Disease relevance of Tcf15

• Meso-substituted cationic porphyrins interact with dsDNA and exhibit different localization patterns in radiation-induced fibrosarcoma cells [1].
• Meso 2, 3, -dimercaptosuccinic acid (DMSA) has been tried successfully in animals as well as in a few cases of human lead and arsenic poisoning [2].

High impact information on Tcf15

• Requirement of the paraxis gene for somite formation and musculoskeletal patterning [3].
• Here we show that in mice homozygous for a paraxis null mutation, cells from the paraxial mesoderm are unable to form epithelia and so somite formation is disrupted [3].
• Meso1, a basic-helix-loop-helix protein involved in mammalian presomitic mesoderm development [4].
• In the medial myotome, where the expression of the myogenic factor Myf5 is required for commitment of myoblasts, the migration pattern of committed myoblasts was altered in the absence of Paraxis [5].
• This delay correlated with an absence of MyoD expression in these regions, indicating that Paraxis is required for commitment of cells from the dorsolateral dermomyotome to the myogenic lineage [5].

Biological context of Tcf15

• Differential regulation of epaxial and hypaxial muscle development by paraxis [5].
• Expression of the muscle-specific myogenin-lacZ transgene was used to examine the formation of the myotome in the paraxis-/- background [5].
• These results suggest that paraxis may regulate early events during chondrogenesis by positively directing transcription of sclerotome-specific genes [6].
• Paraxis is a basic helix-loop-helix protein that positively regulates transcription through binding to specific E-box elements [6].
• These results demonstrate that paraxis regulates somite morphogenesis, and that the function of somites is to pattern the axial skeleton and skeletal muscles [3].

Anatomical context of Tcf15

• Our data demonstrate that Paraxis is an important regulator of a subset of the myogenic progenitor cells from the dorsolateral dermomyotome that are fated to form the non-migratory hypaxial muscles [5].
• Further, in the absence of paraxis, Pax-1 is no longer expressed in the somites and presomitic mesoderm [6].
• Paraxis is a member of this subfamily, and it has been shown to regulate morphogenetic events during somitogenesis, including the transition of cells from mesenchyme to epithelium and maintaining anterior/posterior polarity [6].
• Mice deficient in paraxis exhibit a caudal truncation of the axial skeleton and fusion of the vertebrae [6].
• Paraxis expression precedes that of scleraxis in the region of the somite fated to form the axial skeleton and tendons and is able to direct transcription from an E-box found in the scleraxis promoter [6].

Associations of Tcf15 with chemical compounds

• Meso-to-meso ethyne-bridged tris[(porphinato)zinc(II)] (PZn(3)) near-infrared (NIR) fluorophores (lambda(em)(max) approximately 800 nm) can be rendered sufficiently amphiphilic to enable their facile incorporation into the hydrophobic core of the apo form of low-density lipoprotein (apo-LDL) [7].

Physical interactions of Tcf15

• Paraxis is able to bind to a set of E-boxes that overlaps with the closely related scleraxis [6].

Regulatory relationships of Tcf15

• Significantly, the regulator of adipogenesis Krüppel-like transcription factor 15 gene expression was downregulated in PKBalpha-deficient MEFs but could be restored by expressing an active PKBalpha in the deficient cells [8].

Other interactions of Tcf15

• Here we demonstrate that paraxis can function as a transcriptional activator when it forms a heterodimer with E12 [6].
• Collectively, these data indicate a role for paraxis in maintaining somite polarity that is independent of Notch signaling [9].
• Overexpressing Snail 2 in the chick embryo prevents cyclic Lfng and Meso 1 expression in the PSM and disrupts somite formation [10].

References