Gene Ontology annotation by the MGI curatorial staff, curated orthology

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, accompanied by conservative changes to GO terms applied by UniProt

Automated transfer of experimentally-verified manual GO annotation data to mouse-rat orthologs

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

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

Electronic Gene Ontology annotations created by ARBA machine learning models

UniProt record for Nf1 (Q04690)

Automated transfer of experimentally-verified manual GO annotation data to mouse-human orthologs

Combined Automated Annotation using Multiple IEA Methods

The Nf1 tumor suppressor regulates mouse skin wound healing, fibroblast proliferation, and collagen deposited by fibroblasts.

Neurofibromin deficiency in mice causes exencephaly and is a modifier for Splotch neural tube defects.

Haploinsufficiency for the neurofibromatosis 1 (NF1) tumor suppressor results in increased astrocyte proliferation.

In vitro and in vivo effects of a farnesyltransferase inhibitor on Nf1-deficient hematopoietic cells.

Neurofibromin, the neurofibromatosis type 1 Ras-GAP, is required for appropriate P0 expression and myelination.

Mouse models of tumor development in neurofibromatosis type 1.

Mouse tumor model for neurofibromatosis type 1.

Induction of melanogenic abnormalities in NF1+/- mutant mice by DMBA.

Genetic and biochemical evidence that haploinsufficiency of the Nf1 tumor suppressor gene modulates melanocyte and mast cell fates in vivo.

Nf1 and Gmcsf interact in myeloid leukemogenesis.

The neurofibromatosis type 1 (Nf1) tumor suppressor is a modifier of carcinogen-induced pigmentation and papilloma formation in C57BL/6 mice.

Neurofibromin negatively regulates neurotrophin signaling through p21ras in embryonic sensory neurons.

Nf1;Trp53 mutant mice develop glioblastoma with evidence of strain-specific effects.

Neurofibromatosis 1 (NF1) heterozygosity results in a cell-autonomous growth advantage for astrocytes.

Learning deficits, but normal development and tumor predisposition, in mice lacking exon 23a of Nf1.

Ablation of NF1 function in neurons induces abnormal development of cerebral cortex and reactive gliosis in the brain.

Analysis of melanocyte precursors in Nf1 mutants reveals that MGF/KIT signaling promotes directed cell migration independent of its function in cell survival.

Hyperactivation of p21(ras) and the hematopoietic-specific Rho GTPase, Rac2, cooperate to alter the proliferation of neurofibromin-deficient mast cells in vivo and in vitro.

Neurofibromin regulates G protein-stimulated adenylyl cyclase activity.

Mechanism for the learning deficits in a mouse model of neurofibromatosis type 1.

Glycogen stored in skeletal but not in cardiac muscle in acid alpha-glucosidase mutant (Pompe) mice is highly resistant to transgene-encoded human enzyme.

Nf1 has an essential role in endothelial cells.

Aberrant growth and differentiation of oligodendrocyte progenitors in neurofibromatosis type 1 mutants.

Role of TC21/R-Ras2 in enhanced migration of neurofibromin-deficient Schwann cells.

Somatic inactivation of Nf1 in hematopoietic cells results in a progressive myeloproliferative disorder.

Loss of the nf1 tumor suppressor gene decreases fas antigen expression in myeloid cells.

JCV T-antigen interacts with the neurofibromatosis type 2 gene product in a transgenic mouse model of malignant peripheral nerve sheath tumors.

Glioma formation in neurofibromatosis 1 reflects preferential activation of K-RAS in astrocytes.

Neurofibromin regulates neural stem cell proliferation, survival, and astroglial differentiation in vitro and in vivo.

The HMG-CoA reductase inhibitor lovastatin reverses the learning and attention deficits in a mouse model of neurofibromatosis type 1.

Nf1 haploinsufficiency augments angiogenesis.

Stimulus-evoked release of neuropeptides is enhanced in sensory neurons from mice with a heterozygous mutation of the Nf1 gene.

Neurofibromin binds to caveolin-1 and regulates ras, FAK, and Akt.

Neurofibromin is a novel regulator of RAS-induced signals in primary vascular smooth muscle cells.

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

Nf1+/- mast cells induce neurofibroma like phenotypes through secreted TGF-beta signaling.

Neurofibromin plays a critical role in modulating osteoblast differentiation of mesenchymal stem/progenitor cells.

The neurofibromin GAP-related domain rescues endothelial but not neural crest development in Nf1 mice.

Hyperactivation of p21ras and PI3K cooperate to alter murine and human neurofibromatosis type 1-haploinsufficient osteoclast functions.

An oncogene-tumor suppressor cascade drives metastatic prostate cancer by coordinately activating Ras and nuclear factor-kappaB.

Long-term potentiation in the CA1 hippocampus induced by NR2A subunit-containing NMDA glutamate receptors is mediated by Ras-GRF2/Erk map kinase signaling.

Valosin-containing protein and neurofibromin interact to regulate dendritic spine density.

Social learning and amygdala disruptions in Nf1 mice are rescued by blocking p21-activated kinase.

Identification of genes important for cutaneous function revealed by a large scale reverse genetic screen in the mouse.

Loss of neurofibromin results in neurotrophin-independent survival of embryonic sensory and sympathetic neurons.

Tumour predisposition in mice heterozygous for a targeted mutation in Nf1.

Targeted disruption of the neurofibromatosis type-1 gene leads to developmental abnormalities in heart and various neural crest-derived tissues.

Nf1 deficiency causes Ras-mediated granulocyte/macrophage colony stimulating factor hypersensitivity and chronic myeloid leukaemia.

Nf1-deficient mouse Schwann cells are angiogenic and invasive and can be induced to hyperproliferate: reversion of some phenotypes by an inhibitor of farnesyl protein transferase.

A mouse model for the learning and memory deficits associated with neurofibromatosis type I.

Region-specific astrogliosis in brains of mice heterozygous for mutations in the neurofibromatosis type 1 (Nf1) tumor suppressor.

Falcon deep research synthesis for mouse Nf1