Lgals2 lectin, galactose-binding, soluble 2 [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: Lgals2provided by MGI
Official Full Name: lectin, galactose-binding, soluble 2provided by MGI
Primary source: MGI:MGI:895068
See related: Ensembl:ENSMUSG00000043501 AllianceGenome:MGI:895068
Gene type: protein coding
RefSeq status: VALIDATED
Organism: Mus musculus
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Glires; Rodentia; Myomorpha; Muroidea; Muridae; Murinae; Mus; Mus
Also known as: 2200008F12Rik
Summary: Predicted to enable galactoside binding activity. Predicted to be active in cytoplasm. Is expressed in yolk sac endoderm. Human ortholog(s) of this gene implicated in myocardial infarction. Orthologous to human LGALS2 (galectin 2). [provided by Alliance of Genome Resources, Apr 2022]
Expression: Biased expression in large intestine adult (RPKM 1476.0), duodenum adult (RPKM 691.2) and 8 other tissues See more
Orthologs: human all
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Genomic context

Location:: 15 E1; 15 37.7 cM

Exon count:: 4

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCm39 (GCF_000001635.27)	15	NC_000081.7 (78735060..78739729, complement)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	15	NC_000081.6 (78850860..78855529, complement)

Chromosome 15 - NC_000081.7 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Genomic Sequence:

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Expression

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See details

Project title: Mouse ENCODE transcriptome data
Description: RNA profiling data sets generated by the Mouse ENCODE project.
BioProject: PRJNA66167
Publication: PMID 25409824
Analysis date: n/a

Bibliography

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GeneRIFs: Gene References Into Functions

What's a GeneRIF?

Alternative exon splicing and differential expression in pancreatic islets reveals candidate genes and pathways implicated in early diabetes development.
Title: Alternative exon splicing and differential expression in pancreatic islets reveals candidate genes and pathways implicated in early diabetes development.
Galectin-2 (Gal-2) residues near cysteine residues C57 experienced significant chemical shift changes following S-nitrosylation.
Title: Structural mechanisms for the S-nitrosylation-derived protection of mouse galectin-2 from oxidation-induced inactivation revealed by NMR.
analysis of the effect of low-temperature plasma on the expression of galectin-1, -2, and -3 in the healing skin compared with those of electrocoagulation conducted with a high-frequency electrical coagulator
Title: Galectin expression in healing wounded skin treated with low-temperature plasma: Comparison with treatment by electronical coagulation.
Therefore, Cys(57) is suggested to be responsible for oxidative inactivation of the mGal-2 protein, and protection of the sulfhydryl group of the Cys(57) in mGal-2 by S-nitrosylation is likely important for maintaining mGal-2 protein function in an oxidative environment such as the gastrointestinal tract.
Title: Identification of the cysteine residue responsible for oxidative inactivation of mouse galectin-2.
Studies of specific knock-out mice show that galectin-2 acts through the CD14/toll-like receptor (TLR)-4 pathway. It leads to increased CD40-positive and reduced CD206-positive macrophages around remodeling collateral arteries.
Title: Galectin-2 induces a proinflammatory, anti-arteriogenic phenotype in monocytes and macrophages.
Gal-2 oxidation by H2O2 resulted in the loss of sugar-binding ability, while S-nitrosylation prevented H2O2-inducted inactivation, presumably by protecting the Cys residue(s) in the protein.
Title: S-nitrosylation of mouse galectin-2 prevents oxidative inactivation by hydrogen peroxide.
In normal murine skin, low levels of galectin-2 messenger RNA are detected.
Title: Galectin-2 suppresses contact allergy by inducing apoptosis in activated CD8+ T cells.
Galectin-2 was present in nuclei of murine 3T3 fibroblasts.
Title: Human galectin-2: nuclear presence in vitro and its modulation by quiescence/stress factors.
A comparative profiling has been started in the mouse as a model organism, combining sequence analysis, expression patterns and structural features in the cases of the homodimeric galectins-1, -2 and -7.
Title: Murine homodimeric adhesion/growth-regulatory galectins-1, -2 and -7: comparative profiling of gene/ promoter sequences by database mining, of expression by RT-PCR/immunohistochemistry and of contact sites for carbohydrate ligands by computational chemistry.

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Variation

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Alleles

Alleles of this type are documented at Mouse Genome Informatics (MGI)

Targeted (1)
Endonuclease-mediated (3)

General gene information

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Markers

Lgals2 (e-PCR), detects polymorphism
- UniSTS:516140

AI324147 (e-PCR)
- UniSTS:180789

Gene Ontology Provided by MGI

Function	Evidence Code	Pubs
enables carbohydrate binding	IBA Inferred from Biological aspect of Ancestor more info
enables galactoside binding	IBA Inferred from Biological aspect of Ancestor more info
enables galactoside binding	ISO Inferred from Sequence Orthology more info

Process	Evidence Code	Pubs
involved_in T cell homeostasis	ISO Inferred from Sequence Orthology more info
involved_in cell-cell adhesion	ISO Inferred from Sequence Orthology more info
involved_in positive regulation of apoptotic process	ISO Inferred from Sequence Orthology more info
involved_in positive regulation of inflammatory response	IDA Inferred from Direct Assay more info	PubMed

Component	Evidence Code	Pubs
part_of galectin complex	ISO Inferred from Sequence Orthology more info

General protein information

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Preferred Names: galectin-2

Names: gal-2

NCBI Reference Sequences (RefSeq)

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RefSeqs maintained independently of Annotated Genomes

These reference sequences exist independently of genome builds. Explain

These reference sequences are curated independently of the genome annotation cycle, so their versions may not match the RefSeq versions in the current genome build. Identify version mismatches by comparing the version of the RefSeq in this section to the one reported in Genomic regions, transcripts, and products above.