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Homo sapiens (human) neighbor of BRCA1 lncRNA 2 (NBR2) URS0000A77648_9606

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NBR2: NBR2 is a long non-coding RNA (lncRNA) that plays a crucial role in various biological processes, including cancer development and energy stress response. Knockdown of NBR2 has been shown to abolish the inhibitory effect of curcumin on colorectal cancer cells [PMC9599102]. NBR2 is down-regulated in Ang II-induced myocardial hypertrophy, indicating its importance in myocardial hypertrophy [PMC9275985]. Glucose starvation increases the interaction between NBR2 and endogenous AMPKα, suggesting its involvement in energy stress response [PMC4814347]. In the context of phenformin treatment, NBR2 has been found to contribute to the adaptive response of tumor cells [PMC6901916]. The interaction between NBR2 and AMPK forms a feed-forward loop mechanism that modulates cancer glycolysis and tumor progression [PMC8275123]. Knockdown of NBR2 inhibits AMPKα activity, leading to unchecked cell cycle progression, altered autophagy/apoptosis response, and enhanced tumor formation [PMC7215767]. Under energy stress conditions, NBR2 down-regulates apoptosis while promoting autophagy, thereby inhibiting breast and kidney cancer progression [PMC8674783]. Methylation-dependent repression of NBR2 by MBD2 has been observed [PMC1181861]. The genomic region between BRCA1 and pseudo-BRCA1 genes contains a partial copy of the NBR1 gene known as NBR2. This partial copy is situated head-to-head with BRCA1 gene and may have functional implications [PMC8674783]. The interaction partners or additional proteins involved in the NBR2-AMPK complex are not yet fully understood. However, overexpression of NBR2 inhibits epithelial-mesenchymal transition (EMT) process in thyroid cancer cells, leading to reduced invasion and wound healing [PMC7304297]. The expression level of NBR2 is associated with the progression of various cancers [PMC8674783].

Genome locations

Gene Ontology annotations

Sequence

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GGAUGACGUAAAAGGAAAGAGACGGAAGAGGAAGAAUUCUACCUGAGUUUGCCAUAAAGUGCCUGCCCUCUAGCCUCUACUCUUCCAGUUGCGGCUUAUUGCAUCACAGUAAUUGCUGUACGAAGGUCAGAAUCGCUACCUAUUGUCCAAAGCAGUCGUAAGAAGAGGUCCCAAUCCCCCACUCUUUCCGCCCUAAUGGAGGUCUCCAGUUUCGGUAAAAGUUUCAUUUGAUCUGAAUAGUAUUAAAAUAAAAUACCUGGAUGAGGAAGAUGAAGAGGUGCUGGAAGCCCAGGAAGCACACAUCAAGGCUCCCUUGCCAGCAGGGUGCUGCCAAUAAAAGGUAGUCACGUGGAAUUUGGAAUGUGGAAAGGAGGUAGAAGUCAUCCUUUCCUCCCCUGUAGCAGCAGGCGUGCAGGCUCUGGUGGUCAGCUGGACUCCAUACUCCCCCACCAGUCACCAGCCUGGGGACCGUGGGGCUGCAAGGACCUCAGCAGCGGUGUCCCAAGUUUCCUGACUUCUUCCAUCCUCUGGAAAUCAGCUGUGUUUGCUGAGGAUAAUGGCCUCAAGAUCCAUCUGUGUUCCUACAAAAGAGAUGAUCUUGUUCUUUUUUAUGAUUGCACAUCUUUUGUUCUAACGUUUGGUCCUUCACCUUGGUUCCUGACACAAGGAUUCCUAAAUCCCUUGGAAUUUUCUGCAUGAUAGGAGCGUCCUUUGUUCUCAUGAGGUGACUCUUGGUGGGCUCCUUAUUUGGGGACUGGUCACCAAAAAUACCUAACUAUGGUUGGAAGCUUAGUGCUUUCAGCCCCAUUCCCCAUCCUCUGGGGUGGGGAGCAGAGCUGGAGCUCGAUCAUGCCUGCGUGACAAAGCCUCCAGAAAAAUCCUUGAAAGACAGGACAUGGAGAGCUGCUGGGUUGGCGAACACAUCCAUGUGCCGGGAGGAUGGUGCACCCCAACUCCACAAGGACCCUUCCAGACCUCACCCUGUGUAUCUCUUCAUCUGGCUGUUCAUUUAGCAGCUCCGAGGGCAGGCAUGGUGGCUCAUGCCUGUAAUCCCAGCACUUUGGGAGGCCGAGGCAGGUGGUUCAUCUAAGGUCUGGAGUUCGAGACCAGCCUGGCCAACAUAGCGAGAGCAGCUCCGGUGGCGGGAGGAGUGGCAGCGGCCAGGCAGCCCAGCUUCGCGAAGGCUGUAGGCACACCGCGGCCAGCAGGCACCUGGCACCCACCUUCCCUGCUGCCAGGAUGCCCAAGAAAAAGGUCAGCUCCACCGAAGGGGCUGCCAUGGAAGAGCCCAAGAGGAGAUCAGCGCAAUUGUCAGCUAAACCUCCUGCAAAAGUGGAAGCGAAGCCGAAAAAGGCAGCAGCGAAGGAUAAAUUUUCAGACACAAAAGUGCAAAAAAAGGGAAAAGGGGAGCAAAGGGAAAACAGGCCGAAGUGGCUAACCAAAAAACUAAAGAAGAUUUACCUGCAGAAAACAGGGGAAACGAAAACUGAGGAGAGUCCAGCCUCUGAUGAA

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Publications