Disease relevance of DLX4

• Coexpression of BP1, DLX7 and DLX4 occurred in a significant number of leukemias [1].
• Elevated levels of DLX4 mRNA were detected in a choriocarcinoma derived cell line when compared with a cytotrophoblast cell line and normal placenta [2].
• MATERIALS AND METHODS: Expression of homeodomain proteins DLX4 and HB9 was detected by RT-PCR and immunohistochemically in 24 breast tumors and their corresponding non-malignant tissue [3].
• Further studies demonstrated an inverse correlation between the binding affinity of the BP1 protein for the distal beta-globin silencer sequence and the severity of sickle cell anemia, suggesting a possible role for BP1 in determining the production of hemoglobin S [4].
• Inhibition of beta protein 1 expression enhances beta-globin promoter activity and beta-globin mRNA levels in the human erythroleukemia (K562) cell line [5].

Psychiatry related information on DLX4

• OBJECTIVE: Beta-blocking agents, particularly propranolol, are considered effective in the treatment of neuroleptic-induced akathisia, but considerable controversy exists about the involved receptor subtype(s) [6].
• Oscillatory Beta Activity Predicts Response Speed during a Multisensory Audiovisual Reaction Time Task: A High-Density Electrical Mapping Study [7].
• CONCLUSIONS: Our results confirm that Beta activity is increased in Primary Insomnia [8].
• Future studies in composite transgenic mice developing amyloid plaques, neurofibrillary tangles, and other AD pathology may allow for the determination of the relative contribution of A Beta and non-A Beta components to dementia [9].
• 3. Beta blockers appear to be of use in specific social phobias, like public speaking [10].

High impact information on DLX4

• BACKGROUND & AIMS: Beta-blockers are extensively used to prevent variceal bleeding in patients with large esophageal varices [11].
• BACKGROUND: Beta-blockers and amiodarone reduce the frequency of atrial fibrillation after open-heart surgery but the effectiveness of oral amiodarone in older patients already receiving beta-blockers is unknown [12].
• The relation of treatment adherence to mortality after a myocardial infarction was investigated among 2175 participants in the Beta Blocker Heart Attack Trial, which had data for measures of treatment adherence, clinical severity, and the psychological and social features that may influence post-infarction mortality [13].
• Letter: Beta blocker and blood viscosity [14].
• The results with the Beta isomer consistently indicated that the membranes of DS lysosomes were more rigid than the D samples [15].

Chemical compound and disease context of DLX4

• S100-Beta, melanoma-inhibiting activity, and lactate dehydrogenase discriminate progressive from nonprogressive American Joint Committee on Cancer stage IV melanoma [16].
• Thus, in response to the two days of basal hyperglycaemia, both the basal and stimulated Beta-cell responses were enhanced and there was no evidence for 'glucose toxicity' to the Beta-cells [17].
• Evasion of host defenses by measles virus: wild-type measles virus infection interferes with induction of Alpha/Beta interferon production [18].
• Effect of Beta blockers, particularly carvedilol, on reducing the risk of events after acute myocardial infarction [19].
• Aim of this work was to evaluate the influence of obesity on the kinetics and the antihypertensive effect of two Beta-blockers with different solubility such as: the water-soluble, atenolol and the liposoluble, metoprolol [20].

Biological context of DLX4

• Using fluorescence in situ hybridisation (FISH), DLX4 has been assigned to human chromosome 17q21-q22 [21].
• We predict that DLX3 and DLX4 are closely linked and have arisen through gene duplication and divergence from a common ancestral precursor [21].
• It is predicted that a similar combination of homeobox genes, that includes DLX4, is involved in regulating epithelial-mesenchymal cell interactions in extraembryonic tissues [2].
• Northern analysis revealed two DLX4 transcripts in first trimester placenta of 2.8 and 3.0 kb [2].
• In-situ mRNA hybridization experiments were used to show differential expression of DLX4 at different phases of the endometrial cycle [22].

