Disease relevance of Hes5

• The levels of Hes5 mRNA decreased on days 1 and 3 after the start of reperfusion and the decreased levels of the mRNA returned to the basal level by 5 days after ischemia [1].

High impact information on Hes5

• These findings suggest that Hes5 and Mash1 may be part of the cell-intrinsic timer in the precursor cells [2].
• We show that enforced expression of Hes5 in purified precursor cells strongly inhibits the normal increase in the thyroid hormone receptor protein TR(&bgr;)1, which is thought to be part of the timing mechanism; it also strongly inhibits the differentiation induced by either mitogen withdrawal or thyroid hormone treatment [2].
• In contrast, Hes5 is expressed by a small subset of globose basal cells and by olfactory ensheathing glia in the normal mucosa; Hes5 label disappears from both transiently after lesion [3].
• Tissue exposed to D-APV for 3 days showed higher expression of Hes1 and Hes5 mRNA than did unexposed control tissue [4].

Anatomical context of Hes5

• Changes in the expression of Hes5 and Mash1 mRNA in the adult rat dentate gyrus after transient forebrain ischemia [1].
• Patterns of expression varied considerably between family members, ranging from the limited expression of Mash1 in the neurogenic SGZ of the dentate gyrus to the scattered, widespread profile of Hes5 throughout the dentate gyrus and the hippocampus proper [5].
• To elucidate the mechanism of enhanced progenitor cell proliferation induced by D-APV, we investigated expression of Hes1 and Hes5 mRNA in the ventricular zone of neocortical slices by reverse transcription-polymerase chain reaction [4].

References