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N3537

Sigma-Aldrich

Monoclonal Anti-Neurofibromin antibody produced in mouse

clone NFn27a, ascites fluid

Synonym(s):

Anti-Merlin Schwannomin, Anti-SCH

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About This Item

MDL number:
MFCD03845618
UNSPSC Code:
12352203

biological source

mouse

conjugate

unconjugated

antibody form

ascites fluid

antibody product type

primary antibodies

clone

NFn27a, monoclonal

species reactivity

mouse, human, rat

technique(s)

western blot: 1:100-1:200 using rat brain cytosolic extract

UniProt accession no.

P21359

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... NF1(4763)
mouse ... Nf1(18015)
rat ... Nf1(24592)

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General description

Neurofibromin 1 (NF1) is a tumor suppressor. The gene encoding it is localized on human chromosome 17q11.2 and contains 60 exons.

Immunogen

synthetic peptide corresponding to amino acids 27-41 located at the N-terminus of human neurofibromin.

Biochem/physiol Actions

Neurofibromin 1 (NF1) acts as a negative regulator of RAS (a GTPase). Mutations in the gene encoding it have been associated with neurofibromatosis type 1 and melanoma.

Physical form

Ascites fluid with 15 mM sodium azide as a preservative

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Certificates of Analysis (COA)

Lot/Batch Number
105K4762

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M Adelita Vizcaíno et al.
Human pathology, 46(9), 1323-1330 (2015-07-21)
Recent studies have identified somatic alterations in the gene encoding for neurofibromin (NF1) in a subset of glioblastoma (GBM), usually associated with the mesenchymal molecular subtype. To understand the significance of NF1 genetic alterations in diffuse gliomas in general, we
Meng-Chang Hsiao et al.
American journal of human genetics, 97(2), 238-249 (2015-07-21)
Genomic rearrangements can cause both Mendelian and complex disorders. Currently, several major mechanisms causing genomic rearrangements, such as non-allelic homologous recombination (NAHR), non-homologous end joining (NHEJ), fork stalling and template switching (FoSTeS), and microhomology-mediated break-induced replication (MMBIR), have been proposed.
Michael Krauthammer et al.
Nature genetics, 47(9), 996-1002 (2015-07-28)
We report on whole-exome sequencing (WES) of 213 melanomas. Our analysis established NF1, encoding a negative regulator of RAS, as the third most frequently mutated gene in melanoma, after BRAF and NRAS. Inactivating NF1 mutations were present in 46% of

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