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BAP1 inhibits SLC7A11. 38 / 38
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"Genomic analyses together with robust statistics have revealed that the restoration of BAP1 facilitates the formation of the polycomb repressive deubiquitinase (PR-DUB) complex and inhibits ubiquitinated histone 2A (H2Aub) occupancy on the SLC7A11 promoter."
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"Moreover, BAP1 partially prevents the progression of tumors via SLC7A11 as well as ferroptosis, and cancer-related BAP1 mutants end up losing their capacities to suppress SLC7A11 and to stimulate ferroptosis [25]."
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"In this manner , BAP1 reduces SLC7A11 expression and cysteine uptake , leading lipid peroxidation upregulation and the ferroptosis induction ( 71 ) ."
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"Luciferase reporter assay showed that BAP1-WT could reduce the SLC7A11 promoter, while BAP1-MUT had no effect on the promoter."
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"For instance, BAP1 and p53 inhibited SLC7A11 to induce ferroptosis, while KEAP1 prevented NRF2 from activating SLC7A11 ( xref - xref )."
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"BAP1, as a tumor suppressor, promotes ferroptosis and inhibits cancer cell growth by inhibiting SLC7A11 [94]."
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"The repression of SLC7A11 by BAP1 unveils a potential ferroptosis axis implicated in placental physiology and pathology, shedding light on novel mechanisms underlying pregnancy disorders ."
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"Several studies have revealed that BAP1 can inhibit ubiquitinated histone 2A (H2Aub) occupancy on the SLC7A11 promoter (Zhang et al., 2018)."
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"It has been recently reported that BAP1 facilitates lipid peroxidation and promotes ferroptosis through repressing SLC7A11 [24]."
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"Analysis of our H2Aub ChIP-seq data revealed that restoration of BAP1 WT, but not BAP1 C91A, markedly decreased H2Aub occupancy at both the promoter and gene body of SLC7A11 (XREF_FIG), which was further confirmed by H2Aub ChIP assay on the SLC7A11 promoter and representative exons (XREF_FIG and XREF_SUPPLEMENTARY)."
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"Together, our data suggested a model that the BAP1 containing PR and DUB complex binds on the SLC7A11 promoter, where BAP1 removes ubiquitin from H2Aub, and BAP1 dependent H2Aub reduction on SLC7A11 is associated with BAP1 mediated SLC7A11 repression."
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"BAP1 inhibits tumor development, in part, via SLC7A11 and ferroptosis [48]."
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"It has been reported that BRCA1-associated protein 1, another tumor suppressor, induces ferroptosis by repressing SLC7A11 in a similar way to p53 (Zhang et al., 2018)."
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"Although the precise mechanism by which BAP1 induces SLC7A11 suppression needs to be further investigated, it could regulate the H2A ubiquitination (H2Aub) level on the SLC7A11 promoter, which suppresses the expression of SLC7A11 [58]."
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"Silencing BAP1 up-regulated SLC7A11 and mitigated ferroptosis."
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"These results suggested that BAP1 can mediate SLC7A11 inhibition and neuronal ferroptosis by regulating H2Aub.3.3 FOXO3a regulated BAP1 expression at the transcriptional level."
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"BAP1 inactivation in cancer cells diminishes SLC7A11, leading to tumor ferroptosis resistance without the regulation of NRF2 and ATF4 [120]."
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"We also studied whether NRF2 or ATF4 plays any role in BAP1 mediated SLC7A11 repression."
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"The knockdown of SLC7A11 in UMRC6 cells (a BAP1-deficient renal cancer cell line) marginally affects cancer cell proliferation, suggesting that the BAP1-mediated tumor suppression through regulating SLC7A11 [80]."
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"At the posttranscriptional levels, SLC7A11 is up-regulated by LncRNA HEPFAL and down-regulated by BAP1 and m A reader YTHDC2 (41–43)."
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"p53 and BRCA1 Associated Protein 1 (BAP1) inhibit carcinogenesis in part by antagonizing SLC7A11 and induce ferroptosis (Zhang Y. et al., 2019)."
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"As a deubiquitinating enzyme , BAP1 inhibits the expression of SLC7A11 by reducing the ubiquitination of H2A to inhibit the activity of SLC7A11 promoter ( 23 ) ."
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"Further mechanistic studies demonstrated that BAP1 suppresses SLC7A11 expression partly by deubiquitinating histone 2A ubiquitination to promote ferroptosis ."
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"It was reported that the BRCA1-associated protein 1 (BAP1) tumor suppressor is also able to promote ferroptosis by repressing SLC7A11 [41]."
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"In addition, Zhang et al. discovered that another tumor suppressor BAP1 promoted ferroptosis and inhibited the growth of cancer cells by inhibiting SLC7A11 (49)."
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"Although the precise mechanism by which BAP1 induces SLC7A11 repression needs further elucidation, it was proposed that BAP1, a H2A deubiquitinase, represses SLC7A11 expression by regulating the levels of H2A ubiquitination (H2Aub) on the SLC7A11 promoter (Figure 2) [41]."
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"For example, BAP1 has been found to reduce H2Aub occupancy of the SLC7A11 promoter, leading to the suppression of SLC7A11 expression and contributing to elevated ferroptosis and lipid peroxidation [60]."
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"BAP1 downregulates SLC7A11 by H2Aub deubiquitination on SLC7A11, inhibiting cystine uptake and leading to lipid peroxidation and ferroptosis (Zhang et al., 2018)."
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"Also, BAP1 reversed the effects of Exos oe-GATA-4 on H/R-induced cardiomyocytes' ferroptosis by downregulating SLC7A11."
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"Moreover, TP53 is not needed for BAP1-mediated SLC7A11 suppression [ 100 ]."
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"Two key tumor suppressor proteins , p53 ( TP53 ) ( Jiang et al ., 2015 ) and BAP1 ( Zhang et al ., 2018a ) , independently suppress SLC7A11 expression ."
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"Among these genes, SLC7A11 (encoding the Solute Carrier Family 7 Member 11), an antiporter that imports cystine and exports glutamate, was repressed by BAP1."
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"SLC7A11, one of the subunits of System Xc , cannot only be repressed by miR-672-3p but also downregulated by p53 and BRCA1-associated protein 1 (BAP1) [72–74] (Fig. 3)."
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"For instance, BAP1 and p53 inhibited SLC7A11 to induce ferroptosis, while KEAP1 prevented NRF2 from activating SLC7A11 (34-36)."
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"Epigenetically , BAP1 inhibits SLC7A11 expression through de-ubiquitinating H2A [ 13 ] , while chromatin remodeling factor ARID1A increases SLC7A11 expression [ 14 ] ."
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"Both BAP1 and PRC1 ( the main H2Aub ubiquitin ligase ) inhibit the expression of SLC7A11 [ 54 ] ."
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"Liu M et al believed that SLC7A11-mediated cystine uptake plays a necessary role in the inhibition of lipid peroxidation and cellular ferroptosis and found that NRF2 and activating transcription factor-4 (ATF4) can activate SLC7A11, and SLC7A11 can promote GPX4 protein synthesis by activating the mTORC1-4EBP, while P53, BAP1, ATF3, and BECN1 can inhibit SLC7A11 function."
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"Although the precise mechanism by which BAP1 induces SLC7A11 repression needs further elucidation , it was proposed that BAP1 , a H2A deubiquitinase , represses SLC7A11 expression by regulating the levels of H2A ubiquitination ( H2Aub ) on the SLC7A11 promoter ( Figure 2 ) [ 41 ] ."
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