<scp>CXCR</scp>7 mediates <scp>SDF</scp>1‐induced melanocyte migration

Lee, Eunkyung; Han, Jiyeon; Kim, Kwangmi; Choi, Hyunjung; Cho, Eun‐Gyung; Lee, Tae Ryong

doi:10.1111/pcmr.12024

Cited by 42 publications

(37 citation statements)

References 54 publications

(73 reference statements)

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“…The structural reasons for this differential behavior have not been defined. b-Arrestin coupling correlates with receptor trafficking properties and is required for the scavenger function of ACKR2 [152] and ACKR3 [151,166,167], whereas it appears dispensable for ACKR4 internalization and ligand uptake [126] (see Fig. 3C).…”

Section: B-arrestin-dependent Signaling Propertiesmentioning

confidence: 98%

Overview and potential unifying themes of the atypical chemokine receptor family

Vacchini

Locati

Borroni

2016

Journal of Leukocyte Biology

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Chemokines modulate immune responses through their ability to orchestrate the migration of target cells. Chemokines directly induce cell migration through a distinct set of 7 transmembrane domain G proteincoupled receptors but are also recognized by a small subfamily of atypical chemokine receptors, characterized by their inability to support chemotactic activity. Atypical chemokine receptors are now emerging as crucial regulatory components of chemokine networks in a wide range of physiologic and pathologic contexts. Although a new nomenclature has been approved recently to reflect their functional distinction from their conventional counterparts, a systematic view of this subfamily is still missing. This review discusses their biochemical and immunologic properties to identify potential unifying themes in this emerging family.

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Section: B-arrestin-dependent Signaling Propertiesmentioning

confidence: 98%

Overview and potential unifying themes of the atypical chemokine receptor family

Vacchini

Locati

Borroni

2016

Journal of Leukocyte Biology

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“…Chemokine signalling through CXCL12/CXCR4 is a common mechanism controlling the migration of several cell types along the body axis, such as hematopoietic progenitor cells 40 , vascular endothelial cells 41 , melanocytes 42 and tumour cells 43,44 . In addition to the present results, it has been reported that in the CNS, in addition to CR cells, the migration of cerebellar granule precursors 34 , cortical interneurons 23 , microglia 45 , neural precursor cells 46 , and certain brain tumour cells 33 is also dependent on CXCL12/CXCR4…”

Section: Discussionmentioning

confidence: 99%

Sema3E/PlexinD1 regulates the migration of hem-derived Cajal-Retzius cells in developing cerebral cortex

et al. 2014

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During the development of the cerebral cortex, Cajal-Retzius (CR) cells settle in the preplate and coordinate the precise growth of the neocortex. Indeed, CR cells migrate tangentially from specific proliferative regions of the telencephalon (for example, the cortical hem (CH)) to populate the entire cortical surface. This is a very finely tuned process regulated by an emerging number of factors that has been sequentially revealed in recent years. However, the putative participation of one of the major families of axon guidance molecules in this process, the Semaphorins, was not explored. Here we show that Semaphorin-3E (Sema3E) is a natural negative regulator of the migration of PlexinD1-positive CR cells originating in the CH. Our results also indicate that Sema3E/PlexinD1 signalling controls the motogenic potential of CR cells in vitro and in vivo. Indeed, absence of Sema3E/PlexinD1 signalling increased the migratory properties of CR cells. This modulation implies negative effects on CXCL12/CXCR4 signalling and increased ADF/Cofilin activity.

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“…In this region, non-NCderived mesenchymal cells express Sdf1, suggesting a role for SDF1 signaling transduced exclusively by CXCR7 at this step. Recent studies showed that CXCR7 may promote cell migration 26 or proliferation 27 independently of CXCR4. During heart development, the great arteries derived from cardiac NCs undergo extensive lengthening during septation of the outflow tract.…”

Section: Sdf1 Drives Cardiac Nc Migration and Survival Through The CXmentioning

confidence: 99%

Misregulation of SDF1-CXCR4 Signaling Impairs Early Cardiac Neural Crest Cell Migration Leading to Conotruncal Defects

Escot

Blavet

Härtle

et al. 2013

Circulation Research

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Rationale: Cardiac neural crest cells (NCs) contribute to heart morphogenesis by giving rise to a variety of cell types from mesenchyme of the outflow tract, ventricular septum, and semilunar valves to neurons of the cardiac ganglia and smooth muscles of the great arteries. Failure in cardiac NC development results in outflow and ventricular septation defects commonly observed in congenital heart diseases. Cardiac NCs derive from the vagal neural tube, which also gives rise to enteric NCs that colonize the gut; however, so far, molecular mechanisms segregating these 2 populations and driving cardiac NC migration toward the heart have remained elusive. Objective: Stromal-derived factor-1 (SDF1) is a chemokine that mediates oriented migration of multiple embryonic cells and mice deficient for Sdf1 or its receptors, Cxcr4 and Cxcr7 , exhibit ventricular septum defects, raising the possibility that SDF1 might selectively drive cardiac NC migration toward the heart via a chemotactic mechanism. Methods and Results : We show in the chick embryo that Sdf1 expression is tightly coordinated with the progression of cardiac NCs expressing Cxcr4 . Cxcr4 loss-of-function causes delayed migration and enhanced death of cardiac NCs, whereas Sdf1 misexpression results in their diversion from their normal pathway, indicating that SDF1 acts as a chemoattractant for cardiac NCs. These alterations of SDF1 signaling result in severe cardiovascular defects. Conclusions: These data identify Sdf1 and its receptor Cxcr4 as candidate genes responsible for cardiac congenital pathologies in human.

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CXCR7 mediates SDF1‐induced melanocyte migration

Cited by 42 publications

References 54 publications

Overview and potential unifying themes of the atypical chemokine receptor family

Overview and potential unifying themes of the atypical chemokine receptor family

Sema3E/PlexinD1 regulates the migration of hem-derived Cajal-Retzius cells in developing cerebral cortex

Misregulation of SDF1-CXCR4 Signaling Impairs Early Cardiac Neural Crest Cell Migration Leading to Conotruncal Defects

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