Home
Toolbox
Resource
Workflow
Tutorials
Citations
Downloads
Mutation Al-Predictor Flow
Gene-to-Mutation Flow
News & Insights
Genetic Encyclopedia
Frontiers
Industry Insights
Case Studies
About Us
About the Site
Contact Us
Private Policy
User Agreement
COL4A5 c.1390G>A
ALS1
DMD c.1332-11868C>G
TP53
肌萎缩侧索硬化症1型
USH2A c.8559-2A>G
囊性纤维化
Log In
|
Sign Up
中文
人类
PDIA3 - Protein Disulfide Isomerase Family A Member 3
Alias:
P58
ER60
ERp57
ERp60
ERp61
GRP57
GRP58
PI-PLC
HsT17083
HEL-S-269
HEL-S-93n
Create a favorites folder
Cancel
Confirm
Add To Favorites
Select a favorites
Description
New favorites >>
Cancel
Confirm
Favorite
Basic Information
Sequence Homology
Related Diseases and Mutations
Transcripts & Proteins
Gene Expression
Interactions
Related Mouse Models
Related Drugs
References Literature
这个基因编码一个内质网蛋白,可以与凝集素分子伴侣钙网蛋白和钙联蛋白相互作用,调节新生合成糖蛋白的折叠。这个蛋白曾被认为是磷酸脂酶;然而,已经证明这个蛋白实际上具有蛋白二硫键异构酶活性。人们认为,凝集素和这个蛋白的复合物通过促进其糖蛋白底物中二硫键的形成,来调节蛋白质折叠。这个蛋白还具有防止蛋白质聚集的分子伴侣功能。[RefSeq, 2016年12月提供]
Related ID:
NCBI:2923
ENSEMBL:ENSG00000167004
HGNC:4606
UNIPROT:P30101
OMIM:602046
Basic Information
NCBI
Transcripts
Exons
Length
MW (kDa)
Mutations
Related Diseases
Related Mouse Models
Reference
2923
1
13
26841 bp
56.78
33
--
7
34
PDIA3 Genetics information (+)
GRCh38
Sequence Homology
Related Diseases and Mutations
#
Disease
Anatomical Category
Score
Mutations
No data available
Transcripts & Proteins
Table View
Tile View
#
Transcript
Length(nt)
Exon Count
CDS(bp)
Protein
Length(aa)
No data available
* This data comes from NCBI.
Gene Expression
Tissue-specific RNA expression
Organ
Abundance
Alphabetical
Cell-specific RNA expression
Organ
Abundance
Alphabetical
Interactions
Reset
Acting
Regulation
Detail
Mechanism
Target
Residues
Reference
Score
No data available
Related Mouse Models
Type
Name
MGI
Strain of Origin
Publications
Mutations
No data available
Related Drugs
Name
CAS Number
Status
Phase
Link
No data available
References Literature
Title
PMID
Journal
Year
IF
No Data Found!
Wechat
Mutation Direct
Sequence
Comparison
Al agent
Tutorials
Back to top