Chemokine-like factor 1, a novel cytokine, induces nerve cell migration through the non-extracellular Ca2+-dependent tyrosine kinases pathway

Wang, Zhenzhen; Li, Gang; Chen, Xiaoyu; Zhao, Ming; Yuan, Yu‐He; Wang, Xiaoliang; Chen, Nai‐Hong

doi:10.1016/j.brainres.2009.10.047

Cited by 19 publications

(14 citation statements)

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“…In addition, the quantitative analysis showed that the fluorescence intensity of F-actin from the CKLF1-stimulated group increased significantly compared with the control. Consistent with this finding, supporting data have shown that CKLF1 induces actin polymerization in neuroblastoma cells considered to have arisen from the neural crest [13]. Unexpectedly, we found that the dot-like staining of MAP2 was also enhanced in response to CKLF1 stimulation.…”

Section: Discussionsupporting

confidence: 90%

“…A scratch-wound-healing assay was performed using our previous method [13,17]. Briefly, neurons were seeded at a density of 1 × 10 5 cells/well in 24-well plates and allowed to grow to confluence.…”

Section: Wound-healing Assaysmentioning

confidence: 99%

“…Immunofluorescence staining was performed as reported previously [13]. Primary cortical neuron cultures were grown on poly-D-lysine-coated coverslips.…”

Section: Immunofluorescence Stainingmentioning

confidence: 99%

“…In addition, CKLF1 immunoreactivity was observed in the superficial layer of the cerebral cortex of rats, where neurons terminate their migration during cortical development [12]. Furthermore, CKLF1 showed chemotactic activities in neuroblastoma SH-SY5Y cells [13]. These researches showed the potential role of CKLF1 in cortical development.…”

Section: Introductionmentioning

confidence: 96%

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Chemokine-like factor 1 promotes the migration of rat primary cortical neurons by the induction of actin polymerization

et al. 2014

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Chemokine-like factor 1 (CKLF1), a newly cloned chemotactic cytokine, plays an essential role in immune cell migration. However, the potential role of CKLF1 in the cortical neuronal migration remains unclear. In the present research, by measuring the distance between the margin of brain slices and the leading population of migrating cells, we showed that the extent of cell migration was markedly enhanced in response to CKLF1 treatment, which was significantly inhibited by the simultaneous addition of anti-CKLF1 antibody. By immunofluorescence staining, it was found that CKLF1 induced actin polymerization in primary cerebral cortical neurons. By wound-healing assays, it was found that CKLF1 stimulated the migration of cortical neurons in a dose-dependent manner. In conclusion, our data suggest that CKLF1 promotes the migration of rat primary cerebral cortical neurons by the induction of actin polymerization.

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Section: Discussionsupporting

confidence: 90%

Section: Wound-healing Assaysmentioning

confidence: 99%

“…Immunofluorescence staining was performed as reported previously [13]. Primary cortical neuron cultures were grown on poly-D-lysine-coated coverslips.…”

Section: Immunofluorescence Stainingmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 96%

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Chemokine-like factor 1 promotes the migration of rat primary cortical neurons by the induction of actin polymerization

et al. 2014

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“…2B; Supplemental Fig. S5) encodes a chemokine with a role in muscle development and neuronal migration (Wang et al 2010). Its expression is increased in systemic lupus erythematosus (SLE) and in rheumatoid arthritis (RA), diseases that are nine and three times more common in women, respectively.…”

Section: Resultsmentioning

confidence: 99%

Sex-biased genetic effects on gene regulation in humans

et al. 2012

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Human regulatory variation, reported as expression quantitative trait loci (eQTLs), contributes to differences between populations and tissues. The contribution of eQTLs to differences between sexes, however, has not been investigated to date. Here we explore regulatory variation in females and males and demonstrate that 12%-15% of autosomal eQTLs function in a sex-biased manner. We show that genes possessing sex-biased eQTLs are expressed at similar levels across the sexes and highlight cases of genes controlling sexually dimorphic and shared traits that are under the control of distinct regulatory elements in females and males. This study illustrates that sex provides important context that can modify the effects of functional genetic variants.

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