LMO1 (LIM domain only 1 (rhombotin 1))

Alias (NCBI)	rhombotin 1
	RBTN1
	RHOM1
	TTG1
HGNC (Hugo)	LMO1
HGNC Alias symb	TTG1
	RHOM1
HGNC Previous name	RBTN1
HGNC Previous name	rhombotin 1
LocusID (NCBI)	4004
Atlas_Id	33
Location	11p15.4  [Link to chromosome band 11p15]
Location_base_pair	Starts at 8224309 and ends at 8263878 bp from pter ( according to GRCh38/hg38-Dec_2013)  [Mapping LMO1.png]
Local_order	Telomeric to STK33 gene; centromeric to RIC3 gene.
	LMO1 gene is located between RIC3 and STK33 genes in Chromosome 11p15. The arrow indicates the orientation of the genes.

	Structure of LMO1 gene. The gene consists of 5 exons and several splicing variants were reported.
Description	4,4 kb (from the beginning of the 1st exon to the end of the 5th exon) consisting of 5 exons.
Transcription	mRNA of approximately 700 - 1000 bp, depending on the splicing variants.
Pseudogene	Not reported.

Note
Entity	Neuroblastoma
Disease	Genome-wide association studies revealed a corelation between neuroblastoma and a single nucleotide polymorphism in LMO1 gene, rs110419 (A/G), of which the A allele was shown to promote LMO1 expression and to corelate the cases. The DNA copy number gain of the LMO1 locus due to duplication was also demonstrated to associate with the cases. These findings suggest that the gene has a role in the development and/or progression of neuroblastoma. It was also reported that LMO3 is a neuroblastoma oncogene.
Entity	Apoptosis of the gastric epithelial cells
Note	In some gastric-cancer derived cell lines, LMO1 is upregulated by TGFbeta signalling and induces their apoptosis through enhancing GSDMA expression. This TGFbeta-LMO1-GSDMA cascade is considered a mechanism for apoptosis induction in the gastric epithelial cells, and has a role in maintaining their homeostasis.
	LMO1 induces apoptosis of the pit cells in TGFbeta signalling. This function is assumed to have a role in homeostasis of the gastric epithelium.
Entity	T-cell acute lymphoblastic leukemia (T-ALL)
Disease	Originally, the LMO1 gene was identified at a break point of the translocation t(11;14)(p15;q11), which was frequently observed in T-ALL. Using LMO1 as a probe, LMO2 and LMO3 were identified. LMO1 is expressed in inmature T cells but suppressed in the mature cells, and overexpression of the gene in thymocytes, hematopoeitic progeniter cells located in the thymus, resulted in developing T-ALL in mice. LMO1 acts cooperatively with SCL (Stem cell leukemia) as a transcriptional activator or represser, dependent on the genes and the cells, and enforced expression of LMO1 and SCL in the thymocytes inhibits T-cell differentiation and causes T-ALL. It is known that the LMO1-SCL complex regulates several genes, including suppression of NFKB1 (nuclear factor of kappa light polypeptide gene enhancer in B-cells 1) and PTCRA (pre T-cell antigen receptor alpha), activation of NKX3.1 (NK3 homeobox 1).

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