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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.
Showing 10 out of 122 products:
Human Polyclonal Neurofibromin 1 Primary Antibody for ICC, IHC (fro) - ABIN152500
Kuorilehto, Ekholm, Nissinen, Hietaniemi, Hiltunen, Paavolainen, Penttinen, Peltonen: NF1 gene expression in mouse fracture healing and in experimental rat pseudarthrosis. in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 2006
Show all 4 references for ABIN152500
Guinea Pig Monoclonal Neurofibromin 1 Primary Antibody for IHC (p), IP - ABIN152499
Hisaoka, Hashimoto, Ohguri, Aoki, Okamoto, Tanaka, Okimoto, Nakamura, Ishida: Congenital (infantile) pseudarthrosis of the fibula associated with osteofibrous dysplasia. in Skeletal radiology 2004
Show all 3 references for ABIN152499
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
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Guinea Pig Monoclonal Neurofibromin 1 Primary Antibody for IHC (p), IP - ABIN152498
Tucker, Riccardi, Brown, Fee, Sutcliffe, Vielkind, Wechsler, Wolkenstein, Friedman: S100B and neurofibromin immunostaining and X-inactivation patterns of laser-microdissected cells indicate a multicellular origin of some NF1-associated neurofibromas. in Journal of neuroscience research 2011
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
Spatially- and temporally-controlled postnatal p53 (show TP53 Antibodies) knockdown cooperates with embryonic Schwann cell precursor Nf1 gene loss to promote malignant peripheral nerve sheath tumor formation.
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
A significant correlation between neurofibromin expression and colorectal tumor localization was found, with tumors arising in the colon showing intense NF expression more often than those arising in the rectum; higher expression of NF was more common in tumors not responding to treatment; and tumors with multiple metastases showed higher expression of NF than those with single metastasis
mutation in the NF1 gene is associated with Neurofibromatosis-Noonan Syndrome.
the computational model results have added credibility to the experimental hypothesis of a genetic cause (i.e. Nf1 mutation) for Congenital pseudarthrosis of the tibia
The pattern of growth differs substantially in deletion and non-deletion neurofibromatosis 1 patients, but the pathogenic basis for this difference is unknown.
Fine mapping of meiotic NAHR-associated crossovers causing large NF1 deletions has been reported.
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%).
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