Difference between revisions of "LINC01826"
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LINC01826:long intergenic non-protein coding RNA 1826 | LINC01826:long intergenic non-protein coding RNA 1826 | ||
| − | lnc-MKI67IP-3 | + | lnc-MKI67IP-3 <ref name="ref1" /> |
| − | |||
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===Cellular Localization=== | ===Cellular Localization=== | ||
| − | Lnc-MKI67IP-3 is primarily localized in the cytoplasm | + | Lnc-MKI67IP-3 is primarily localized in the cytoplasm <ref name="ref1" />. |
| + | |||
===Function=== | ===Function=== | ||
[[File:LncRNA-MKI167-3.JPG|right|thumb|400px|'''Lnc-MKI67IP-3 could bind to let-7e as a miRNA sponge''' <ref name="ref1" />.]] | [[File:LncRNA-MKI167-3.JPG|right|thumb|400px|'''Lnc-MKI67IP-3 could bind to let-7e as a miRNA sponge''' <ref name="ref1" />.]] | ||
| − | + | ||
| + | These results indicate that Lnc-MKI67IP-3 might play important roles in the inflammatory responses of VECs and development of atherosclerosis <ref name="ref1" />. Lnc-MKI67IP-3 acts as a sponge or competing endogenous RNA (ceRNA) for let-7e, suppressing its pro-inflammatory effects, and let-7e decreased lnc-MKI67IP-3 expression, thereby forming a positive feedback loop to aggravate inflammation <ref name="ref1" />. Moreover, lnc-MKI67IP-3 is also abnormal in oxLDL-treated VECs and atherosclerotic plaques <ref name="ref1" />. | ||
===Regulation=== | ===Regulation=== | ||
| − | Let-7e mimic significantly down-regulate lnc-MKI67IP-3 expression, while let-7e inhibitor markedly up-regulate this expression and let-7e inhibitor could be considered as an inducer of lnc-MKI67IP-3, just like vitamin C.<ref name="ref1" /> | + | Let-7e mimic significantly down-regulate lnc-MKI67IP-3 expression, while let-7e inhibitor markedly up-regulate this expression and let-7e inhibitor could be considered as an inducer of lnc-MKI67IP-3, just like vitamin C <ref name="ref1" />. |
| + | |||
| + | ===Expression=== | ||
| + | In human umbilical vein endothelial cells (HUVECs) treated with ox-LDL for different times, lnc-MKI67IP-3 is significantly down-regulated <ref name="ref1" />. | ||
| + | |||
===Diseases=== | ===Diseases=== | ||
| − | Inflammatory response in vascular endothelial cells | + | Inflammatory response in vascular endothelial cells, atherosclerosis <ref name="ref1" /> |
| − | |||
| − | |||
===Sequence=== | ===Sequence=== | ||
Latest revision as of 02:43, 1 September 2017
Contents
Annotated Information
Name
LINC01826:long intergenic non-protein coding RNA 1826
lnc-MKI67IP-3 [1]
Cellular Localization
Lnc-MKI67IP-3 is primarily localized in the cytoplasm [1].
Function
These results indicate that Lnc-MKI67IP-3 might play important roles in the inflammatory responses of VECs and development of atherosclerosis [1]. Lnc-MKI67IP-3 acts as a sponge or competing endogenous RNA (ceRNA) for let-7e, suppressing its pro-inflammatory effects, and let-7e decreased lnc-MKI67IP-3 expression, thereby forming a positive feedback loop to aggravate inflammation [1]. Moreover, lnc-MKI67IP-3 is also abnormal in oxLDL-treated VECs and atherosclerotic plaques [1].
Regulation
Let-7e mimic significantly down-regulate lnc-MKI67IP-3 expression, while let-7e inhibitor markedly up-regulate this expression and let-7e inhibitor could be considered as an inducer of lnc-MKI67IP-3, just like vitamin C [1].
Expression
In human umbilical vein endothelial cells (HUVECs) treated with ox-LDL for different times, lnc-MKI67IP-3 is significantly down-regulated [1].
Diseases
Inflammatory response in vascular endothelial cells, atherosclerosis [1]
Sequence
>XR_001739207.1 PREDICTED: Homo sapiens uncharacterized LOC107985818 (LOC107985818), ncRNA
000081 AGTTGATGAG AAGTGTCTGC TTCCATTGCC CGTGAATCCC TAACAGAATG GTGCCAGGCT CCACCAGGAG ACCTTCCTGA 000160
000161 GTCCCATCTG AAAGCCTCCA CCTGAATGCG TCCCTCATTT TAATGACCCA GCCAGGCTAC CTCTGAAGAG AAGGGCAGTT 000240
000241 CTCAGCAGCC TGAGGGGTGC TGGTAGAGAC ATACCAAAAG TGTTGTTGGT GCCACCTTTT TGCAAGAGAT GAAGAGAAAG 000320
000321 TTCC
Labs working on this lncRNA
- The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Ministry of Public Health; The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine; Qilu Hospital, Shandong University, Jinan, China.
