Competitive combined Nav1.7/KIF5b protein binding site polypeptide structure

A protein binding site and competitive binding technology, applied in the field of competitively binding Nav1.7/KIF5b protein binding site polypeptide structure, can solve problems such as expression interference and inability to completely relieve pain, reduce abnormal upregulation, and relieve neuropathy rational pain effect

Inactive Publication Date: 2016-11-09
丁坦
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

The study also showed that: Na v Although the expression changes of 1.8 / 1.9 are related to pain sensation, interference with its expression cannot completely relieve pain

Method used

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Examples

Experimental program
Comparison scheme
Effect test

Embodiment Construction

[0031] Embodiment of the present invention is described below, and embodiment does not constitute limitation of the present invention:

[0032] Published 6 groups competitively binding Na v 1.7 / KIF5b protein binding site polypeptide structural sequence is as follows:

[0033] , ILVHSLFSMLIMCTILTNCIFMTM

[0034] , NVEYTFTGIYTFESLIKILA

[0035] , PWNWLDFVVIVFAYLTEFV

[0036] , ALRTFRVLRALKTISVIPGL

[0037] , VMILTVFCLSVFALIGLQLFMGNL

[0038] , MIFFVVVIFLGSFYLINLILAVVAMA

[0039] The modified peptide sequence can compete for the binding of Na v 1.7 / KIF5b protein binding site, highly selective reduction of Na v 1.7 Transport from cytoplasm to membrane, thereby reducing Na on DRG membrane v The abnormal up-regulation of 1.7 may alleviate the occurrence of neuropathic pain as a result.

[0040]

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PUM

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Abstract

The invention relates to the field of medicine, in particular to a competitive combined Nav1.7/KIF5b protein binding site polypeptide structure. The sequence of the structure is one of ILVHSLFSMLIMCTILTNCIFMTM, NVEYTFTGIYTFESLIKILA, PWNWLDFVVIVFAYLTEFV, ALRTFRVLRALKTISVIPGL, VMILTVFCLSVFALIGLQLFMGNL and MIFFVVVIFLGSFYLINLILAVVAMA. The modified polypeptide sequence can be competitively combined with a Nav1.7/KIF5b protein binding site, transfer of Nav1.7 from endochylema to cell membranes is highly selectively reduced, so abnormal increase of Nav1.7 on DRG cell membranes is reduced, and consequentially nerve pathological pain may be relieved.

Description

technical field [0001] The invention relates to the field of medicines, in particular to a polypeptide structure for competitively binding Nav1.7 / KIF5b protein binding sites. Background technique [0002] Neuropathic pain (NeP) is one of the common clinical chronic pains. The current clinical treatment for neuropathic pain is mainly based on drugs, but it cannot fundamentally completely shield the generation of pain. Utilizing the advanced technology of modern life science research, through molecular biology and gene interference and other technologies, in-depth study of kinesin and pain-causing key Na after nerve injury + The causal relationship between intracellular transport of channel proteins and neuropathic pain reveals the root cause of neuropathic pain and possible inhibitory targets from the perspective of intracellular transport in nerve cells. Prediction, peptide construction and modification, treatment of neuropathic pain. [0003] The study found that: Na + A...

Claims

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Application Information

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Patent Type & Authority Applications(China)
IPC IPC(8): C07K7/08C07K14/47A61K38/10A61K38/16A61P25/00
CPCC07K7/08A61K38/00C07K14/47A61K2300/00
Inventor 丁坦王哲张传健
Owner 丁坦
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