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Homo sapiens (human) FOXF1 adjacent non-coding developmental regulatory RNA (FENDRR) URS0000759D4A_9606

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FENDRR: FENDRR enhances the polarization of M1 macrophages via the STAT1 signaling [PMC8395204]. FENDRR expression was correlated with genome-wide expression profiles in patients with COAD/READ [PMC8490734]. FENDRR was found to interact with the 3'UTR of Sox2 mRNA [PMC8806690]. The rs1424019 A>G polymorphism in the FENDRR promoter was genotyped and its role in gene regulation was investigated [PMC9225451]. FENDRR was shown to reduce the activity of MMP2/MMP9 and protect against gastric cancer cell metastasis [PMC4237812]. The expression of FENDRR was associated with tumor stage in COAD/READ patients [PMC7109049]. The expression levels of FENDRR and PGC-1α decreased significantly after ox-LDL treatment in HAECs [PMC8072360]. FENDRR negatively regulated the post-transcriptional expression of ABCB1 and ABCC1, contributing to doxorubicin resistance in osteosarcoma cells [PMC9891159]. FENDRR exhibited a protective effect against H2O2-induced cardiomyocyte injury in a mouse model of MI/R injury [PMC9891159]. Overexpression of FENDRR decreased caspase-1 activity levels in hypoxia HPAECs, indicating a protective effect against cell injury [PMC9594874]. FENDRR formed an RNA-DNA triplex within the promoter of DRP1, leading to decreased transcription by promoting DRP1 promoter methylation [PMC9594874]. YTHDF2 recognized m6A-modified lncRNA FENDR and promoted its degradation [PMC9635867]. FENDRR functions as an important tumor suppressor in NSCLC [PMC8797579]. FENDRR binding with SRSF9 may inhibit mTOR signaling [PMC8395204]. Protein-coding genes co-expressed with MEF2C-AS1 are associated with RAS and TGF-beta signaling pathway [PMC6067087]. FENDRR up-regulation inhibited the expression of ABCC10 in A549/DDP cells [PMC6855145]. FENDRR inhibited the immunosuppressive ability of Treg cells [PMC7757045]. FENDRR was found to be selectively recognized by specific human miRNAs and lncRNAs [PMC8698532]. Overexpression of FENDRR had opposite effects in CAFs [PMC8315042]. Adenovirus-mediated FENDRR transfer into the lungs reduced fibrotic lesions and collagen deposition [PMC8395204]. TGF-β1/Smad3 signal inhibited the expression of FENDRR in pulmonary fibrosis [PMC8136122]. FENDRR was found to be physically associated with PRC2 [PMC7911649]. FENDRR inhibits breast cancer cell proliferation and promotes cell apoptosis [PMC5857152]. A mutant mouse with a modification of the FENDRR gene exhibited developmental defects [PMC4409293]. FENDRR plays a role in regulating FOXC2 expression in gastric cancer cells [PMC8044876]. FENDRR is involved in the development of vascular or malignant diseases [PMC9854786]. The coding potential of FENDRR was analyzed using CSF analysis [PMC8797579]. The triplex-forming sites of lncRNAs, including FENDRR, were predicted using a specific strategy [PMC5648039]. The role of FENDRR in cell migration and invasion was explored in colorectal cancer [PMC7768317]. High expression levels of FENDRR were associated with better prognosis in HNSCC patients [PMC8315042].

