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Cell surface receptor for SEMA4A and for class 3 semaphorins, such as SEMA3A, SEMA3C and SEMA3E. Additionally we are shipping Plexin D1 Antibodies (78) and Plexin D1 Kits (1) and many more products for this protein.
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Authors found that the PlexinD1 cleavage product binds to actin rods, pathological aggregate-like structures which had so far been described for age-related neurodegenerative diseases. Data suggest a novel disease mechanism for SMA involving formation of actin rods as a molecular sink for a cleaved PlexinD1 fragment leading to dysregulation of receptor signaling.
Measuring electrical impedance allows real-time monitoring of changes in endothelial cell morphology and adhesion induced by SEMA3E (show SEMA3E Proteins) via plexin D1
Plexin D1 plays a role in collagen contraction in human lung fibroblasts.
Findings suggest that Plexin-D1/class III semaphorin (Sema3E (show SEMA3E Proteins)) axis is triggered in systemic sclerosis (SSc (show CYP11A1 Proteins)) endothelium.
finding that PLXND1 and REV3L mutations are responsible for a proportion of MBS (show PPP1R12A Proteins) patients suggests that de novo mutations in other genes might account for other MBS (show PPP1R12A Proteins) patients
The data indicate that Plexin-D1 operates in a cell context-specific fashion, mediating different synaptogenic outcomes depending upon neuron type.
Plxnd1 is a novel regulator of VAT growth, body fat distribution, and insulin (show INS Proteins) sensitivity in both zebrafish and humans
The identification and characterization of SH3BP1 (show SH3BP1 Proteins) as a novel downstream effector of Sema3E (show SEMA3E Proteins)-PlexinD1 provides an explanation for how extracellular signals are translated into cytoskeletal changes and unique cell behavior.
It is therefore suggested that SEMA3C (show SEMA3C Proteins) signaling, propagated through the heterodimer receptor plexin-D1/neuropilin (show NRP1 Proteins), is important for truncus arteriosus septation
A critical role of Sema3E (show SEMA3E Proteins)/Plexin D1 interaction in tumor resistance to apoptosis.
GIPC1 (show GIPC1 Proteins) forms a domain-swapped dimer in an autoinhibited conformation that hinders binding of both PlexinD1 and myosin VI (show MYO6 Proteins). PlexinD1 binding to GIPC1 (show GIPC1 Proteins) releases the autoinhibition, promoting its interaction with myosin VI (show MYO6 Proteins). GIPCs and myosin VI (show MYO6 Proteins) interact through two distinct interfaces and form an open-ended alternating array.
Sema3G (show SEMA3G Proteins) induces cell collapse in an Nrp2 (show NRP2 Proteins)/PlexinD1-dependent manner.
Our results demonstrate that sema3e (show SEMA3E Proteins)/plexin D1 modulates IS formation and Ag-scanning activities of thymocytes within thymic tissues.
Sema3E (show SEMA3E Proteins)/PlexinD1 signaling controls the motogenic potential of Cajal-Retzius (CR) cells in vitro and in vivo. Absence of Sema3E (show SEMA3E Proteins)/PlexinD1 signalling increased the migratory properties of CR cells.
Sema3E (show SEMA3E Proteins)-PlexinD1 signaling is involved in the development of CNV. Stimulation of the pathway has therapeutic potential for CNV.
Proprioceptive sensory afferents that express PlexinD1 avoid forming monosynaptic connections with neurons in Sema3E (show SEMA3E Proteins)(+) motor pools yet are able to form direct connections with neurons in Sema3E (show SEMA3E Proteins)(off) motor pools.
beta1 integrin adhesion is controlled by the plexinD1-sema3E (show SEMA3E Proteins) axis in mice
Data an association between Plexin-B2 (show PLXNB2 Proteins) and Plexin-D1 with the negative regulation of IL-12 (show IL12A Proteins)/IL-23p40 in DCs.
This study demonstrated that Sema3E (show SEMA3E Proteins) and Plexin-D1 specify the degree of glutamatergic connectivity between a specific source and target in the complex circuitry of the basal ganglia.
Sema3d (show SEMA3D Proteins) regulates collective endothelial cell migration in zebrafish through two separate mechanisms. Mesenchymal Sema3d (show SEMA3D Proteins) guides outgrowth of the common cardinal (show CARD8 Proteins) vein via repulsion and signals through PlexinD1.
Somite expression of known vascular guidance cues, efnb2, sema3a2, and plexinD1 are disrupted, suggesting that the inter-somitic vessel vascular phenotype is due to disruption of these cues.
We show that proper blood vessel pathfinding requires the endothelial receptor PlexinD1 and semaphorin signals, and we identify mutations in plexinD1 in the zebrafish vascular patterning mutant out of bounds
Loss of plxnB2 (show PLXNB2 Proteins) results in delayed ISV sprouting identical to that seen in sema3e (show SEMA3A Proteins) morphants, while loss of plexinD1 in out of bounds (obd) mutants results in precocious ISV sprouting.
Cell surface receptor for SEMA4A and for class 3 semaphorins, such as SEMA3A, SEMA3C and SEMA3E. Plays an important role in cell-cell signaling, and in regulating the migration of a wide spectrum of cell types. Regulates the migration of thymocytes in the medulla. Regulates endothelial cell migration. Plays an important role in ensuring the specificity of synapse formation. Mediates anti-angiogenic signaling in response to SEMA3E. Required for normal development of the heart and vasculature.
, out of bounds
, plexin D1
, LOW QUALITY PROTEIN: plexin-D1