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GeneQ18028594· pop 5· linked from 7 articles

Also known as DLG4, HUGL, HUGL-1, HUGL1, LLGL, Lgl1, Mgl1, LLGL1, scribble cell polarity complex component

Lethal(2) giant larvae protein homolog 1 is a protein that in humans is encoded by the LLGL1 gene.

In the Vinony graph

Vinony's link graph records 7 inbound references to LLGL1, and connects out to PubMed, human chromosome 17 and Ensembl genome database project.

It is catalogued under the topic Genes on human chromosome 17.

Vinony links it to 5 Wikipedia language editions.

Gene data

LLGL1
Name
LLGL scribble cell polarity complex component 1
Type
protein-coding
Position
18,225,542–18,244,876 (+)
Aliases
DLG4, HUGL, HUGL-1, HUGL1, LLGL, Lgl1, Mgl1
RefSeq RNA
NM_004140.4, XM_011523849.3, XM_011523850.3, XM_011523851.3, XM_011523852.3
RefSeq protein
NP_004131.4, XP_011522151.1, XP_011522152.1, XP_011522153.1, XP_011522154.1

This gene encodes a protein that is similar to a tumor suppressor in Drosophila. The protein is part of a cytoskeletal network and is associated with nonmuscle myosin II heavy chain and a kinase that specifically phosphorylates this protein at serine residues. The gene is located within the Smith-Magenis syndrome region on chromosome 17. [provided by RefSeq, Jul 2008].

via MyGene.info

Wikidata facts

Instance of
gene
Show 8 more facts
HomoloGene ID
31220
found in taxon
Homo sapiens
genomic start
18225635
genomic end
18148189
cytogenetic location
17p11.2
expressed in
caudate nucleus
Sources (4)

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Encyclopedic overview

2 sections
Contents
  • References
  • Further reading

Lethal(2) giant larvae protein homolog 1 is a protein that in humans is encoded by the LLGL1 gene.

This gene encodes a protein that is similar to a tumor suppressor in Drosophila. The protein is part of a cytoskeletal network and is associated with nonmuscle myosin II heavy chain and a kinase that specifically phosphorylates this protein at serine residues. The gene is located within the Smith-Magenis syndrome region on chromosome 17.

Excerpted from Wikipedia’s “LLGL1” article, available under the CC BY-SA 4.0 licence.

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