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Cell surface receptor for SEMA4A and for class 3 semaphorins, such as SEMA3A, SEMA3C and SEMA3E. Zusätzlich bieten wir Ihnen Plexin D1 Antikörper (72) und Plexin D1 Kits (1) und viele weitere Produktgruppen zu diesem Protein an.
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Measuring electrical impedance allows real-time monitoring of changes in endothelial cell morphology and adhesion induced by SEMA3E (zeige SEMA3E Proteine) via plexin D1
Plexin D1 plays a role in collagen contraction in human lung fibroblasts.
Findings suggest that Plexin-D1/class III semaphorin (Sema3E (zeige SEMA3E Proteine)) axis is triggered in systemic sclerosis (SSc (zeige CYP11A1 Proteine)) endothelium.
finding that PLXND1 and REV3L mutations are responsible for a proportion of MBS (zeige PPP1R12A Proteine) patients suggests that de novo mutations in other genes might account for other MBS (zeige PPP1R12A Proteine) 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 (zeige INS Proteine) sensitivity in both zebrafish and humans
The identification and characterization of SH3BP1 (zeige SH3BP1 Proteine) as a novel downstream effector of Sema3E (zeige SEMA3E Proteine)-PlexinD1 provides an explanation for how extracellular signals are translated into cytoskeletal changes and unique cell behavior.
It is therefore suggested that SEMA3C (zeige SEMA3C Proteine) signaling, propagated through the heterodimer receptor plexin-D1/neuropilin (zeige NRP1 Proteine), is important for truncus arteriosus septation
A critical role of Sema3E (zeige SEMA3E Proteine)/Plexin D1 interaction in tumor resistance to apoptosis.
Strong expression of plexD1 was detected in endothelial cells of cervical cancer samples, yet no expression was seen in endothelial cells of normal cervical tissues, which suggests a potential role of PlexD1 in cervical cancer-associated angiogenesis
GIPC1 (zeige GIPC1 Proteine) forms a domain-swapped dimer in an autoinhibited conformation that hinders binding of both PlexinD1 and myosin VI (zeige MYO6 Proteine). PlexinD1 binding to GIPC1 (zeige GIPC1 Proteine) releases the autoinhibition, promoting its interaction with myosin VI (zeige MYO6 Proteine). GIPCs and myosin VI (zeige MYO6 Proteine) interact through two distinct interfaces and form an open-ended alternating array.
Sema3G (zeige SEMA3G Proteine) induces cell collapse in an Nrp2 (zeige NRP2 Proteine)/PlexinD1-dependent manner.
Our results demonstrate that sema3e (zeige SEMA3E Proteine)/plexin D1 modulates IS formation and Ag-scanning activities of thymocytes within thymic tissues.
Sema3E (zeige SEMA3E Proteine)/PlexinD1 signaling controls the motogenic potential of Cajal-Retzius (CR) cells in vitro and in vivo. Absence of Sema3E (zeige SEMA3E Proteine)/PlexinD1 signalling increased the migratory properties of CR cells.
Sema3E (zeige SEMA3E Proteine)-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 (zeige SEMA3E Proteine)(+) motor pools yet are able to form direct connections with neurons in Sema3E (zeige SEMA3E Proteine)(off) motor pools.
beta1 integrin adhesion is controlled by the plexinD1-sema3E (zeige SEMA3E Proteine) axis in mice
Data an association between Plexin-B2 (zeige PLXNB2 Proteine) and Plexin-D1 with the negative regulation of IL-12 (zeige IL12A Proteine)/IL-23p40 in DCs.
This study demonstrated that Sema3E (zeige SEMA3E Proteine) and Plexin-D1 specify the degree of glutamatergic connectivity between a specific source and target in the complex circuitry of the basal ganglia.
a novel role of Sema3E-Plexin-D1 function in modulating angiogenesis via a VEGF-induced feedback mechanism
Sema3d (zeige SEMA3D Proteine) regulates collective endothelial cell migration in zebrafish through two separate mechanisms. Mesenchymal Sema3d (zeige SEMA3D Proteine) guides outgrowth of the common cardinal (zeige CARD8 Proteine) 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 (zeige PLXNB2 Proteine) results in delayed ISV sprouting identical to that seen in sema3e (zeige SEMA3A Proteine) 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