Difference between revisions of "MIAT"
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MIAT knockdown could affect the proliferation,apoptosis and migration of Human lens epithelial cells (HLECs) upon oxidative stress <ref name="ref1" />. | MIAT knockdown could affect the proliferation,apoptosis and migration of Human lens epithelial cells (HLECs) upon oxidative stress <ref name="ref1" />. | ||
Revision as of 14:37, 29 June 2016
Contents
Characteristics
MIAT, was specifically up-regulated both in the plasma fraction of whole blood and aqueous humor of cataract patients [1].
Cellular Localization
In epithelial cell.[1].
Function
Figure 1.LncRNA‐MIAT is shown as a cataract‐specific biomarker. [1].
MIAT knockdown could affect the proliferation,apoptosis and migration of Human lens epithelial cells (HLECs) upon oxidative stress [1].
MIAT acted as a ceRNA, and formed a feedback loop with Akt and miR-150-5p to regulate HLEC function [1].
Regulation
MTT assay revealed that MIAT knockdown significantly decreased the HLEC viability.[1].
Diseases
- Neuroendocrine prostate cancer (NEPC)
Expression
LncRNA-MIAT was significantly up-regulated in cataractous lenses [1].
Labs working on this lncRNA
- Eye Hospital, Nanjing Medical University, Nanjing, China.
- The Fourth School of Clinical Medicine, Nanjing Medical University, Nanjing, China.
