Disease relevance of DLX2

• In leukemic patients affected by the t(4;11)(q21;q23) chromosomal abnormality, the expression of DLX2, DLX3, and DLX4 was virtually abrogated [1].
• In addition, the initial assignments into sFv pools based on phage ELISA readings allowed the segregation of individual anti-TES1 sFvs into discrete or minimally overlapping intrabody pools [2].
• Establishment and characterization of human immature teratoma cell line (TES-1) [3].

High impact information on DLX2

• Upon integration into the striatal GZ, cortical stem cells down-regulate Emx1 and up-regulate Dlx2, which is a homeobox gene characteristic of the developing striatum and striatal neural stem cells [4].
• Altogether these data suggest a molecular mechanism for tooth development involving Dlx2 gene expression in ARS patients [5].
• From isolated clones in the 30N and 60N size groups, two predominant RNA sequences, TES1 (30N) and TES33 (60N), have been shown to catalyze the synthesis of different thioesters using various acyl adenylates as the substrates [6].
• A zebrafish forebrain-specific zinc finger gene can induce ectopic dlx2 and dlx6 expression [7].
• We report the expression of neurexin 1, Neuro D1, dlx1, and dlx2 in untreated and cAMP treated epithelial prostate cells [8].

Biological context of DLX2

• Induction of apoptosis by fenretinide in tumor cell lines correlates with DLX2, DLX3 and DLX4 gene expression [9].
• Our data support the notion that DLX2, 3, 4 genes could participate in the control of 4HPR-mediated apoptosis, making them important molecules for the monitoring of therapy efficacy in cancer patients [9].
• DLX2 (TES1), a homeobox gene of the Distal-less family, assigned to conserved regions on human and mouse chromosomes 2 [10].
• Dlx2, Lymphoid Enhancer Factor (Lef-1) and Msx2 transcription factors are required for several developmental processes [11].
• The Dlx2 and Dlx5 homeobox genes have been shown to be critical for bone formation both in vitro and in vivo [12].

Anatomical context of DLX2

• Using cell-specific markers and antibodies to ventral homeodomain transcription factors, NKX2.1 and DLX2, we show here that a subpopulation of early oligodendrocyte progenitor cells (OPCs) in the human telencephalon may originate in the ganglionic eminence (GE) [13].
• Dlx2 activates the Msx2 promoter in several cell lines and binds DNA as a monomer and dimer [11].
• Immunohistochemical analysis revealed that necdin was coexpressed with Dlx2, Dlx5, or MAGE-D1 in a subpopulation of embryonic forebrain cells [14].
• Lateral cells appearing to emanate from r4 express both hoxb2 and dlx2, suggesting that they are neural crest [15].
• PITX2 binds to bicoid and bicoid-like elements in the Dlx2 promoter and activates this promoter 45-fold in CHO cells [16].

Other interactions of DLX2

• Forced expression of fez induces ectopic expression of dlx2 and dlx6, two genes involved in brain development [7].
• To understand the control of gene expression by these factors, chromatin immunoprecipitation (ChIP) assays identified Msx2 as a downstream target of Dlx2 and Lef-1 [11].

Analytical, diagnostic and therapeutic context of DLX2

• To identify co-factors that regulate DLX function we utilized the yeast two-hybrid assay, and found a DLX interacting protein (DIP2) which binds to the N-terminal region of DLX2 via a PDZ domain [17].
• Co-immunoprecipitation and protein pull-down experiments demonstrate Lef-1 physically interacts with Dlx2 [11].

References