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KLF10

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GENERAL INFORMATION

Gene name

 KLF10

Gene description

 Kruppel-like factor 10

Protein class

 Predicted intracellular proteins
Transcription factors

Predicted localization

 Intracellular

Number of transcripts

 2
SHOW MORE

HUMAN PROTEIN ATLAS INFORMATION

Summary

RNA cell category

 Expressed in all

Protein evidence

 Evidence at protein level

Main location

 Not available

DATA RELIABILITY

Reliability score

 Pending cell analysis.

ASSAYS
RNA expression

RNA EXPRESSION OVERVIEW
RNA cell line category: Expressed in all
Organ
Origin
Category
Expression
Alphabetical
Cell lines sorted after organ of phenotypic resemblance.

GENE INFORMATION

Gene name

 KLF10 (HGNC Symbol)

Synonyms

 EGRA, TIEG, TIEG1

Description

 Kruppel-like factor 10 (HGNC Symbol)

Entrez gene summary

 This gene encodes a member of a family of proteins that feature C2H2-type zinc finger domains. The encoded protein is a transcriptional repressor that acts as an effector of transforming growth factor beta signaling. Activity of this protein may inhibit the growth of cancers, particularly pancreatic cancer. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jun 2013]

Chromosome

 8

Cytoband

 q22.3

Chromosome location (bp)

 102648779 - 102655902

Protein evidence

 Evidence at protein level (all genes)

Ensembl

 ENSG00000155090 (version 83.38)

Entrez gene

 7071

UniProt

 Q13118 (UniProt - Evidence at protein level)

neXtProt

 NX_Q13118

Antibodypedia

 KLF10 antibodies

PROTEIN BROWSER
KLF10-001
KLF10-002

PROTEIN INFORMATION

Splice variant

UniProt

Protein class

Gene ontology

Length & mass

Signal peptide
(predicted)

Transmembrane regions
(predicted)
KLF10-001
ENSP00000285407
ENST00000285407
Q13118 [Direct mapping]
Krueppel-like factor 10
Show all
Predicted intracellular proteins
Transcription factors
   Zinc-coordinating DNA-binding domains
Protein evidence (Ezkurdia et al 2014)
Show all
GO:0000122 [negative regulation of transcription from RNA polymerase II promoter]
GO:0001046 [core promoter sequence-specific DNA binding]
GO:0001501 [skeletal system development]
GO:0003700 [transcription factor activity, sequence-specific DNA binding]
GO:0005515 [protein binding]
GO:0005634 [nucleus]
GO:0006351 [transcription, DNA-templated]
GO:0006355 [regulation of transcription, DNA-templated]
GO:0007179 [transforming growth factor beta receptor signaling pathway]
GO:0007267 [cell-cell signaling]
GO:0007623 [circadian rhythm]
GO:0008283 [cell proliferation]
GO:0008285 [negative regulation of cell proliferation]
GO:0009267 [cellular response to starvation]
GO:0030282 [bone mineralization]
GO:0035019 [somatic stem cell population maintenance]
GO:0042752 [regulation of circadian rhythm]
GO:0045672 [positive regulation of osteoclast differentiation]
GO:0045892 [negative regulation of transcription, DNA-templated]
GO:0046872 [metal ion binding]
GO:1901653 [cellular response to peptide]
Show all
 480 aa
52.6 kDa 		No 0
KLF10-002
ENSP00000379222
ENST00000395884
Q13118 [Direct mapping]
Krueppel-like factor 10
Show all
Predicted intracellular proteins
Transcription factors
   Zinc-coordinating DNA-binding domains
Protein evidence (Ezkurdia et al 2014)
Show all
GO:0000122 [negative regulation of transcription from RNA polymerase II promoter]
GO:0001046 [core promoter sequence-specific DNA binding]
GO:0001501 [skeletal system development]
GO:0003700 [transcription factor activity, sequence-specific DNA binding]
GO:0005515 [protein binding]
GO:0005634 [nucleus]
GO:0006351 [transcription, DNA-templated]
GO:0007179 [transforming growth factor beta receptor signaling pathway]
GO:0007267 [cell-cell signaling]
GO:0008283 [cell proliferation]
GO:0008285 [negative regulation of cell proliferation]
GO:0009267 [cellular response to starvation]
GO:0042752 [regulation of circadian rhythm]
GO:0045892 [negative regulation of transcription, DNA-templated]
GO:0046872 [metal ion binding]
Show all
 469 aa
51.4 kDa 		No 0

Contact

The Project

The Human Protein Atlas

The Human Protein Atlas project is funded
by the Knut & Alice Wallenberg foundation.