Product nameAnti-Neurofibromin antibody
See all Neurofibromin primary antibodies
DescriptionRabbit polyclonal to Neurofibromin
Tested applicationsSuitable for: WB, IPmore details
Species reactivityReacts with: Mouse, Human, Zebrafish
Predicted to work with: Rat, Rabbit, Horse, Cow, Chimpanzee, Ferret, Rhesus monkey, Gorilla, Orangutan, Elephant
The epitope recognized maps to a region between residue 2760 and the C terminus (residue 2818) of human Neurofibromin 1 using the numbering given in entry NP_000258.1 (GeneID 4763).
- WB: HeLa, 293T, TCMK-1 and NIH3T3 whole cell lysates. IP: HeLa whole cell lysate.
Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
Storage bufferPreservative: 0.1% Sodium azide
Constituents: 0.021% PBS, 1.764% Sodium citrate, 1.815% Tris
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab17963 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/1000 - 1/10000. Predicted molecular weight: 319 kDa.|
|IP||Use a concentration of 2 - 10 µg/ml.|
FunctionStimulates the GTPase activity of Ras. NF1 shows greater affinity for Ras GAP, but lower specific activity. May be a regulator of Ras activity.
Involvement in diseaseDefects in NF1 are the cause of neurofibromatosis type 1 (NF1) [MIM:162200]; also known as von Recklinghausen syndrome. A disease characterized by patches of skin pigmentation (cafe-au-lait spots), Lisch nodules of the iris, tumors in the peripheral nervous system and fibromatous skin tumors. Individuals with the disorder have increased susceptibility to the development of benign and malignant tumors.
Defects in NF1 are a cause of juvenile myelomonocytic leukemia (JMML) [MIM:607785]. JMML is a pediatric myelodysplastic syndrome that constitutes approximately 30% of childhood cases of myelodysplastic syndrome (MDS) and 2% of leukemia. Germline mutations of NF1 account for the association of JMML with type 1 neurofibromatosis (NF1).
Defects in NF1 are the cause of Watson syndrome (WS) [MIM:193520]. WS is characterized by the presence of pulmonary stenosis, cafe-au-lait spots, and mental retardation. WS is considered as an atypical form of NF1.
Defects in NF1 are a cause of familial spinal neurofibromatosis (FSNF) [MIM:162210]. Familial spinal NF is considered to be an alternative form of neurofibromatosis, showing multiple spinal tumors.
Defects in NF1 are a cause of neurofibromatosis-Noonan syndrome (NFNS) [MIM:601321]. NFNS is characterized by manifestations of both NF1 and Noonan syndrome (NS). NS is a disorder characterized by dysmorphic facial features, short stature, hypertelorism, cardiac anomalies, deafness, motor delay, and a bleeding diathesis.
Defects in NF1 may be a cause of colorectal cancer (CRC) [MIM:114500].
Sequence similaritiesContains 1 CRAL-TRIO domain.
Contains 1 Ras-GAP domain.
- Information by UniProt
- DKFZp686J1293 antibody
- FLJ21220 antibody
- Neurofibromatosis Noonan syndrome antibody
All lanes : Anti-Neurofibromin antibody (ab17963) at 0.1 µg/ml
Lane 1 : HeLa whole cell lysate in NETN lysis buffer
Lane 2 : 293T whole cell lysate in NETN lysis buffer
Lane 3 : Jurkat whole cell lysate in NETN lysis buffer
Lane 4 : TCMK-1 whole cell lysate in NETN lysis buffer
Lane 5 : NIH3T3 whole cell lysate in NETN lysis buffer
Lysates/proteins at 50 µg per lane.
Developed using the ECL technique.
Predicted band size: 319 kDa
Exposure time: 75 seconds
Whole cell lysate (0.5-1.0mg per IP reaction; 20% of IP loaded) from HeLa cells prepared using NETN lysis buffer.
Lane 1: IP using rabbit anti-Neurofibromin antibody.
Lane 2: IP using ab17963 at 6 µg per reaction.
Lane 3: Control IgG.
For western blotting, ab17963 was used at 1 µg/ml.
This product has been referenced in:
- Moutal A et al. CRMP2-Neurofibromin Interface Drives NF1-related Pain. Neuroscience 381:79-90 (2018). IF . Read more (PubMed: 29655575) »
- Yzaguirre AD et al. Loss of neurofibromin Ras-GAP activity enhances the formation of cardiac blood islands in murine embryos. Elife 4:e07780 (2015). WB . Read more (PubMed: 26460546) »