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
MAP4K4 - Mitogen-activated Protein Kinase Kinase Kinase Kinase 4
Alias:
HGK
NIK
MEKKK4
FLH21957
HEL-S-31
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
这个基因编码的蛋白质是丝氨酸/苏氨酸蛋白激酶家族的成员。这个激酶已被证明能特异性地激活MAPK8/JNK。通过这个激酶激活MAPK8被发现受到MAP3K7/TAK1、MAP2K4/MKK4和MAP2K7/MKK7的显性负突变体的抑制,这表明这个激酶可能通过MAP3K7-MAP2K4-MAP2K7激酶级联来发挥作用,并调节TNF-α信号通路。已经发现了编码不同异构体的可变剪接转录变异体。[由RefSeq,2008年7月提供]
Related ID:
NCBI:9448
ENSEMBL:ENSG00000071054
HGNC:6866
UNIPROT:O95819
OMIM:604666
Basic Information
NCBI
Transcripts
Exons
Length
MW (kDa)
Mutations
Related Diseases
Related Mouse Models
Reference
9448
51
33
196984 bp
142.10
92
--
8
20
MAP4K4 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