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Gene Ontology annotations

Sequence

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AGCAGACAGCGCGGGCUGGGAGCGCCGGCAAGGGCGGCCCUCGCGCACCUGGCUGCCAGCCCGCAGGGGGCUCGCACGCAGACCUGCCCUUGCCACCUCAGCGCUCGGGUGCGGGCUGGGGGCGGUGGAGCCACGAAAGGUGGUGCCGAGAGCGGAGCGCAGGACAGCGCAGGAGCCCCGGCGCAUCGCGGCGCGCACAGACCCAGGAUUACUUCAUGCACAUAAAAGAAAACGCAACUACAGUGGACCCUGAACAACCUAUGGCCUGCAGCCACUGAAGAAUGCUUGCAUAAGGAGCUCUUCUCUGCACAUACCCCGACACAGUGAUGGUAUCUUGCAGCUGCUGCUUCUGUCCAAGGCACUGCAGCCUACUCGUCAAAAGCCCGAAGCCCAGCUCUGCCAGCAGUGCACUGUGUGCUCUUAGGAAACAGAGAAGCAAAGAAGUUAGCAAGCUUGUUUUGGCAGAAGAAAAAACACAAAAUACCCAACCACAGAUCCUCAAAAAUAUUGCUAAGCACUAAUUUUGCUAACAUGUUAGACAGCCUUCGGAUCUAGGCAAUCUUGUUCCUCAGCUGGAAAGAGUUCCUGCCAGCCAUGUGAUUCCAAAUCCACCCUGGACAUAUGGGGAUAAUGAGAAAAUCAGCUCCGGCCUUCCCUGGCCUUCCAGCCAAGUGAAUGGGGGCAUCCCCUGGUGCUUCAGCCCGGGGCCCACCCAGAGGAUGCUAGCUGGCCUGCAGAGGCCUCAACCAUGCCCUCCUGGACUCAGGUAAGACUGAGGUUUCCAUGCCCUCAAAACAAUUGUUCAGACAAAAACUCACUGCCCAGGUCAAAGUCACAGCACCAGAAAGCCAACCUGAGGAUGAAGACAAAGCUCUUUGUUGGCACAGUCCCCUGAUCAUUCGAGGUCAGCAUCUCCAUCAAAAUGGACCCAAUGCUGAGGCAAGAAGGAGAACAUCACUGUUAAGAAGGUAAUGAGUCACAAAUGCUAUUUCGAUGGUUUUCUUUGAAAGAAAUACACAGAACCAAACCAAUUUUAAUUAAAGAUCUUGUCUUUGUAAUCAGGCAGCCACAAAUGAAGGCAAAACUGCUUUCAUGUGGCAUAAUAUACACAGAGCUGAACUAGUUUUCCCAUAAAAGGGCAGGUUCUUUUCUUCAAAUAAGAAAAGAGUUUGUUCCUAACAAUAUGGGGGAUGCAACAGAAAGCUGUCUUUUGCAAAGUAUAAAAUUGCAGAUCCUCCCGUGGAAGCCAUUUCUUGAUGCUAAACCAAUGCGAACGUUUGCCAAACGCACAUGCGAGCCGGGAUUAUCCUACCCUUUGAGAUUAGACAUGUGAUCCUGAUUUUUAAGUGAAAAACGCAGCCAGAGGCCAAAUAAACAUACCUACAAGUACAUCGAAAGCUCAAAUGGUUGAGAAAUGAUUGUAACACACCCCGGUGUGUAUUUCUGAGGAAGAAUCAACAUGCACAUGGAAAUUGAUGUUUUGAUUUUUAAUUUUAAAACGACGACAGAACUGAAAUACCUCCCCUAACUAGGUCCACUGAAACCAGUGAGGAGAUAAUCAUUUUCAGUUAAAUAUGCAUGUAAUUUAAUAAUCCACAGAUGGAAAAUGCAUUUGAGGUGGACUGAACACAGCCAGGAGUUUUUGCUUAUCGACAGCACUGAAUCCUGCCUUGACUAGAGAGACUCGUCAUGUGAUCAACUGUGGCCAGAGGGCAUCCUGCAGACAGCUCCUGUCACACCACACUGACCAGACUCUUAUGAGUAUUUAAGCAUCUUCAGGGAAGCGAUUGACUGUCUUAUAAUGGUCUUACAAGUACGGAACUUUAUUACCUGCUAAUAAUCAGAGCACAUGAUGGCACAAUAGAAUAUACGAGUGAAGUUCUAAAUGCAAGGUUGUUCUUAUUCUGUGAGUGGCAAAACUCAUGCAGUGAGCAGAUAAAGCUGGCAGGAGGCAUUGGCGCCCUAAUGCUGGGCACUAACCACCUGCCCGGACUGCGAAUAUCUGUUGGGUCCUUUCUAUAUCUGGUCUAUUCUCGUGUUUGAUUAUAUCCUGGUGGCAAGAAUAGCAAAAUCAACUCUCCUUCCUAUCCCAUGUGGAGAGGCAUGAUUUGAGUCAGAGAGCAUUAUCCUCUCUGCGUUAUCCAACCCCAUGUCCCAUGAUGCACUUUGUAGACAAGCAAGUGUCCCUGGUGGAGAAUCCACAGCCACACAUCCUCAUUGGUUGCAAGGAUCAGUGUCCAAUAUCUACUGCCAUGAUCAUUCUCAGUUUUACAUCCACAGAGCUUCAUAGAAUUCUAACACCACAGGUCCAAGUAGAGGUUUUGGCCUCAGAGUGGGCUAGAUUCCACCUCUGACAGCAGCUGUGGGACUGUUUUUCCAUCUGUAAAAUGGAGACAAGAGUAUCACCUACCUCAUGGUGUUGGUGGGAUCGUUAAACAGAAUUCCGAUCAUGAAACCCUUAGCCUGCUCCCUGCAUAGGCUGCAUGCGCUCAGUGAGCUAUGGCUCUGUUUCAUGCUGACUUUACCAUCAUGUAAGCAGUUUUAAAAAUGCUAGAAGCUUUAGUCAUAGAAUUACCAUAUGAUACAGCCUACUGCAGAGUCCAGAGGCUGAGGCAGGAGAGUUACUUGAACCUGGGAGGCGGAGGUUGCAGUGAGCCAAGAUCGCGCCACUGCACUCCAGCCUGGGCAACAGAGUGAGAUUCUGUCUCAACACAAAAAAGAAGACAUGUGUCCCCAUCACAGUAUCAUACAGAGUGCUUCCACUGCCCUAAAAUACCCUGUGCUCUUCCUAUUCAUCCCUCUCUUCAACCCCAGCAACCACUGAUCCUUUUACCAUCUCCAUGGUUUUGCCUUUCCCAGAAUGUCAUAUUGUUGGAAUCAUACGCUAUGUAGCCUUUGCAAAUGGGCUUCUUUCACCGAGCAAUGUGCAUUGAAGGUGCCUCUAUGACUUUUCAAGGGUUGAUAGCUCAUUCCUUUUUAUUGCUAAAUAAUAUUCCAUUGUCUGAAUGUACCACAUUUUGUUUAUCCAUUCACCUACUAAAGGACAUCUUGGUUGCUUCCAAGUUUGGGCAAUUAUAAAUAAAACUGCUAUAAACAUUG

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Publications