======= LYNX1 ======= == Gene Information == * **Official Symbol**: LYNX1 * **Official Name**: Ly6/neurotoxin 1 * **Aliases and Previous Symbols**: N/A * **Entrez ID**: [[https://www.ncbi.nlm.nih.gov/gene/?term=66004|66004]] * **UniProt**: [[https://www.uniprot.org/uniprot/P0DP58|P0DP58]] * **Interactions**: [[https://thebiogrid.org/search.php?search=LYNX1&organism=9606|BioGRID]] * **PubMed articles**: [[https://www.ncbi.nlm.nih.gov/pubmed/?term=gene%20LYNX1|Open PubMed]] * **OMIM**: [[https://omim.org/entry/606110|Open OMIM]] == Function Summary == * **Entrez Summary**: N/A * **UniProt Summary**: Acts in different tissues through interaction to nicotinic acetylcholine receptors (nAChRs) (PubMed:21252236). The proposed role as modulator of nAChR activity seems to be dependent on the nAChR subtype and stoichiometry, and to involve an effect on nAChR trafficking and its cell surface expression, and on single channel properties of the nAChR inserted in the plasma membrane. Modulates functional properties of nicotinic acetylcholine receptors (nAChRs) to prevent excessive excitation, and hence neurodegeneration. Enhances desensitization by increasing both the rate and extent of desensitization of alpha- 4:beta-2-containing nAChRs and slowing recovery from desensitization. Promotes large amplitude ACh-evoked currents through alpha-4:beta-2 nAChRs. Is involved in regulation of the nAChR pentameric assembly in the endoplasmic reticulum. Shifts stoichiometry from high sensitivity alpha-4(2):beta-2(3) to low sensitivity alpha-4(3):beta-2(2) nAChR (By similarity). In vitro modulates alpha-3:beta-4-containing nAChRs. Reduces cell surface expression of (alpha-3:beta-4)(2):beta-4 and (alpha-3:beta- 4)(2):alpha-5 nAChRs suggesting an interaction with nAChR alpha- 3(-):(+)beta-4 subunit interfaces and an allosteric mode. Corresponding single channel effects characterized by decreased unitary conductance, altered burst proportions and enhanced desensitization/inactivation seem to depend on nAChR alpha:alpha subunit interfaces and are greater in (alpha-3:beta-2)(2):alpha-3 when compared to (alpha-3:beta-2)(2):alpha-5 nAChRs (PubMed:28100642). Prevents plasticity in the primary visual cortex late in life (By similarity). {ECO:0000250|UniProtKB:P0DP60, ECO:0000269|PubMed:21252236, ECO:0000269|PubMed:28100642}. |UPAR LY6| |acetylcholine receptor inhibitor activity| |ion channel inhibitor activity| |acetylcholine receptor regulator activity| |acetylcholine receptor binding| |synaptic transmission, cholinergic| |negative regulation of signaling receptor activity| |regulation of neurotransmitter receptor activity| |anchored component of membrane| |regulation of signaling receptor activity| |dendrite| |chemical synaptic transmission| |anterograde trans-synaptic signaling| |trans-synaptic signaling| |synaptic signaling| |endoplasmic reticulum| |cell-cell signaling| |negative regulation of molecular function| |membrane| \\ === CRISPR Data === No hits were found. No correlation found to any other genes in chemogenomics. Global Fraction of Cell Lines Where Essential: N/A ^Tissue^Fraction Of Cell Lines Where Essential^ == Essentiality in NALM6 == * **Essentiality Rank**: 7395 * **Expression level (log2 read counts)**: -3.42 {{:chemogenomics:nalm6 dist.png?nolink |}}