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Retinoic acid (simplified nomenclature for all-trans-retinoic acid) is a metabolite of vitamin A 1 (all-trans-retinol) that is required for embryonic development, male fertility, regulation of bone growth and immune function. [2] All-trans-retinoic acid is required for chordate animal development, which includes all higher animals from fish to ...
Establishment of the forelimb field (but not hindlimb field) requires retinoic acid signaling in the developing trunk of the embryo from which the limb buds emerge. [ 2 ] [ 3 ] Also, although excess retinoic acid can alter limb patterning by ectopically activating Shh or Meis1/Meis2 expression, genetic studies in mouse that eliminate retinoic ...
This endoplasmic reticulum protein acts on retinoids, including all-trans-retinoic acid (RA), with both 4-hydroxylation and 18-hydroxylation activities. This enzyme regulates the cellular level of retinoic acid which is involved in regulation of gene expression in both embryonic and adult tissues.
Retinoic acid via the retinoic acid receptor influences the process of cell differentiation and, hence, the growth and development of embryos. During development, there is a concentration gradient of retinoic acid along the anterior-posterior (head-tail) axis. Cells in the embryo respond to retinoic acid differently depending on the amount present.
The hindbrain, for example, is patterned by Hox genes, which are expressed in overlapping domains along the anteroposterior axis under the control of retinoic acid. The 3 ′ (3 prime end) genes in the Hox cluster are induced by retinoic acid in the hindbrain, whereas the 5 ′ (5 prime end) Hox genes are not induced by retinoic acid and are ...
During development, retinoic acid, a metabolite of vitamin A, is used to stimulate the growth of the posterior end of the organism. [12] Retinoic acid binds to retinoic acid receptors that acts as transcription factors to regulate the expression of Hox genes. Exposure of embryos to exogenous retinoids especially in the first trimester results ...
This enzyme is involved in the catabolism of all-trans- and 9-cis-retinoic acid, and thus contributes to the regulation of retinoic acid levels in cells and tissues. [6] CYP26C1 was found to show no expression in colorectal cancer cells or normal colonic epithelium. [7]
Although endogenous retinoic acid is required in higher vertebrates to limit the caudal Fgf8 domain needed for somitogenesis in the trunk (but not tail), some studies also point to a possible role of retinoic acid in ending somitogenesis in vertebrates that lack a tail (human) or have a short tail (chick). [16]