManual Assertion Based On ExperimentIMP:ARUK-UCL
Hematopoietic stem cell migration to bone marrowManual Assertion Based On ExperimentIMP:UniProtKB
Heterotypic cell-cell adhesionManual Assertion Based On ExperimentIDA:ARUK-UCL
Leukocyte migration involved in inflammatory responseIEA:Ensembl
Maintenance of blood-brain barrier1 PublicationNAS:ARUK-UCL
MyelinationIEA:Ensembl
Myeloid progenitor cell differentiationIEA:Ensembl
Negative regulation of cell adhesion mediated by integrinManual Assertion Based On ExperimentIMP:ARUK-UCL
Negative regulation of integrin activationManual Assertion Based On ExperimentIMP:ARUK-UCL
Neutrophil homeostasisIEA:Ensembl
Positive regulation of cellular extravasationManual Assertion Based On ExperimentIMP:ARUK-UCL
Positive regulation of membrane permeabilityManual Assertion Based On ExperimentIMP:ARUK-UCL
Protein localization to cell junctionManual Assertion Based On ExperimentIMP:ARUK-UCL
Protein localization to cell surfaceManual Assertion Based On ExperimentIMP:ARUK-UCL
Regulation of actin cytoskeleton organization by cell-cell adhesionIEA:Ensembl
Regulation of neutrophil chemotaxisManual Assertion Based On ExperimentIDA:UniProtKB
Spermatid developmentIEA:Ensembl
Transmission of nerve impulseIEA:Ensembl

Cell membrane; Cell junction; Cell junction, desmosome; Cell junction, tight junction. Detected in the acrosome region in developing spermatids (By similarity).
In epithelial cells, it is expressed at desmosomes but not at tight junctions (PubMed:15194813).
Localizes at the cell surface of endothelial cells; treatment of endothelial cells with vascular endothelial growth factor stimulates recruitment of JAM3 to cell-cell contacts (PubMed:15994945).
Soluble form of JAM-C: Secreted

Hemorrhagic destruction of the brain with subependymal calcification and cataracts (HDBSCC):
A syndrome characterized by congenital cataracts and severe brain abnormalities apparently resulting from hemorrhagic destruction of the brain parenchyma, including the cerebral white matter and basal ganglia. Patients manifest profound developmental delay, and other neurologic features included seizures, spasticity, and hyperreflexia. The clinical course is very severe resulting in death in infancy. Brain imaging shows multifocal intraparenchymal hemorrhage with associated liquefaction and massive cystic degeneration, and calcification in the subependymal region and in brain tissue.

Extracellular: 32-241
Helical: 242-262
Cytoplasmic: 263-310

Proteolytically cleaved from endothelial cells surface into a soluble form by ADAM10 and ADAM17; the release of soluble JAM3 is increased by proinflammatory factors.
S-palmitoylated by ZDHHC7. S-palmitoylation promotes expression at tight junctions.