l 739749 has been researched along with Neurofibromatosis 1 in 2 studies
*Neurofibromatosis 1: An autosomal dominant inherited disorder (with a high frequency of spontaneous mutations) that features developmental changes in the nervous system, muscles, bones, and skin, most notably in tissue derived from the embryonic NEURAL CREST. Multiple hyperpigmented skin lesions and subcutaneous tumors are the hallmark of this disease. Peripheral and central nervous system neoplasms occur frequently, especially OPTIC NERVE GLIOMA and NEUROFIBROSARCOMA. NF1 is caused by mutations which inactivate the NF1 gene (GENES, NEUROFIBROMATOSIS 1) on chromosome 17q. The incidence of learning disabilities is also elevated in this condition. (From Adams et al., Principles of Neurology, 6th ed, pp1014-18) There is overlap of clinical features with NOONAN SYNDROME in a syndrome called neurofibromatosis-Noonan syndrome. Both the PTPN11 and NF1 gene products are involved in the SIGNAL TRANSDUCTION pathway of Ras (RAS PROTEINS). [MeSH]
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 1 (50.00) | 18.2507 |
| 2000's | 1 (50.00) | 29.6817 |
| 2010's | 0 (0.00) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Akunuru, S; Chiamvimonvat, N; Ratner, N; Vázquez, AE; Xu, Y; Yamoah, EN | 1 |
| Kim, HA; Ling, B; Ratner, N | 1 |
2 other study(ies) available for l 739749 and Neurofibromatosis 1
| Article | Year |
|---|---|
Gene-targeted deletion of neurofibromin enhances the expression of a transient outward K+ current in Schwann cells: a protein kinase A-mediated mechanism.
Topics: Animals; Cells, Cultured; Cyclic AMP-Dependent Protein Kinases; Enzyme Inhibitors; Ganglia, Spinal; Gene Targeting; Genes, ras; Genotype; Ion Channel Gating; Mice; Mice, Inbred C57BL; Mice, Mutant Strains; Neurofibromatosis 1; Neurofibromin 1; Oligopeptides; Patch-Clamp Techniques; Potassium; Potassium Channel Blockers; Schwann Cells; Signal Transduction | 2002 |
Nf1-deficient mouse Schwann cells are angiogenic and invasive and can be induced to hyperproliferate: reversion of some phenotypes by an inhibitor of farnesyl protein transferase.
Topics: Alkyl and Aryl Transferases; Animals; Axons; Biomarkers; Blood; Cell Division; Cells, Cultured; Colforsin; Cyclic AMP-Dependent Protein Kinases; Enzyme Activation; Enzyme Inhibitors; Glia Maturation Factor; Hyperplasia; Mice; Mice, Mutant Strains; Mutation; Myelin P0 Protein; Neoplasm Invasiveness; Neovascularization, Pathologic; Nerve Growth Factors; Nerve Tissue Proteins; Neurofibromatosis 1; Neurofibromin 1; Oligopeptides; Phenotype; Protein Prenylation; Proteins; Schwann Cells; Transferases | 1997 |