Role of TC21/R-Ras2 in enhanced migration of neurofibromin-deficient Schwann cells

Huang, Yuan; Rangwala, Fatima; Fulkerson, Patricia C.; Ling, Bowen; Reed, E.; Cox, Adrienne D.; Kamholz, John; Ratner, Nancy

doi:10.1038/sj.onc.1207075

Cited by 38 publications

(42 citation statements)

References 58 publications

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“…We showed that the PI3-kinase inhibitor, LY294002, attenuates the increased migration of Nf1-/-trigeminal neural crest cells; we have also decreased invasive capacity by treating these cells with the MAP kinase inhibitors PD98059 and U0126 (data not shown). These data are consistent with results using neurofibromindeficient Schwann cells derived from E12.5 dorsal root ganglia (Huang et al, 2004). In order to increase the likelihood that these data will be published, we have added two sets of experiments over the past year: 1) characterization of expression of neural crest markers in the cell populations used (trigeminal neural crest, branchial arch mesenchymal, limb bud mesenchymal), 2) additional inhibitor studies with both the embryonic cell populations and the sarcoma cell lines.…”

Section: Invasiveness Of Nf1-neural Crest Cells (Revised Sow Task 2)supporting

confidence: 82%

Cell Motility and Invasiveness of Neurofibromin-Deficient Neural Crest Cells and Malignant Triton Tumor Lines. Addendum

Vogel¹

2006

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Section: Invasiveness Of Nf1-neural Crest Cells (Revised Sow Task 2)supporting

confidence: 82%

Cell Motility and Invasiveness of Neurofibromin-Deficient Neural Crest Cells and Malignant Triton Tumor Lines. Addendum

Vogel¹

2006

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“…2B and 3B). NF1 mediates the inactivation of classic RAS proteins (e.g., KRAS and HRAS) but also nonclassic RAS proteins, including RRAS2 (26). siRNAs targeting KRAS and RRAS2 both caused 4OHT sensitivity, and KRAS silencing also caused moderate ICI182,780 sensitivity (Figs.…”

Section: Resultsmentioning

confidence: 99%

Genome-wide functional screen identifies a compendium of genes affecting sensitivity to tamoxifen

Mendes-Pereira

Sims

Dexter

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

119

125

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Therapies that target estrogen signaling have made a very considerable contribution to reducing mortality from breast cancer. However, resistance to tamoxifen remains a major clinical problem. Here we have used a genome-wide functional profiling approach to identify multiple genes that confer resistance or sensitivity to tamoxifen. Combining whole-genome shRNA screening with massively parallel sequencing, we have profiled the impact of more than 56,670 RNA interference reagents targeting 16,487 genes on the cellular response to tamoxifen. This screen, along with subsequent validation experiments, identifies a compendium of genes whose silencing causes tamoxifen resistance (including BAP1 , CLPP , GPRC5D , NAE1 , NF1 , NIPBL , NSD1 , RAD21 , RARG , SMC3 , and UBA3 ) and also a set of genes whose silencing causes sensitivity to this endocrine agent ( C10orf72 , C15orf55/NUT , EDF1 , ING5 , KRAS , NOC3L , PPP1R15B , RRAS2 , TMPRSS2 , and TPM4 ). Multiple individual genes, including NF1 , a regulator of RAS signaling, also correlate with clinical outcome after tamoxifen treatment.

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“…PAKs (p21-activated kinases) have also been implicated in SC transformation (Tang et al, 1998). R-Ras and R-Ras2/TC21 may mediate some effects of Nf1 loss in SCs (Huang et al, 2004).…”

Section: Schwann Cell Tumorsmentioning

confidence: 99%

Mechanisms and Roles of Axon-Schwann Cell Interactions

Corfas¹,

Velardez²,

Ko³

et al. 2004

J. Neurosci.

176

130

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Schwann cells (SCs) cover most of the surface of all axons in peripheral nerves. Axons and these glial cells are not only in intimate physical contact but also in constant and dynamic communication, each one influencing and regulating the development, function, and maintenance of the other. In recent years, there has been significant progress in the understanding of the molecular mechanisms of axon-Schwann cell interactions, particularly those relevant for postnatal development and maintenance of nerve function and structure. In this review, we discuss recent progress in four aspects of axon-Schwann cell interactions, including the roles of the neuregulin1 (NRG1)-erbB signaling pathway, the mechanisms underlying the formation and function of the node of Ranvier, the role of perisynaptic Schwann cells at the neuromuscular junction, and the mechanisms that generate Schwann cell tumors.Along the entire length of mammalian peripheral nerves, axons of motor, sensory, and autonomic neurons are in close association with SCs. The intimate contact between SCs and peripheral axons provided a first indication that these cells interact in important ways. In the mature nervous system, Schwann cells can be divided into four classes: myelinating cells (MSCs), nonmyelinating cells (NMSCs), perisynaptic Schwann cells (PSCs) (also known as terminal Schwann cells), and satellite cells of peripheral ganglia. These classes are based on their morphology, biochemical makeup, and the neuronal types (or area of their axons) with which they associate. MSCs, the best characterized SC, wrap around all large-diameter axons, including all motor neurons and some sensory neurons. Each MSC associates with a single axon and creates the myelin sheath necessary for saltatory nerve conduction (Fig. 1 A). NMSCs associate with small-diameter axons of C-fibers emanating from many sensory and all postganglionic sympathetic neurons. Each NMSC wraps around several sensory axons to form a Remak bundle, keeping individual axons separated by thin extensions of the Schwann cell body (Fig. 1 B).

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Role of TC21/R-Ras2 in enhanced migration of neurofibromin-deficient Schwann cells

Cited by 38 publications

References 58 publications

Cell Motility and Invasiveness of Neurofibromin-Deficient Neural Crest Cells and Malignant Triton Tumor Lines. Addendum

Cell Motility and Invasiveness of Neurofibromin-Deficient Neural Crest Cells and Malignant Triton Tumor Lines. Addendum

Genome-wide functional screen identifies a compendium of genes affecting sensitivity to tamoxifen

Mechanisms and Roles of Axon-Schwann Cell Interactions

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