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
SSX1 - SSX Family Member 1
Alias:
SSRC
CT5.1
SPGFX5
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
这个基因的产物属于高度同源的滑膜肉瘤X(SSX)断裂蛋白家族。这些蛋白质可能作为转录抑制因子发挥作用。它们还能在癌症患者中引发自发的体液和细胞免疫反应,并成为癌症疫苗免疫治疗中的潜在有用靶点。这个基因以及SSX2和SSX4家族成员参与了t(X;18)(p11.2;q11.2)易位,这是所有滑膜肉瘤的特征性发现。这个易位导致染色体18上的滑膜肉瘤易位基因与染色体X上的一个SSX基因融合。编码的杂交蛋白质可能负责转化活性。这个基因的可变剪接导致多个转录变异体。在染色体X上已经发现了一个相关的假基因。[RefSeq,2013年7月提供]
Related ID:
NCBI:6756
ENSEMBL:ENSG00000126752
HGNC:11335
UNIPROT:Q16384
OMIM:312820
Basic Information
NCBI
Transcripts
Exons
Length
MW (kDa)
Mutations
Related Diseases
Related Mouse Models
Reference
6756
2
8
12053 bp
21.93
21
2
--
6
SSX1 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