Entry Detail

General Information

Database ID: LDA0001695
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:MALAT1
Full Name:metastasis associated lung adenocarcinoma transcript 1
Category:LncRNA
Species:Homo sapiens
Synonyms:HCN|LINC00047|NCRNA00047|NEAT2|PRO2853
Chromosome:11
Strand:+
Coordinate:
Start Site(bp):65497738End Site(bp):65506516
External Links:
Ensembl ID:ENSG00000251562
Ensembl Transcript ID:N/A
Entrez Gene:378938.0
NONCODE ID:N/A
RefSeq Accession:NR_002819.4

 

ncRNA Association Statistics

Total Associated Disease Number:204   
More Information
Causal Disease Number:132
Network:
Top Causal Diseases:
Breast Neoplasms  (Score: 1)
Breast Neoplasms  (Score: 1)
Coronary Artery Disease  (Score: 1)
Stomach Neoplasms  (Score: 1)
Colorectal Neoplasms  (Score: 1)
tongue squamous cell carcinoma  (Score: 1)
Colorectal Neoplasms  (Score: 1)
Stomach Neoplasms  (Score: 1)
Carcinoma, Non-Small-Cell Lung  (Score: 1)
Carcinoma, Renal Cell  (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//RNA Pull-Down//Western Blot//Transfection//Tunel//CCK8//qRT-PCR//Flow Cytometry//RIP//Luciferase Report Assay//Cell Proliferation Assay//Colony Formation Assay
Weak Evidence:

 

Reference

[1] PubMed ID:34240756
Disease Name:Acute Kidney Injury
Sample:serum samples from AKI patients
Dysfunction Pattern:Interaction(miR-204/APOL1 pathway)
Validated Method:RNA Pull-Down//Western Blot//Transfection//Tunel//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay
Description: From the results, lncRNA MALAT1 was strongly elevated in serum samples from AKI patients, with the high sensitivity and specificity concerning differentiating AKI patients from healthy controls.After co-transfection with MALAT1 silencing and miR-204 inhibition, we found that miR-204 could counteract the effects of MALAT1 on HK-2 cell progression and inflammation after under hypoxic conditions. Finally, NF-κB signaling was inactivated while APOL1 expression was increased in HK-2 cells after hypoxia treatment, and lncRNA MALAT1 inhibition reactivated NF-κB signaling while suppressed APOL1 expression by sponging miR-204.
Causality:Yes
Causal Description:Silencing of MALAT1 could reverse hypoxia-triggered promotion of HK-2 cell apoptosis. Meanwhile, the increase of IL-1β, IL-6, and TNF-α after hypoxia treatment could be repressed by MALAT1 knockdown as well.
Clinical-realted Application:

[2] PubMed ID:29115409
Disease Name:Acute Kidney Injury
Sample:kidney injury specimens and NRK-52E cells
Dysfunction Pattern:Interaction(miR-146a/NF-κB signaling pathway)
Validated Method:In Vivo Experiment//Western Blot//Transfection//qRT-PCR//RIP//Cell Proliferation Assay
Description:The expression levels of miR-146a were lower in the kidney injury specimens and NRK-52E cells, compared with those in the controls. MALAT1 knockdown and the overexpression of miR-146a reduced the production of phosphorylated inhibitor of NF-κB and np65 protein. miR?146a was found to be transcriptionally induced by NF-κB, and miR-146a repressed the pro-inflammatory NF-κB pathway and downstream transcription factors. Taken together, these data indicated that the MALAT1/miR?146a/NF-κB pathway exerted key functions in LPS-induced AKI, and provided novel insights into the mechanisms of this therapeutic candidate for the treatment of the disease.
Causality:No
Causal Description:
Clinical-realted Application: