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Protein

Alpha-conotoxin Lo1a

Gene
N/A
Organism
Conasprella longurionis (Cone snail) (Conus longurionis)
Status
Reviewed-Annotation score: -Experimental evidence at protein leveli

Functioni

Alpha-conotoxins act on postsynaptic membranes, they bind to the nicotinic acetylcholine receptors (nAChR) and thus inhibit them. This peptide is active on neuronal nAChRs alpha-7/CHRNA7 (IC50 of 3.24 µM), alpha-3-beta-4/CHRNA3-CHRNB4, alpha-4-beta-2/CHRNA4-CHRNB2, and alpha-4-beta-4/CHRNA4-CHRNB4. 10 µM of this peptide inhibits these receptors by 85%, 40%, 19%, and 13%, respectively.1 Publication

Miscellaneous

Does not show effect on the muscle nAChRs alpha-1-beta-1-epsilon-delta/CHRNA1-CHRNB1-CHRNE-CHRND (adult subtype) and alpha-1-beta-1-gamma-delta/CHRNA1-CHRNB1-CHRNG-CHRND (fetal subtype).1 Publication

GO - Molecular functioni

Keywordsi

Molecular functionAcetylcholine receptor inhibiting toxin, Ion channel impairing toxin, Neurotoxin, Postsynaptic neurotoxin, Toxin

Names & Taxonomyi

Protein namesi
Recommended name:
Alpha-conotoxin Lo1a
OrganismiConasprella longurionis (Cone snail) (Conus longurionis)
Taxonomic identifieri1077918 [NCBI]
Taxonomic lineageiEukaryotaMetazoaLophotrochozoaMolluscaGastropodaCaenogastropodaNeogastropodaConoideaConidaeConasprellaFusiconus

Subcellular locationi

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionGraphics by Christian Stolte; Source: COMPARTMENTS

Keywords - Cellular componenti

Secreted

Pathology & Biotechi

Mutagenesis

Feature keyPosition(s)DescriptionActionsGraphical viewLength
Mutagenesisi18D → RRR: Is more potent at the alpha-7 nAChR (IC(50)=1.06 uM), and surprinsingly inhibits the adult muscle subtype alpha-1/beta-1/delta/epsilon (IC(50)=1.47 uM or 82% when 10 uM of the peptide are tested), but not the fetal subtype alpha-1/beta-1/delta/gamma. 1 Publication1
Mutagenesisi18Missing : Is more potent at the alpha-7 nAChR (IC(50)=0.80 nM), and surprinsingly inhibits the adult muscle subtype alpha-1/beta-1/delta/epsilon (IC(50)=4.40 uM or 80% when 10 uM of the peptide are tested), and the fetal muscle subtype alpha-1/beta-1/delta/gamma (38% when 10 uM of the peptide are tested). 1 Publication1

PTM / Processingi

Molecule processing

Feature keyPosition(s)DescriptionActionsGraphical viewLength
PeptideiPRO_00004301711 – 18Alpha-conotoxin Lo1a1 PublicationAdd BLAST18

Amino acid modifications

Feature keyPosition(s)DescriptionActionsGraphical viewLength
Disulfide bondi3 ↔ 91 Publication
Disulfide bondi4 ↔ 171 Publication

Keywords - PTMi

Disulfide bond

Expressioni

Tissue specificityi

Expressed by the venom duct.

Structurei

Secondary structure

118
Legend: HelixTurnBeta strandPDB Structure known for this area
Show more details

3D structure databases

SMRiX1WB75
ModBaseiSearch...
MobiDBiSearch...

Family & Domainsi

Domaini

The cysteine framework is I (CC-C-C).

Sequence similaritiesi

Belongs to the conotoxin A superfamily.Curated

Family and domain databases

InterProiView protein in InterPro
IPR009958 Conotoxin_a-typ
IPR018072 Conotoxin_a-typ_CS
PfamiView protein in Pfam
PF07365 Toxin_8, 1 hit
PROSITEiView protein in PROSITE
PS60014 ALPHA_CONOTOXIN, 1 hit

Sequencei

Sequence statusi: Complete.

Length:18
Mass (Da):1,935
Last modified:May 14, 2014 - v1
Checksum:i3B5A473B4BD1698C
GO

Mass spectrometryi

Molecular mass is 1930.12 Da from positions 1 - 18. Determined by MALDI. 1 Publication

Similar proteinsi

Entry informationi

Entry nameiCA1A_CONLG
AccessioniPrimary (citable) accession number: X1WB75
Entry historyiIntegrated into UniProtKB/Swiss-Prot: September 3, 2014
Last sequence update: May 14, 2014
Last modified: September 12, 2018
This is version 14 of the entry and version 1 of the sequence. See complete history.
Entry statusiReviewed (UniProtKB/Swiss-Prot)
Annotation programAnimal Toxin Annotation Program

Miscellaneousi

Keywords - Technical termi

3D-structure, Direct protein sequencing
UniProt is an ELIXIR core data resource
Main funding by: National Institutes of Health

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