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Trichostatin A (TSA, a HDAC inhibitor) addition significantly attenuates MTX unsensitivity caused by dysfunction of LMO2/ZEB1 signaling. In conclusion, these findings have identified a molecular mechanism underlying LMO2/ZEB1-mediated leukaemogenesis, paving a way for treating T-ALL with a new strategy of epigenetic inhibitors.
Genome-wide analysis indicated that LMO2 is required at the hemangioblast stage to position the TAL1/LMO2/LDB1 complex to regulatory elements that are important for the establishment of the hematopoietic developmental program.
DNM2 mutations cooperate with Lmo2 T-cell oncogenes by enhancing IL-7 signalling.
Hhex regulates Kit to promote radioresistance of self-renewing thymocytes in Lmo2-transgenic mice.
HHEX is a direct transcriptional target of LMO2 consistent with its concordant gene expression.
GATA2 and Lmo2 cooperatively regulate VEGF-induced angiogenesis and lymphangiogenesis via NRP2.
a regulatory hierarchy of HOX control of LMO2 in normal development
Lyl1 is critical for all oncogenic functions of Lmo2, including upregulation of a stem cell-like gene signature, aberrant self-renewal of thymocytes, and subsequent generation of T-cell leukemia.
A model in which the distal control region functions through a chromatin looping mechanism to contact and enhance Lmo2 transcription specifically in erythroid cells.
Studied the solution structure of Lmo2(LIM2) /Ldb1(LID) complex. Results show modular binding of tandem LIM domains in Lmo2 to tandem linear motifs in Ldb1 is accompanied by several disorder-to-order transitions/ conformational changes in both proteins.
Studies demonstrate that Etv2 is expressed during and required for yolk sac hematoendothelial development, and that Lmo2 is one of the downstream targets of Etv2.
This result raises the possibility that oncogenic Lck may activate Lmo2 promoter through direct interaction.
Data show that thymic expression of the Tal1 and Lmo2 oncogenes results in rapid development of T-ALL, and similar to T-ALL patients, more than half the leukemic mice develop spontaneous mutations in Notch1.
Notch1 mutation and Arf inactivation appear to independently cooperate in no requisite order with Lmo2 overexpression in inducing T-ALL, and all 3 events remained insufficient to guarantee immediate tumor development.
DNA-binding activity of Tal1 is not required to cooperate with Lmo2 to cause leukemia in mice
The molecular basis of Lmo2-induced T-cell acute lymphoblastic leukemia.
Results suggest that alterations in gene expression of Gata6, Tspan8, S100a8, and Lmo2 may act via novel pathways that play functionally important roles in Men1-associated tumor progression.
findings show that Lmo2 promotes the self-renewal of preleukemic thymocytes, providing a mechanism by which committed T cells can then accumulate additional genetic mutations required for leukemic transformation
there is no mandatory role for LMO2 in lymphoid development, implying that its specific role in T-cell tumorigenesis results from a reprogramming of gene expression after enforced expression in T-cell precursors
Scl/Lmo2 complex does not appear to autoregulate, as neither gene's expression is affected by depletion of the other
the data in this study revealed a novel crosstalk between LMO2 and the Wnt signaling pathway during tumorigenesis and suggested that LMO2 might be a tumor suppressor in certain solid tumors.
LMO2 has a predominantly cytoplasmic location in breast cancer cells. LMO2 interaction with cofilin1 regulates actin cytoskeleton dynamics, promoting tumor cell invasion and metastasis.
These data indicate that Lhx2 is capable of blocking proliferation of T-ALL-derived cells by both LMO2-dependent and -independent means. We propose Lhx2 as a new molecular tool for anti-T-ALL drug development.
stromal LMO2 may be responsible for zonal characteristic of Prostate cancer
The transcriptional factor LMO2 regulates endothelial proliferation and angiogenesis in vitro.
This article demonstrates a novel and unexpected function of the LMO2 oncogenic transcription factor in controlling DNA replication that we unravelled via an unbiased proteome-wide screen for LMO2-interacting partners.
Findings suggest that LMO2 loss may be a good predictor for the presence of MYC translocation in large B-cell lymphoma.
FOXP3 binds LMO2 in vitro, resulting in decreased interaction between LMO2 and TAL1, providing a molecular mechanism for FOXP3-mediated transcriptional modulation in T-ALL.
recurrent activating intronic mutations of LMO2, a prominent oncogene in T-cell acute lymphoblastic leukemia (T-ALL). Heterozygous mutations were identified in PF-382 and DU.528 T-ALL cell lines in addition to 3.7% of pediatric (6 of 160) and 5.5% of adult (9 of 163) T-ALL patient samples.
Data indicate a novel functional mechanism of LMO2 in facilitating the delivery of actin monomers to the branched microfilament and increasing lamellipodia/filopodia formation in basal-type breast cancer cells.
we demonstrate previously unrecognized mechanisms by which LMO2 alters human T-cell development in vivo; these mechanisms correlate with human T-ALL leukemogenesis.
this study revealed a novel function of LMO2 involving in the regulatory hierarchy of UBA6-USE1-FAT10ylation pathway by targeting the E1 enzyme UBA6.
LMO2 is a useful marker for immunophenotypic assessment of thymic neoplasms.
LMO2 was associated with increased levels of cytosolic p27(Kip1) protein.
that suppression of MIR223 expression, as compared with controls, is associated with lack of differentiation and adverse cytogenetic profile, but unrelated with LMO2 protein expression or overall survival.
Alanine scanning mutagenesis of the LIM interaction domain of LDB1 revealed a discrete motif, R(320)LITR, required for LMO2 binding.
LMO2 expression was elevated in GBM tissues and inversely correlated with prognosis of GBM patients. Taken together, our findings describe novel dual roles of LMO2 to induce tumorigenesis and angiogenesis.
Diagnostic Utility of the Germinal Center-associated Markers GCET1, HGAL, and LMO2 in Hematolymphoid Neoplasms.
Data show that the Lim domain only 2 (LMO2) regulatory element (element-25) region consists of transcription factor GATA2-binding myeloid ennhancer and RUNX protein-binding T-cell repressor.
Cryptic chromosomal rearrangements in the LMO2 gene were associated with T-cell acute lymphoblastic leukemia.
The transcriptional factor LMO2 regulates endothelial proliferation and angiogenesis in vitro. Furthermore, LMO2 is required for angiogenesis and tissue healing in vivo. Thus, LMO2 is a critical determinant of vascular and tissue regeneration.
a loss-of-function mutation in lmo2, a gene specifically required for hematopoiesis and vascular development, results in failure of optic fissure closure
in the absence of inducers of erythroid or myeloid haematopoiesis, Scl/Tal1-Lmo2-induced haemangioblasts differentiate into endothelial cells
Transcriptional regulation of lmo2 promoter during hematopoietic and vascular development in zebrafish is elucidated.
LMO2 encodes a cysteine-rich, two LIM-domain protein that is required for yolk sac erythropoiesis. The LMO2 protein has a central and crucial role in hematopoietic development and is highly conserved. The LMO2 transcription start site is located approximately 25 kb downstream from the 11p13 T-cell translocation cluster (11p13 ttc), where a number T-cell acute lymphoblastic leukemia-specific translocations occur. Alternative splicing results in multiple transcript variants encoding different isoforms.
, LIM domain only 2 (rhombotin-like 1)
, LIM domain only protein 2
, LIM only 2
, T-cell translocation protein 2
, cysteine-rich protein TTG-2
, T-cell translocation gene 2
, rhombotin 2
, rhombotin-like 1
, LIM domain only-2