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Contralateral migration of oculomotor neurons is regulated by Slit/Robo signaling. Results demonstrate that a migratory subset of motor neurons respond to floor plate-derived Slit repulsion to properly control the timing of contralateral migration.
While Slit1 and Robo2 are only expressed in peripheral axons and their cell bodies, Slit2, Slit3 and Robo1 are also expressed in satellite cells of the dorsal root ganglion, Schwann cells and fibroblasts of peripheral nerves.
These observations from mutant Slit and Robo mice give great support for Slit/Robo role in neural crest cell migration during Enteric Nervous System development.
Data indicate the roles of Slit1/Robo1 and Netrin1/DCC signals in positioning motor neuron cell bodies.
a role for Slit1 in corpus callosum development
Robo-2-mediated targeting of P2 axons along the dorsoventral axis of the OB is controlled by Slit-1 expression
This study demonistrated that production of IPCs is enhanced in Robo1/2 and Slit1/2 mutants, suggesting that Slit/Robo signaling modulates the transition between primary and intermediate progenitors.
Disruption of either the Robo1 or Slit1 genes accelerates progression of thalamocortical axons in vivo.
Slit1 has a dual context-dependent role in thalamocortical axons formation
Robo1 and Robo2 are expressed in the nucleus origin of the tract of the postoptic commissure TPOC (nTPOC), while Slit expression domains flank the TPOC trajectory.
Nkx2.9 controls SACMN axon exit from the mammalian spinal cord by regulating Robo-Slit signaling
Data show that only Nck2 is required for the Slit1-induced changes in cortical neuron morphology in vitro.
These results indicate that Slit1/2 - Robo1/2 signaling is critical during the initial establishment of dopaminergic pathways, with roles in the dorsoventral positioning and precise pathfinding of these ascending longitudinal axons.
The results of this study suggested that the Slit1 secreted by new neurons alters the morphology of astrocytes through the astrocytes' Robo receptors, thereby promoting the fast migration of new neurons in contact with the astrocytes.
role in antagonizing netrin-1 attractive effects during migration of inferior olivary neurons
Slit proteins control the development of the lateral olfactory tract
Analysis of alternative splicing and conserved domains in human and mouse slit genes
our results suggest that Slit1 signaling may be involved in the regulation of molar tooth shape by regulating epithelial cell proliferation and formation of EFA of the crown.
Data suggest that the Slit family of axon guidance molecules (Slit 1-3) and their Robo 1 and 2 receptors contribute to the topographic targeting of basal vomeronasal axons.
The Slit receptors Robo2 and Robo3/Rig-1 are expressed in the subventricular zone and the rostral migratory stream and Slit1 and Slit2 are present in the adult septum and are responsible for both the septum and the CP repulsive activity in vitro
Findings show that SLIT1 is a direct target of SUV39H2 which binds to its promoter and catalyzes H3K9 tri-methylation to silence SLIT1 expression.
evidence showing that Slit1 and Slit2 proteins are selective inhibitors and repellents for dorsally projecting, but not for ventrally projecting, cranial motor axons
In fetal and embryonic stem cell cultures Slit-1 inhibited neurite outgrowth.
heparin/HS is an integral component of the minimal Slit-Robo signaling complex and serves to stabilize the relatively weak Slit-Robo interaction
Slits are negative regulators of Sdf1 and Cxcr4 in breast cancer cells.
A specific signaling pathway downstream of Fgfr1 controls in a cell-autonomous manner slit1 forebrain expression and identifies a specific growth factor receptor for in vivo control of the expression of a key embryonic axon guidance cue.
Slit acts via Robo2 in dendrites as a branching/growth factor but not in guidance, while Robo2 and Robo3 function in concert in axons to mediate axonal interactions and respond to Slits as guidance factors
These results suggested that the role of SLIT1 is altered postnatally and that this is particularly important for prefrontal connectivity in the Old World monkey cortex.
slit1a and slit1b are both expressed in the midline, hypochord, telencephalon, and hindbrain.
During motor axon regeneration, col4a5 destabilizes axons probing inappropriate trajectories to ensure target-selective regeneration, possible through slit1a.
Genetic analysis showed that Caspase-3, Caspase-9, and p38 MAPK interacted with Slit1a-Robo2 signaling.
Study shows that the laminar specificity of retinotectal connections does not depend on self-sorting interactions among retinal ganglion cells axons; rather, tectum-derived Slit1, signaling through axonal Robo2, guides neurites to their target layer.
Data show that Hedgehog signaling is required for commissure formation, glial bridge formation, and the restricted expression of the guidance molecules slit1a, slit2, slit3 and sema3d.
Slits inhibit arborization and synaptogenesis in the central nervous system.
Robo2 acted initially to split the tract of the postoptic commissure into discrete fascicles upon entering a broad domain of Slit1a expression in the ventrocaudal diencephalon.
homolog of Drosophila slit\; may play a role in protein-protein interactions during midline formation in the central nervous system\; specifically expressed in fetal and adult forebrain neurons
slit homolog 1 protein
, multiple EGF-like domains protein 4
, multiple epidermal growth factor-like domains protein 4
, multiple epidermal growth factor-like domains 4
, slit homolog 1 (Drosophila)
, slit homolog 1
, slit homolog 1 protein-like