Falcon deep research synthesis for human HRAS
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HRAS is a small GTPase molecular switch whose core GO annotations should prioritize GTP binding, GTPase activity, Ras protein signal transduction, positive regulation of MAPK cascade, and plasma membrane/Golgi membrane localization, while distal oncogenic mutant phenotypes should be curated conservatively.
"“Ras protein signal transduction” and “positive regulation of MAPK cascade” are generally **core** for HRAS, but very specific outcome terms (e.g., “cell cycle progression” as a default) should be restricted to contexts with strong, direct, wild-type evidence."
Aiolos transcription factor controls cell death in T cells by regulating Bcl-2 expression and its cellular localization.
RA-GEF, a novel Rap1A guanine nucleotide exchange factor containing a Ras/Rap1A-associating domain, is conserved between nematode and humans.
Increased oxidative stress with gene alteration in urinary bladder urothelium after the Chernobyl accident.
Involvement of Ras and Ral in chemotactic migration of skeletal myoblasts.
Regulation of a novel human phospholipase C, PLCepsilon, through membrane targeting by Ras.
Prenylated Rab acceptor protein is a receptor for prenylated small GTPases.
Nedd4 regulates ubiquitination and stability of the guanine-nucleotide exchange factor CNrasGEF.
The putative tumor suppressor RASSF1A homodimerizes and heterodimerizes with the Ras-GTP binding protein Nore1.
The complex of Arl2-GTP and PDE delta: from structure to function.
Ras and Rap control AMPA receptor trafficking during synaptic plasticity.
Novel raf kinase protein-protein interactions found by an exhaustive yeast two-hybrid analysis.
Structural evidence for feedback activation by Ras.GTP of the Ras-specific nucleotide exchange factor SOS.
Alternative splicing of the human proto-oncogene c-H-ras renders a new Ras family protein that trafficks to cytoplasm and nucleus.
Ras regulates assembly of mitogenic signalling complexes through the effector protein IMP.
Structural analysis of autoinhibition in the Ras activator Son of sevenless.
RIN1 is an ABL tyrosine kinase activator and a regulator of epithelial-cell adhesion and migration.
Regulation of p53 translation and induction after DNA damage by ribosomal protein L26 and nucleolin.
The RAP1 guanine nucleotide exchange factor Epac2 couples cyclic AMP and Ras signals at the plasma membrane.
GTP-Ras disrupts the intramolecular complex of C1 and RA domains of Nore1.
Release of RASSF1C from the nucleus by Daxx degradation links DNA damage and SAPK/JNK activation.
Catalytic competence of the Ras-GEF domain of hSos1 requires intra-REM domain interactions mediated by phenylalanine 577.
GTP binding is essential to the protein kinase activity of LRRK2, a causative gene product for familial Parkinson's disease.
Binding of ras to phosphoinositide 3-kinase p110alpha is required for ras-driven tumorigenesis in mice.
Spatial regulation of Raf kinase signaling by RKTG.
Transformation efficiency of RasQ61 mutants linked to structural features of the switch regions in the presence of Raf.
A novel switch region regulates H-ras membrane orientation and signal output.
Membrane-dependent signal integration by the Ras activator Son of sevenless.
Novel type of Ras effector interaction established between tumour suppressor NORE1A and Ras switch II.
Regulation of growth and survival of activated T cells by cell-transducing inhibitors of Ras.
Differences in flexibility underlie functional differences in the Ras activators son of sevenless and Ras guanine nucleotide releasing factor 1.
Reassessment of the role of FKBP38 in the Rheb/mTORC1 pathway.
Nucleocytoplasmic transport of Alp7/TACC organizes spatiotemporal microtubule formation in fission yeast.
Ras membrane orientation and nanodomain localization generate isoform diversity.
Role of the histone domain in the autoinhibition and activation of the Ras activator Son of Sevenless.
Allosteric gating of Son of sevenless activity by the histone domain.
An oncogene-tumor suppressor cascade drives metastatic prostate cancer by coordinately activating Ras and nuclear factor-kappaB.
Genetic and functional characterization of putative Ras/Raf interaction inhibitors in C. elegans and mammalian cells.
A human MAP kinase interactome.
Modulation of guanine nucleotides bound to Ras in NIH3T3 cells by oncogenes, growth factors, and the GTPase activating protein (GAP).
PAQR10 and PAQR11 mediate Ras signaling in the Golgi apparatus.
p37δ is a new isoform of PI3K p110δ that increases cell proliferation and is overexpressed in tumors.
Oncogenic Ras and B-Raf proteins positively regulate death receptor 5 expression through co-activation of ERK and JNK signaling.
Nilotinib and MEK inhibitors induce synthetic lethality through paradoxical activation of RAF in drug-resistant chronic myeloid leukemia.
Wnt4 inhibits cell motility induced by oncogenic Ras.
Charting the molecular links between driver and susceptibility genes in colorectal cancer.
Integrated RAS signaling defined by parallel NMR detection of effectors and regulators.
Protein interaction switches coordinate Raf-1 and MST2/Hippo signalling.
Using an in situ proximity ligation assay to systematically profile endogenous protein-protein interactions in a pathway network.
Allosteric effects of the oncogenic RasQ61L mutant on Raf-RBD.
The RAS-Binding Domain of Human BRAF Protein Serine/Threonine Kinase Exhibits Allosteric Conformational Changes upon Binding HRAS.
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.
Architecture of the human interactome defines protein communities and disease networks.
Interrogating the protein interactomes of RAS isoforms identifies PIP5K1A as a KRAS-specific vulnerability.
UBIAD1 suppresses the proliferation of bladder carcinoma cells by regulating H-Ras intracellular trafficking via interaction with the C-terminal domain of H-Ras.
GGTase3 is a newly identified geranylgeranyltransferase targeting a ubiquitin ligase.
A reference map of the human binary protein interactome.
Interactome Mapping Provides a Network of Neurodegenerative Disease Proteins and Uncovers Widespread Protein Aggregation in Affected Brains.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
A protein interaction landscape of breast cancer.
A protein network map of head and neck cancer reveals PIK3CA mutant drug sensitivity.
Systematic discovery of mutation-directed neo-protein-protein interactions in cancer.
Structure-function analysis of the SHOC2-MRAS-PP1C holophosphatase complex.
A Proteomic Approach Identifies Isoform-Specific and Nucleotide-Dependent RAS Interactions.
Multimodal cell maps as a foundation for structural and functional genomics.
Solution structure and dynamics of ras p21.GDP determined by heteronuclear three- and four-dimensional NMR spectroscopy.
Normal and oncogenic p21ras proteins bind to the amino-terminal regulatory domain of c-Raf-1.
Ras-related proteins in signal transduction and growth control.
Identification of a novel Rac1-interacting protein involved in membrane ruffling.
Ras activation in platelets after stimulation of the thrombin receptor, thromboxane A2 receptor or protein kinase C.
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a.
Protein binding and signaling properties of RIN1 suggest a unique effector function.
Mechanism of activation of the Caenorhabditis elegans ras homologue let-60 by a novel, temperature-sensitive, gain-of-function mutation.
The Ras-RasGAP complex: structural basis for GTPase activation and its loss in oncogenic Ras mutants.
Regional polysterism in the GTP-bound form of the human c-Ha-Ras protein.
Regulation of Sos activity by intramolecular interactions.
Identification of Nore1 as a potential Ras effector.
The structural basis of the activation of Ras by Sos.
Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling.
A non-farnesylated Ha-Ras protein can be palmitoylated and trigger potent differentiation and transformation.