Entry Detail

General Information

Database ID: LDA0007795
Species: Homo sapiens
Confidence Score: 0.985791
Contents: >> ncRNA Information
>> ncRNA Association Statistics
>> Disease Information
>> Disease Association Statistics
>> Evidence Support
>> Reference
Causality: Yes
Clinical Significance: Unknown

 


ncRNA Information

Reference Genome Note: GRCh38 for human lncRNAs; GRCm39 for mouse lncRNAs; mRatBN7.2 for rat lncRNAs; hg19 for human circRNAs; mm9 for mouse circRNAs.

ncRNA Symbol:NEAT1
Full Name:nuclear paraspeckle assembly transcript 1
Category:LncRNA
Species:Homo sapiens
Synonyms:LINC00084|NCRNA00084|TP53LC15|TncRNA|VINC
Chromosome:11
Strand:+
Coordinate:
Start Site(bp):65422798End Site(bp):65445540
External Links:
Ensembl ID:ENSG00000245532
Ensembl Transcript ID:N/A
Entrez Gene:283131.0
NONCODE ID:N/A
RefSeq Accession:NR_131012.1

 

ncRNA Association Statistics

Total Associated Disease Number:190   
More Information
Causal Disease Number:146
Network:
Top Causal Diseases:
Parkinson Disease  (Score: 1)
Ovarian Neoplasms  (Score: 1)
Non-alcoholic Fatty Liver Disease  (Score: 1)
Parkinson Disease  (Score: 1)
Leukemia, Myeloid, Acute  (Score: 1)
Osteosarcoma  (Score: 1)
Osteosarcoma  (Score: 1)
Leukemia, Myeloid, Acute  (Score: 1)
Colorectal Neoplasms  (Score: 1)
Carcinoma, Hepatocellular  (Score: 1)
More Information

 

 

Disease Information

 Disease OntologyMeSH
Disease ID:D058186
Disease Name:Acute Kidney Injury
Category:MeSH
Type:Urogenital Diseases
Define:Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.
Alias:Acute Kidney Injury//Acute Kidney Injuries//Kidney Injuries, Acute//Kidney Injury, Acute//Acute Renal Injury//Acute Renal Injuries//Renal Injuries, Acute//Renal Injury, Acute//Renal Insufficiency, Acute//Acute Renal Insufficiencies//Renal Insufficiencies, Acute//Acute Renal Insufficiency//Kidney Insufficiency, Acute//Acute Kidney Insufficiencies//Kidney Insufficiencies, Acute//Acute Kidney Insufficiency//Kidney Failure, Acute//Acute Kidney Failures//Kidney Failures, Acute//Acute Renal Failure//Acute Renal Failures//Renal Failures, Acute//Renal Failure, Acute//Acute Kidney Failure

 

Disease Association Statistics

Total Associated ncRNA Number:30   
More Information
Causal ncRNA Number:30
Network:
Top Causal ncRNAs:
NEAT1  (Score: 0.985791)
MALAT1  (Score: 0.985791)
NEAT1  (Score: 0.985791)
MALAT1  (Score: 0.985791)
PVT1  (Score: 0.731059)
Kcnq1ot1  (Score: 0.731059)
H19  (Score: 0.731059)
CASC2  (Score: 0.731059)
SNHG14  (Score: 0.731059)
hsa_circ_0020339  (Score: 0.731059)
More Information

 

Evidence Support

Strong Evidence:In Vivo Experiment//Northern Blot//Western Blot//ISH//Transfection//qPCR//Tunel//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Cell Apoptosis Assay//ELISA//IHC//ChIP
Weak Evidence:

 

Reference

[1] PubMed ID:35600150
Disease Name:Acute Kidney Injury
Sample:AKI cell models
Dysfunction Pattern:Interaction(miR-22-3p/CXCL12/NF-κB )
Validated Method:In Vivo Experiment//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//ELISA
Description: NEAT1 was overexpressed and miR-22-3p was underexpressed in sepsis patients and lipopolysaccharide (LPS)-induced AKI cell models. In summary, our data showed that NEAT1 promoted LPS-induced HK2 cell injury via regulating the miR-22-3p/CXCL12/NF-κB signaling pathway, suggesting that NEAT1 knockdown might be a potential pathway for alleviating sepsis-induced AKI.
Causality:Yes
Causal Description:Knockdown of NEAT1 could promote viability and suppress apoptosis and the inflammatory response in LPS-induced HK2 cells.
Clinical-realted Application:

[2] PubMed ID:35619557
Disease Name:Acute Kidney Injury
Sample:TECs
Dysfunction Pattern:Interaction(miR-129-5p)
Validated Method:In Vivo Experiment//Northern Blot//Western Blot//ISH//qPCR//Tunel//RIP//Luciferase Report Assay//RNA-seq//Cell Apoptosis Assay//IHC//ChIP
Description:By high-throughput RNA sequencing, we found that Neat1_2, a transcript variant of Neat1, was upregulated in 40-min ischemia/reperfusion injury (IRI), which resulted in the development of renal fibrotic lesions. The upregulation of Neat1_2 in hypoxia-treated TECs was attributed to p53 transcriptional regulation.Mechanistically, Neat1_2 shares miRNA response elements with FADD, CASP-8, and CASP-3. Neat1_2 competitively binds to miR-129-5p and prevents miR-129-5p from decreasing the levels of FADD, CASP-8, and CASP-3, and ultimately facilitates TEC apoptosis. Increased expression of Neat1_2 associated with kidney injury and TEC apoptosis was recapitulated in human AKI, highlighting its clinical relevance.
Causality:Yes
Causal Description:Gain- and loss-of-function studies, both in vitro and in vivo, demonstrated that Neat1_2 promoted apoptosis of injured TECs induced by IRI and caused tubulointerstitial inflammation and fibrosis.
Clinical-realted Application: