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NF1 product appears to function as a negative regulator of the ras signal transduction pathway. Additionally we are shipping Neurofibromin 1 Kits (5) and Neurofibromin 1 Proteins (3) and many more products for this protein.
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Human Polyclonal Neurofibromin 1 Primary Antibody for IF, ELISA - ABIN1534476
Wallace, Marchuk, Andersen, Letcher, Odeh, Saulino, Fountain, Brereton, Nicholson, Mitchell: Type 1 neurofibromatosis gene: identification of a large transcript disrupted in three NF1 patients. in Science (New York, N.Y.) 1990
Show all 2 references for ABIN1534476
Polymorphism in the neurofibromin gene, Nf1, is associated with antagonistic selection on wing size and development time in Drosophila melanogaster.
The N-terminal region of NF1 mediates the interaction with Fak56 and is required for the signaling activity and presynaptic localization of NF1
These results identify dAlk as an upstream activator of dNf1-regulated Ras signaling responsible for several dNf1 defects, and they implicate human Alk (show ALK Antibodies) as a potential therapeutic target in NF1
memory-related functions of Rut (show ADCY5 Antibodies)-AC are both Nf1-dependent and -independent, that Nf1 mediates the formation of two distinct memory components within a single neuron population.
survival of a subset of midline glia cells depends upon direct suppression of the proapoptotic protein HID via the EGF receptor (show EGFR Antibodies)/RAS/MAPK (show MAPK1 Antibodies) pathway
role in insulin (show INS Antibodies)-mediated proliferation of Schneider cells
preliminary crystallographic characterization of a novel segment (homologous to the yeast Sec14p lipid exchange protein) from the neurofibromatosis type 1 protein
Effect of neurofibromatosis type I mutations on a novel pathway for adenylyl cyclase activation requiring neurofibromin and Ras
Loss of NF1 can give rise to non-cell-autonomous developmental defects, implicate aberrant Ras-mediated signaling in larval neurons as the primary cause of the NF1 growth deficiency.
Neurofibromin regulates longevity and stress resistance through cAMP regulation of mitochondrial respiration and ROS (show ROS1 Antibodies) production, and NF1 may be treatable using catalytic antioxidants.
DNA variants in the NF1 gene are associated with genetic disposition to bovine spongiform encephalopathy.
study shows negative regulation of Ras (show RAB1A Antibodies) pathway through GAP activity of NF1 limits oligodendrocyte progenitor cell (OPC) proliferation and motility during development; provides insight into oncogenic mechanisms by which NF1 loss contributes to glial tumors
identification and characterization of nf1a and nf1b, orthologues of NF1, that show neural crest and cardiovascular defects resulting from morpholino knockdown, including vascular and cardiac valvular abnormalities
These findings demonstrate a role for Ras-GAP (show RASA1 Antibodies) activity in suppressing the hemogenic potential of the heart and restricting growth of neural crest-derived tissues.
identified p21Ras-dependent hyperphosphorylation of Pu.1 within the nucleus of Nf1 haploinsufficient myelomonocytic osteoclast precursors, providing a novel therapeutic target for the potential treatment of NF1 associated osteolytic manifestations.
Targeted gene deletion of TP53 (show TP53 Antibodies), Pten (show PTEN Antibodies), and NF1 in mouse brain causes glioblastoma.
Data indicated a critical role for Nf1 in regulating multiple mesenchymal stem/progenitor cells functions, including migration and adhesion through both the PI3-K (show PIK3CA Antibodies) and MAPK (show MAPK1 Antibodies) pathways.
this is the first demonstration that different germline NF1 gene mutations differentially dictate neurofibromin function in the brain.
Data suggest that bi-allelic loss of Nf1 induces autonomous adrenal hyper-activity. Nf1 seems involved in the regulation of adrenal cortex function in mice and humans.
FGFR1 (show FGFR1 Antibodies) signaling in hypertrophic chondrocytes is attenuated by the Ras-GAP (show RASA1 Antibodies) neurofibromin during endochondral bone formation
Low levels of NF1 expression were associated with primary and acquired resistance of lung adenocarcinomas to EGFR (show EGFR Antibodies) Thymidine Kinase (show TK1 Antibodies) Inhibitors in patients.
eurofibromin differentially controls neural stem cell (NSC) proliferation and multilineage differentiation through the selective use of the PI3K/AKT (show AKT1 Antibodies) and RAF (show RAF1 Antibodies)/MEK (show MDK Antibodies) pathways
Double-deficient RASA1 (show RASA1 Antibodies)-neurofibromin 1 mice developed T cell acute lymphoblastic leukemia/lymphoma, which originated at an early point in T cell development and was dependent on activating mutations in the Notch1 (show NOTCH1 Antibodies) gene.
Neurofibromin mediates Ras deactivation.
NF1 mutation is not associated with the risk of optic pathway glioma in Neurofibromatosis type 1 patients.
proposed technique is cheap and reliable, and could ideally be performed as a preliminary biochemical screening before molecular analysis of the Neurofibromatosis type 1 gene
Of the ten reported cases of NF1 due to R681X, one has presented with optic glioma and none with precocious puberty.
Thirty distinct NF1 mutations were identified in 32 patients. Thirteen mutations were novel and most were frameshift mutations (33.3%).
Constitutional missense mutations at p.Arg1809 affect 1.23% of unrelated NF1 probands in the UAB cohort, therefore this specific NF1 genotype-phenotype correlation will affect counseling and management of a significant number of patients.
Data suggest SPRED1 (show SPRED1 Antibodies) EVH1 domain interacts with NF1 GRD domain [N-term. 16AA/C-term. 20AA of GTPase-activating protein (show RASA1 Antibodies)-related domain]; SPRED1 (show SPRED1 Antibodies) EVH1 and NF1 GRD mutations observed in Legius syndrome reduce binding affinity between EVH1/GRD domains.
Novel 1948delT and 541C>T mutations in NF1 associated with sporadic neurofibromatosis type 1.
This study suggests that inactivating NF1 mutations outside the context of neurofibromatosis may be the oncogenic mechanism for a subset of sporadic gastrointestinal stromal tumors
The complexity of the splicing regulatory elements present in exon 9 is most likely responsible for the fact that mutations in this region represent 25% of all exonic changes that affect splicing in the NF1 gene.
This gene product appears to function as a negative regulator of the ras signal transduction pathway. Mutations in this gene have been linked to neurofibromatosis type 1, juvenile myelomonocytic leukemia and Watson syndrome. The mRNA for this gene is subject to RNA editing (CGA>UGA->Arg1306Term) resulting in premature translation termination. Alternatively spliced transcript variants encoding different isoforms have also been described for this gene.
neurofibromin 1 (neurofibromatosis, von Recklinghausen disease, Watson disease)
, neurofibromatosis 1
, neurofibromatosis factor 1
, neurofibromatosis type 1
, neurofibromin 1
, neurofibromatosis-related protein NF-1
, Neurofibromatosis type 1