Anatomical context of DLX4

• DLX4 may also have a role in the regulation of the genes important for trophoblast invasion since the level of expression in trophoblast cell lines reflects invasive potential [2].
• In term placenta, DLX4 was expressed in the syncytiotrophoblast [2].
• Higher levels of DLX4 expression were observed in proliferative phase endometrial epithelium compared with secretory phase endometrial epithelium [22].
• Homeobox genes DLX4 and HB24 are expressed in regions of epithelial-mesenchymal cell interaction in the adult human endometrium [22].
• In situ hybridization studies at first trimester human placental sections revealed that DLX4 was expressed predominantly in the cytotrophoblast stem cell layer [2].

Associations of DLX4 with chemical compounds

• Induction of apoptosis by fenretinide in tumor cell lines correlates with DLX2, DLX3 and DLX4 gene expression [23].
• SETTING: 25 hospitals or clinical settings in the United States and Canada that participated in the Beta Blocker Heart Attack Trial, including the Health Insurance Plan substudy [24].
• The BP-1/6C3 antigen is a phosphorylated cell surface glycoprotein that can be identified by monoclonal antibodies on mouse pre-B cells, immature B cells, and certain stromal cell lines from bone marrow [25].
• We analyzed two mutations that affect fruit pigmentation in tomato (Lycopersicon esculentum): Beta (B), a single dominant gene that increases beta-carotene in the fruit, and old-gold (og), a recessive mutation that abolishes beta-carotene and increases lycopene [26].
• Binding of YY1 to the Proximal Region of the Murine Beta Interferon Promoter Is Essential To Allow CBP Recruitment and K8H4/K14H3 Acetylation on the Promoter Region after Virus Infection [27].

Physical interactions of DLX4

• Strong linkage disequilibrium of a HbE variant with the (AT)9(T)5 repeat in the BP1 binding site upstream of the beta-globin gene in the Thai population [28].
• HMG-I(Y) also binds to a second oligonucleotide containing a BP1 binding site located in a negative control region upstream of the delta-globin gene, suggesting a role for HMG-I(Y) in repression of adult globin genes [29].

Regulatory relationships of DLX4

• Thus, we conclude that DLX-7 is expressed in hematopoietic cells and that the inhibition of its expression results in the decreased levels of GATA-1 and c-myc genes, with an accompanying induction of apoptosis [30].

Other interactions of DLX4

• BP1, a homeodomain-containing isoform of DLX4, represses the beta-globin gene [4].
• Isolation and identification of homeobox genes from the human placenta including a novel member of the Distal-less family, DLX4 [21].
• The comparison of MSX-2, DLX-5, and DLX-7 expression patterns during the early stages of development of different human tooth types showed the existence of spatially ordered sequences of homeogene expression along the vestibular/lingual axis of dental epithelium [31].
• To establish some relationships between those reported human syndromes, previous experimental data in mice, and the expression patterns of MSX and DLX homeogenes in the human dentition, we investigated MSX-2, DLX-5, and DLX-7 expression patterns and compared them in orofacial tissues of 7.5- to 9-wk-old human embryos by using in situ hybridization [31].
• Protein-binding analysis reveals that the 5' region contains three elements bound by trans-acting factors, beta-protein 1 (BP1) and beta-protein 2 (BP2) [32].

Analytical, diagnostic and therapeutic context of DLX4

• Antibodies were raised to the homeodomain proteins DLX4, HB9 and HB24 and immunohistochemistry was performed on 3 moderately-differentiated tumors and their corresponding non-malignant colon tissue samples [33].
• We mapped this new distal-less family member BP1 to chromosome 17q21-22 by FISH and PCR, which is the same locus to which DLX7 has been mapped [34].
• Mobility shift assays demonstrated that both BP1 and DLX7 proteins, synthesized in vitro, bind to the same BP1 binding site [34].
• Sequence analyses of the DLX3 and DLX7 genes suggest AIHHT is not due to genetic mutations or polymorphisms in the exons of these genes [35].
• Site-directed mutagenesis of binding sites for the repressor proteins BP1 and BP2 in the upstream portion of the beta globin gene flanking region led to a 4-6 fold increase in promoter activity [36].

References