Difference between revisions of "LINC01826"

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(Created page with "==Annotated Information== ===Approved Symbol=== LINC01826 ===Approved Name=== long intergenic non-protein coding RNA 1826 ===Previous Symbols=== _ ===Synonyms=== lnc-MKI67IP-3...")
 
 
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==Annotated Information==
 
==Annotated Information==
===Approved Symbol===
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===Name===
LINC01826
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LINC01826:long intergenic non-protein coding RNA 1826
===Approved Name===
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long intergenic non-protein coding RNA 1826
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lnc-MKI67IP-3 <ref name="ref1" />
===Previous Symbols===
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_
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===Cellular Localization===
===Synonyms===
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Lnc-MKI67IP-3 is primarily localized in the cytoplasm <ref name="ref1" />. 
lnc-MKI67IP-3
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===Chromosome===
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===Function===
2q14.3
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[[File:LncRNA-MKI167-3.JPG|right|thumb|400px|'''Lnc-MKI67IP-3 could bind to let-7e as a miRNA sponge''' <ref name="ref1" />.]]
===RefSeq ID===
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_
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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" />.
===OMIM ID===
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_
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===Regulation===
===RefSeq(supplied by NCBI)===
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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" />.
XR_001739207
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===pubmed IDs===
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===Expression===
28195197
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In human umbilical vein endothelial cells (HUVECs) treated with ox-LDL for different times, lnc-MKI67IP-3 is significantly down-regulated <ref name="ref1" />.
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===Diseases===
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Inflammatory response in vascular endothelial cells, atherosclerosis <ref name="ref1" />
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===Sequence===
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>XR_001739207.1 PREDICTED: Homo sapiens uncharacterized LOC107985818 (LOC107985818), ncRNA
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<dnaseq>CTGAACGCTAAGAACAACAGAACGTAAGACTGACAGTTGACTTATCATAATGATATCCTTCTTTCCCATT
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GAAAAAATGTAGTTGATGAGAAGTGTCTGCTTCCATTGCCCGTGAATCCCTAACAGAATGGTGCCAGGCT
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CCACCAGGAGACCTTCCTGAGTCCCATCTGAAAGCCTCCACCTGAATGCGTCCCTCATTTTAATGACCCA
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GCCAGGCTACCTCTGAAGAGAAGGGCAGTTCTCAGCAGCCTGAGGGGTGCTGGTAGAGACATACCAAAAG
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TGTTGTTGGTGCCACCTTTTTGCAAGAGATGAAGAGAAAGTTCC</dnaseq>
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==Labs working on this lncRNA==
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*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.
 +
==References==
 +
<references>
 +
<ref name="ref1">
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Lin Z, Ge J, Wang Z, Ren J, Wang X, Xiong H, Gao J, Zhang Y, Zhang Q. Let-7e
 +
modulates the inflammatory response in vascular endothelial cells through ceRNA
 +
crosstalk. Sci Rep. 2017 Feb 14;7:42498.
 +
</ref>
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</references>

Latest revision as of 02:43, 1 September 2017

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

Lnc-MKI67IP-3 could bind to let-7e as a miRNA sponge [1].

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

000001 CTGAACGCTA AGAACAACAG AACGTAAGAC TGACAGTTGA CTTATCATAA TGATATCCTT CTTTCCCATT GAAAAAATGT 000080
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.

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 Lin Z, Ge J, Wang Z, Ren J, Wang X, Xiong H, Gao J, Zhang Y, Zhang Q. Let-7e modulates the inflammatory response in vascular endothelial cells through ceRNA crosstalk. Sci Rep. 2017 Feb 14;7:42498.