Disease relevance of Hlxb9

• We constructed a lentivirus vector to express HB9 and GFP in NSCs and examined the consequences of HB9 expression on other transcription factors and cell differentiation [1].

High impact information on Hlxb9

• Thus, Hlxb9 is key to normal pancreas development and function [2].
• During mouse development, the dorsal and ventral pancreatic buds and mature beta-cells in the islets of Langerhans express Hlxb9 [2].
• In absence of Hlxb9 expression, the dorsal region of the gut epithelium fails to initiate a pancreatic differentiation program [3].
• Thus, dorsally Hlxb9 is required for specifying the gut epithelium to a pancreatic fate and ventrally for ensuring proper endocrine cell differentiation [3].
• Presumptive MN progenitors and postmitotic MNs express HB9, whereas only a small population of interneurons located ventrally to the central canal express this factor [4] [5].

Biological context of Hlxb9

• The homeobox gene Hlxb9, which is essential for the initiation of the pancreatic program in the dorsal foregut endoderm, is still expressed in Raldh2--/-- dorsal epithelium but the number of HB9-expressing cells is severely reduced [6].
• In contrast, simultaneous transfection of Ngn2 and HB9 cDNA increased the expression of Isl1/2, a motoneuron marker, when the cells were maintained in medium supplemented with retinoic acid, forskolin, and sonic hedgehog [7].
• In the transgenic mice used in our study, the HB9 promotor controlled the expression of the reporter gene enhanced green fluorescent protein (eGFP), giving rise to GFP+ motoneurons and ventral interneurons [8].
• These results indicate that HB9 protein might be involved in chick tarsometatarsal scale and feather development and that nuclear import of HB9 protein might be regulated by these NLS sequences in the homeodomain [9].
• ES cells were obtained from a transgenic mouse line in which the gene for enhanced green fluorescent protein (eGFP) is expressed under the control of the promotor of the MN specific homeobox gene Hb9 [10].

Anatomical context of Hlxb9

• Persistent expression of Hlxb9 in the pancreatic epithelium impairs pancreatic development [11].
• Requirement for the homeobox gene Hb9 in the consolidation of motor neuron identity [12].
• In embryonic chick spinal cord, the ectopic expression of MNR2 or Hb9 is sufficient to trigger MN differentiation and to repress the differentiation of an adjacent population of V2 interneurons [12].
• Forced expression of the motor neuron determinant HB9 in neural stem cells affects neurogenesis [1].
• Coculture of NSFCs trans-fected with Ngn2-HB92 or Olig2 and HB9 with purified chicken skeletal muscle demonstrated frequent contacts that resembled neuromuscular junctions [7].

Associations of Hlxb9 with chemical compounds

• The expression of the vesicular glutamate transporter 2 in axon terminals of HB9/GFP interneurons indicated that these were glutamatergic interneurons [8].

Other interactions of Hlxb9

• 5. At earlier stages, only a dorsal bud rudiment forms transiently and expresses the transcription factors Ipf1 and Hlxb9 but lacks the key transcription factor involved in the acquisition of a pancreatic fate, Ptf1a, as well as all endocrine precursor cells [13].
• We showed that all these factors were present in neural progenitors derived from mouse ES cells, whereas NSCs derived from the rat embryonic spinal cord expressed neither HB9 nor Islet1 and contained low levels of Nkx6.1 and LIM3 [1].
• NSFCs transfected with Olig2, Ngn2, and HB9 alone exhibited no phenotypic lineage restriction [7].

Analytical, diagnostic and therapeutic context of Hlxb9

• Furthermore, we observed precise distribution of HB9 protein by immunoelectron microscopy [9].

References