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ARL4D

CANCER ATLAS

Gene description

 ADP-ribosylation factor-like 4D

Protein class

 Predicted intracellular proteins

Protein evidence

 Evidence at protein level
Colorectal cancer
Breast cancer
Prostate cancer
Lung cancer
Liver cancer

STAINING SUMMARY
HPA060379

GENE INFORMATION

Gene name

 ARL4D (HGNC Symbol)

Synonyms

 ARF4L

Description

 ADP-ribosylation factor-like 4D (HGNC Symbol)

Entrez gene summary

 ADP-ribosylation factor 4D is a member of the ADP-ribosylation factor family of GTP-binding proteins. ARL4D is closely similar to ARL4A and ARL4C and each has a nuclear localization signal and an unusually high guanine nucleotide exchange rate. This protein may play a role in membrane-associated intracellular trafficking. Mutations in this gene have been associated with Bardet-Biedl syndrome (BBS). [provided by RefSeq, Jul 2008]

Chromosome

 17

Cytoband

 q21.31

Chromosome location (bp)

 43398959 - 43401137

Protein evidence

 Evidence at protein level (all genes)

Ensembl

 ENSG00000175906 (version 83.38)

Entrez gene

 379

UniProt

 P49703 (UniProt - Evidence at protein level)

neXtProt

 NX_P49703

Antibodypedia

 ARL4D antibodies

PROTEIN BROWSER
ARL4D-001

PROTEIN INFORMATION

Splice variant

UniProt

Protein class

Gene ontology

Length & mass

Signal peptide
(predicted)

Transmembrane regions
(predicted)
ARL4D-001
ENSP00000322628
ENST00000320033
P49703 [Direct mapping]
ADP-ribosylation factor-like protein 4D
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Predicted intracellular proteins
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GO:0003924 [GTPase activity]
GO:0005515 [protein binding]
GO:0005525 [GTP binding]
GO:0005622 [intracellular]
GO:0005634 [nucleus]
GO:0005730 [nucleolus]
GO:0005737 [cytoplasm]
GO:0005886 [plasma membrane]
GO:0006886 [intracellular protein transport]
GO:0007165 [signal transduction]
GO:0007264 [small GTPase mediated signal transduction]
GO:0009306 [protein secretion]
GO:0015031 [protein transport]
GO:0016020 [membrane]
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 201 aa
22.2 kDa 		No 0

Contact

The Project

The Human Protein Atlas

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