Peptide record

TPDB71934

Neurotoxin standard
90 amino acids
Basic Information
3D PDB MODEL
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TPDB71934
Neurotoxin
Toxicity and safety peptides
NTxPred2
standard
No
A 90-aa standard natural neurotoxin peptide sequence curated from NTxPred2, with an available 3D structural model.
Sequence
MKTAMLIAVLGFCAALCFVESSHEEEREAAVYLTDLVSKAESAIKRGIPCRCDKNSDELNGEQSYMNGNCGDGWKKCRSVNAIFNCCQRV
Physicochemical Analysis
C420H674N122O134S11
A
9929.37
5.68
12
12
34
-1
21.97
-0.192
72.67
Mammalian: 30 hour Yeast: >20 hour E.coli: >10 hour
8980
90.44
27
Residue Composition
number
9
A
5
R
6
N
4
D
8
C
8
E
2
Q
6
G
1
H
4
I
6
L
6
K
3
M
3
F
1
P
7
S
2
T
1
W
2
Y
6
V
Amino Acid Distribution
A: 9 R: 5 N: 6 D: 4 C: 8 E: 8 Q: 2 G: 6 H: 1 I: 4 L: 6 K: 6 M: 3 F: 3 P: 1 S: 7 T: 2 W: 1 Y: 2 V: 6
Chemical Descriptors
90
C420H674N122O134S11
9929.37
5.68
-1
21.97
-0.192
Evidence Records 1 records
Evidence 1 Activity

Activity

Neurotoxin
FUNCTION: Cardioactive peptide that acts on voltage-gated sodium channels (hNav1.5/SCN5A) and voltage-gated potassium channels (Kv) (PubMed:23356888, PubMed:24749540). The activity on sodium channels consists of inhibition on sodium current inactivation with no significant effect on current activation. This effect may be caused by direct interaction of the toxin with sodium channel site-3 (PubMed:23356888, PubMed:24749540). The activity on potassium channels consists of a significant increase of the amplitude of the transient component of the potassium current, shifting the current threshold to more negative membrane potentials. These effects are concentration-dependent and reversible and may be due to a direct interaction between the toxin and the voltage-sensing domain of the channel (PubMed:24749540). Physiologically, this toxin increases the amplitude of cardiomyocyte contraction and slows the late phase of the twitch relaxation velocity with no induction of spontaneous twitching. It increases action potential duration of cardiomyocytes with no effect on its threshold and on the cell resting potential. On insects, it shows neurotoxic activity to the blowfly larvae S.falculaty, causing an immediate spasm that progressed to body contraction and paralysis. {ECO:0000269|PubMed:23356888, ECO:0000269|PubMed:24749540}.

Target

voltage-gated sodium channel (Nav) voltage-gated potassium channel (Kv) proton-gated sodium channel / ASIC

Source & Reference

NA
UniProtKB/Swiss-Prot Tox-Prot

Other

Exaiptasia diaphana (Tropical sea anemone) (Aiptasia pulchella)
Neurotoxin Ion channel impairing toxin Potassium channel impairing toxin Voltage-gated potassium channel impairing toxin Voltage-gated sodium channel impairing toxin
Cardioactive peptide that acts on voltage-gated sodium channels (hNav1.5/SCN5A) and voltage-gated potassium channels (Kv) (PubMed:23356888, PubMed:24749540). The activity on sodium channels consists of inhibition on sodium current inactivation with no significant effect on current activation.
Delta-aiptatoxin-Adi1a (Delta-ATTX-Adi1a) (Ion channel modifier Ade-1) (Ade1)
sea anemone
Sea anemone sodium channel inhibitory toxin family
Evidence at protein level
Cleavage on pair of basic residues Direct protein sequencing Disulfide bond Ion channel impairing toxin Myotoxin Nematocyst Neurotoxin Potassium channel impairing toxin Reference proteome Secreted Signal Toxin Voltage-gated potassium channel impairing toxin Voltage-gated sodium channel impairing toxin
Additional Detail Fields 6 fields
Cleavage on pair of basic residues Direct protein sequencing Disulfide bond Ion channel impairing toxin Myotoxin Nematocyst Neurotoxin Potassium channel impairing toxin Reference proteome Secreted Signal Toxin Voltage-gated potassium channel impairing toxin Voltage-gated sodium channel impairing toxin
Neurotoxin Ion channel impairing toxin Potassium channel impairing toxin Voltage-gated potassium channel impairing toxin Voltage-gated sodium channel impairing toxin
Evidence at protein level
Sea anemone sodium channel inhibitory toxin family
Delta-aiptatoxin-Adi1a (Delta-ATTX-Adi1a) (Ion channel modifier Ade-1) (Ade1)
sea anemone