p75NTR enhances PC12 cell tumor growth by a non-receptor mechanism involving downregulation of cyclin D2

Fritz, Melinda; Mirnics, Z. K.; Nylander, Karen D.; Schor, Nina F.

doi:10.1016/j.yexcr.2006.06.029

Cited by 6 publications

(5 citation statements)

References 52 publications

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“…In addition, p75NTR plays an important role in the regulation of cell cycle and -amyloid formation [5,6]. Previous studies have shown that NFκB, JNK, p53, ceramide, and other molecules are involved in p75NTR apoptotic signal transduction [7][8][9][10][11].…”

Section: P75ntr and Bfar Interaction Effects On Signal Pathwaymentioning

confidence: 99%

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p75NTR signal transduction suppressed by BFAR and p75NTR interactions

Shi

Huo

2012

Sci. China Life Sci.

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p75NTR is a low-affinity nerve growth factor receptor, which promotes cell proliferation as a positive modulator of high-affinity receptor TrkA, as well as binds with cell ligands to induce apoptosis and mediate death signals. To analyze the regulatory mechanisms of p75NTR, the present study utilized a new membrane yeast two-hybrid system to screen a human fetal brain cDNA library. Results identified BFAR, a novel protein that interacts with p75NTR. Interaction specificity was verified by membrane yeast two-hybrid co-transformation assays, in vitro GST pull-down assays, and in vitro co-immunoprecipitation assays. The fluorescent subcellular localization assay revealed that the two proteins co-localized within the cytoplasm. BFAR overexpression in PC-12 and HEK293T cells inhibited the NFκB and JNK signaling pathway, as determined with the luciferase test. Co-transfected p75NTR and BFAR in HEK293T or PC-12 cells, respectively, increased the percentage of cells in the G2/M phase, decreased the number of S-phase cells, and did not change the number of G0/G1-phase cells. p75NTR, BFAR, membrane yeast two-hybrid, protein-protein interaction, apoptosis

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Section: P75ntr and Bfar Interaction Effects On Signal Pathwaymentioning

confidence: 99%

“…Suppression of p75NTR expression in PC-12 cells has been shown to induce up-regulation of cyclin D2 [5]. In addition, over-expression of BFAR impacts multiple signaling pathways in PC-12 cells to varying degrees.…”

Section: Bfar Over-expression Affects the Cell Cyclementioning

confidence: 99%

p75NTR signal transduction suppressed by BFAR and p75NTR interactions

Shi

Huo

2012

Sci. China Life Sci.

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“…p75NTR 介导细胞凋亡的现象已经被广泛证实 [2,3] . 此外, p75NTR 在调节细胞周期和淀粉样蛋白形成方面发挥了关键的作用 [4,5] . 大量研究表明, NFκB, JNK, p53 和神经酰胺等多种分子参与了 p75NTR 凋亡图 4 p75NTR 和 BFAR 在 HeLa 细胞中的共定位图像 5(B)).…”

Section: P75ntr 与 Bfar 相互作用对不同信号通路的影响unclassified

“…曾有报道, 在 PC-12 细胞中抑制 p75NTR 的表达可导致细胞周期蛋白 D2(cyclin D2)表达上调 [4] . 本研究也发现, 在 PC-12 细胞中过表达 BFAR 对多个信号通路都有不同程度的影响.…”

Section: 过表达 Bfar 对细胞周期的影响unclassified

BFAR 与p75NTR 的蛋白相互作用抑制p75NTR信号转导

施¹,

李²,

霍³

2011

Sci. Sin.-Vitae

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“…CCND2 forms a complex with and functions as a regulatory subunit of CDK4 or CDK6, whose activity is required for cell cycle G1/S transition by interacting with the tumor suppressor protein Rb. Upregulation of CCND2 can decrease proliferation and growth of tumors both in vitro and in vivo (35,36). Interestingly, overexpression of cyclin D2 protein efficiently inhibited cell cycle progression and DNA synthesis in primary human and established murine fibroblasts indicating that cyclin D2 can induce a non-proliferative state, possibly through sequestration of the CDK2 catalytic subunit (37).…”

Section: -------------------------------------------------Ingenuity Cmentioning

confidence: 99%

Genetic alterations after carbon ion irradiation in human lung adenocarcinoma cells

Fokas

You²,

Juricko³

et al. 2010

Int J Oncol

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Abstract. The aim of this study was to investigate the difference in gene expression profiles of human lung adenocarcinoma cells and identify genes whose expression is altered by heavy ions but not X-rays. The lung adenocarcinoma cell line A549 was irradiated with carbon ion beams and X-rays using biologically equivalent doses (2 Gy and 6 Gy, respectively). The transcriptional profiling was determined with a high density cDNA microarray containing 11.800 genes, and genetic network and gene ontology analysis was performed. The changes in selected genes involved were validated by quantitative real-time polymerase chain reaction (qRT-PCR). The microarray analysis identified 49 mapped, network-eligible genes, the expression level of which was altered by carbon ions but not by X-rays. From these, 29 were upregulated while 20 genes were downregulated 4 h postirradiation with carbon ions in A549 cells, as compared to the control. Among these, three genes (CCND2, RARG and E2F5) were involved in the aryl hydrocarbon receptor signalling and G1/S cell cycle checkpoint pathways. The microarray data were corroborated by qRT-PCR analysis of the selected genes (p<0.05). Our findings provide information on the genetic signature of carbon ions in human lung adenocarcinoma cells and add to the understanding of the complicated molecular response to carbon ion irradiation.

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p75NTR enhances PC12 cell tumor growth by a non-receptor mechanism involving downregulation of cyclin D2

Cited by 6 publications

References 52 publications

p75NTR signal transduction suppressed by BFAR and p75NTR interactions

p75NTR signal transduction suppressed by BFAR and p75NTR interactions

BFAR 与p75NTR 的蛋白相互作用抑制p75NTR信号转导

Genetic alterations after carbon ion irradiation in human lung adenocarcinoma cells

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