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[′hō·mē·ə‚bäks]
(cell and molecular biology)
A highly conserved sequence of deoxyribonucleic acid (DNA) that occurs in the coding region of development-controlling regulatory genes and codes for a protein domain that is similar in structure to certain DNA-binding proteins and is thought to be involved in the control of gene expression during morphogenesis and development.
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Ryan JF, Mazza ME, Pang K, Matus DQ, Baxevanis AD, Martindale MQ, Finnerty JR (2007) Pre-Bilaterian Origins of the Hox Cluster and the Hox Code: Evidence from the Sea Anemone, Nematostella vectensis.
(10) When inputs and infrastructure variables were included (kind of school, school stratification, number of teachers, school location, number of libraries, computer classrooms, laboratories, among others) following Hox, none of them help explain the variation in the adjusted average achievement among schools (See Appendix 1).
qRT-PCR: quantitative real-time polymerase chain reaction; UVB: ultraviolet B; HOTAIR: HOX antisense intergenic RNA.
For example, the formulation of a common question in the study of HOX proteins "Given the high degree of sequence conservation of the HD between HOX proteins and therefore conservation of the DNA binding sites recognized by these HDs, how do the HOX proteins function to specifically direct specific segmental identities during development?" asserts that there is phenotypic specificity of TF function; a mechanism for specificity is assumed and sought at the outset.
Therefore, we reviewed the published literature for the role of HOX genes during differentiation of three main types of SC, namely, (i) embryonic SCs, (ii) adult SCs (hematopoietic SCs, colonic SCs, and mesenchymal SCs), and (iii) induced pluripotent SCs.
These observations strongly indicate that deregulation of HOX pathways is a dominant mechanism of leukemia transformation [10, 18].
Increased Hox activity mimics the teratogenic effects of excess retinoic acid signaling.
HOX includes a critical set of genes that help control the embryo's development plan from head to toe.
As suggested by Hox (2002, p.59), all interaction effects between two continuous variables are modeled by comparing the effects of the interaction on those in the 25th and 75th percentiles of the moderating variable.
The ICCs at care group level were calculated by dividing the variation at care group level by the total variation (Hox 2002).
Thus, our present study attempted to identify HOX genes involved in LSCC pathogenesis through a HOX gene expression profile analysis.
Each vertebra embryologically formed from combination of caudal half of one sclerotome and the cranial half of succeeding sclerotome regulated by HOX genes.