Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity.

Annotation inferences using phylogenetic trees

Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword mapping

Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping

Gene Ontology annotation based on curation of immunofluorescence data

Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara.

Automatic assignment of GO terms using logical inference, based on inter-ontology links.

Electronic Gene Ontology annotations created by ARBA machine learning models

Combined Automated Annotation using Multiple IEA Methods.

The NF1 locus encodes a protein functionally related to mammalian GAP and yeast IRA proteins.

Somatic mutations in the neurofibromatosis 1 gene in human tumors.

Aberrant regulation of ras proteins in malignant tumour cells from type 1 neurofibromatosis patients.

The protein product of the neurofibromatosis type 1 gene is expressed at highest abundance in neurons, Schwann cells, and oligodendrocytes.

The sec14 homology module of neurofibromin binds cellular glycerophospholipids: mass spectrometry and structure of a lipid complex.

Neurofibromin is actively transported to the nucleus.

T2 hyperintensities in children with neurofibromatosis type 1 and their relationship to cognitive functioning.

Angiogenic expression profile of normal and neurofibromin-deficient human Schwann cells.

Neurofibroma-associated growth factors activate a distinct signaling network to alter the function of neurofibromin-deficient endothelial cells.

SPRED2 loss-of-function causes a recessive Noonan syndrome-like phenotype.

5-HT(6) receptor recruitment of mTOR as a mechanism for perturbed cognition in schizophrenia.

Bipartite interaction between neurofibromatosis type I protein (neurofibromin) and syndecan transmembrane heparan sulfate proteoglycans.

Neurofibromatosis type 1 protein and amyloid precursor protein interact in normal human melanocytes and colocalize with melanosomes.

Interaction between a Domain of the Negative Regulator of the Ras-ERK Pathway, SPRED1 Protein, and the GTPase-activating Protein-related Domain of Neurofibromin Is Implicated in Legius Syndrome and Neurofibromatosis Type 1.

Interrogating the protein interactomes of RAS isoforms identifies PIP5K1A as a KRAS-specific vulnerability.

Defining the membrane proteome of NK cells.

Regulation of RAS by GAPs

Loss-of-function NF1 variants don't stimulate RAS GTPase activity

RAS GAPs stimulate RAS GTPase activity

KBTBD7:CUL3:RBX1 ubiquitinates NF1

NF1 is degraded by the proteasome

RAS GAPs bind RAS:GTP

SPRED dimer binds NF1

Deep research on NF1 function

Cyberian deep research on NF1 function