抗LMO2 (1A9-3B11)抗体 | Anti-LMO2 (1A9-3B11) Antibody

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価格

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Image

	Western Blot: LMO2 Antibody (1A9-3B11) [NB110-78626] - Detection of LMO2 in Ramos cell lysate.
	Immunocytochemistry/Immunofluorescence: LMO2 Antibody (1A9-3B11) [NB110-78626] - Immunofluorescent labeling of LMO2 (green) in tonsil tissue.
	Immunohistochemistry-Paraffin: LMO2 Antibody (1A9-3B11) [NB110-78626] - IHC analysis of formalin fixed paraffin-embedded (FFPE) human tonsil using LMO2 antibody at 1:500 on a Bond Rx autostainer (Leica Biosystems). The assay involved 20 minutes of heat induced antigen retrieval (HIER) using 10mM sodium citrate buffer (pH 6.0) and endogenous peroxidase quenching with peroxide block. The sections were incubated with primary antibody for 30 minutes and Bond Polymer Refine Detection (Leica Biosystems) with DAB was used for signal development followed by counterstaining with hematoxylin. Whole slide scanning and capturing of representative images was performed using Aperio AT2 (Leica Biosystems). Nuclear with some cytoplasmic staining was observed. Staining was performed by Histowiz.

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Background

LMO2 (LIM-only protein 2) is a nuclear transcriptional regulator essential for normal blood cell development and it exerts its effects by mediating protein-protein interactions as well as by nucleating multicomponent transcriptional complexes. LMO2 interacts with LDB1 (LIM domain binding protein 1) through the tandem LIM domains of LMO2 and LID (LIM interaction domain) of LDB1. LMO2 also interacts with bHlH proteins TAL1/SCL, BEX2 and KDM5A, and form complex with TAL1/SCL. It functions with TAL1/SCL in the regulation of RBCs development and with LDB1 to maintain erythroid precursors in immature state. LMO2 has been associated with the maintenance of hematopoietic stem cells, RBCs differentiation, and angiogenesis in both normal development as well as during carcinogenesis. Disruption of LMO2 in mice causes death in midway through embryonic development as they do not develop RBCs. Excessive expression of LMO2 in T-cells, through either chromosomal translocations or retroviral insertion of gene therapy vectors, as well as transgenic overexpression of LMO2 in mouse model leads to the onset of T-cell acute lymphoblastic leukemia (T-ALL).

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