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suggested that the expression levels of Lmo3 and/or Hen2 could determine the fate of stem cells by inhibiting Hes1 function during nervous system development and might be a trigger of aberrant neurogenesis in vivo
These results support a role for LMO3 in regulating behavioral responses to ethanol, potentially through its actions in the nucleus accumbens.
Gbx2 (show GBX2 Proteins) regulates thalamocortical axon guidance by modifying the LIM (show PDLIM5 Proteins) and Robo codes.
when tested for behavioral responses to ethanol, transgenic mice exhibited altered ethanol sedation and consumption that correlated with Lmo3 expression levels; results suggest a role for Lmo3 in ethanol-related behaviors in mice
Results suggest that all four members of the LIM (show PDLIM5 Proteins)-only family -- LMO1 (show LMO1 Proteins), 2, 3, and 4 -- are important regulators of distinct developmental pathways.
Data show that the calcium- and integrin-binding protein CIB (show CIB1 Proteins) as an LMO3-binding protein, which binds via the second LIM (show PDLIM5 Proteins) domain (LIM2 (show LHX2 Proteins)) of LMO3.
SH3BP5 (show SH3BP5 Proteins), LMO3, and SNAP25 (show SNAP25 Proteins) were expressed in diffuse large B-cell lymphoma cells and associated with clinical features.
LMO3 attenuates GATA4 (show GATA4 Proteins)-dependent, BMP2 (show BMP2 Proteins)-mediated inflammatory endothelial activation.
MiR (show MLXIP Proteins)-101 decreased the expression of LMO3 by reversing the methylation status of the LMO3 promoter and by inhibiting the presence of the methylation-related histones H3K4me2 and H3K27me3 and increasing the presence of H3K9me3 and H4K20me3 on the promoter.
LMO3 as a regulator of human adipogenesis and could contribute a mechanism resulting in visceral-fat accumulation in obesity due to excess glucocorticoids.
suggest that LMO3 is a transcriptional signal transducer in NKX2-1 (show NKX2-1 Proteins)-amplified lung adenocarcinomas
We confirmed that the expression of LMO3 in squamous cell carcinoma is regulated by DNA methylation (show HELLS Proteins) of its specific promoter region.
The present results suggest that a transcriptional complex of LMO3 and HEN2 (show NHLH2 Proteins) may contribute to the genesis and malignant phenotype of neuroblastoma (show ARHGEF16 Proteins) by inhibiting HES1 which suppresses the transactivation of Mash1 (show ASCL1 Proteins).
LMO3 acts as a co-repressor of p53 (show TP53 Proteins), suppressing p53 (show TP53 Proteins)-dependent transcriptional regulation without inhibition of its DNA-binding activity.
The deregulated expression of neuronal-specific LMO3 and HEN2 (show NHLH2 Proteins) contributes to the genesis and progression of human neuroblastoma (show ARHGEF16 Proteins) in a lineage-specific manner.
The protein encoded by this gene belongs to the rhombotin family of cysteine-rich LIM domain oncogenes. This gene is predominantly expressed in the brain. Related family members, LMO1 and LMO2 on chromosome 11, have been reported to be involved in chromosomal translocations in T-cell leukemia. Many alternatively spliced transcript variants have been found for this gene.
LIM domain only protein 3
, LIM domain only 3 (rhombotin-like 2)
, LIM domain only 3
, lim domain only protein 3
, neuronal-specific transcription factor DAT1
, dopamine-inducible LIM-domain transcription factor DAT1
, LIM only 3
, LIM domain only protein 1