REFERENCES


Choose an author or browse all
Choose the species or browse all
Choose a criteria for sorting
 Reverse sorting
Search for a protein
Search for a single PMID
Download references as CSV

Select O-GlcNAc references filter

Click to expand (2 results)


Wang Z, Liu Y, Ma L, Sun H, Tang Y. O-GlcNAcylation Mediated by OGA Activates NEK7/NLRP3 Pathway to Promote Pyroptosis in Parkinson's Disease. Journal of cellular and molecular medicine 2025 29(19) 41066511
Abstract:
Parkinson's disease (PD) is a neurodegenerative disorder characterised by pyroptosis. O-GlcNAcylation, regulated solely by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA), has been shown to mitigate PD. This study aimed to investigate whether pyroptosis and PD pathogenesis are modulated by O-GlcNAcylation. In PD model cells, O-GlcNAc protein levels were downregulated, while OGA expression was upregulated. Knockdown of OGA significantly protected BV2 cells from LPS-induced injury by inhibiting pyroptosis. Inhibition of OGA notably increased the O-GlcNAc levels of NEK7. Furthermore, O-GlcNAcylated NEK7 protein levels were significantly reduced by mutations at T170 or T172, whereas phosphorylated NEK7 protein levels were downregulated only by mutations at T172. Co-immunoprecipitation (co-IP) confirmed the endogenous interaction between NEK7 and NLRP3, which was weakened by OGA knockdown. In animal experiments, OGA deficiency significantly reduced motor dysfunctions and dopaminergic neurodegeneration in MPTP-treated mice. OGT deficiency abolished the protective effects of OGA knockdown against MPTP-induced injury. Additionally, OGT inhibition in OGA knockdown mice promoted pyroptosis. Collectively, these findings indicate that high OGA levels decrease O-GlcNAcylation in PD, thereby promoting pyroptosis via the activation of the NEK7/NLRP3 pathway.
O-GlcNAc proteins:
NEK7
Species: Mus musculus
Download
Zaro BW, Batt AR, Chuh KN, Navarro MX, Pratt MR. The Small Molecule 2-Azido-2-deoxy-glucose Is a Metabolic Chemical Reporter of O-GlcNAc Modifications in Mammalian Cells, Revealing an Unexpected Promiscuity of O-GlcNAc Transferase. ACS chemical biology 2017 12(3) 28135057
Abstract:
Glycans can be directly labeled using unnatural monosaccharide analogs, termed metabolic chemical reporters (MCRs). These compounds enable the secondary visualization and identification of glycoproteins by taking advantage of bioorthogonal reactions. Most widely used MCRs have azides or alkynes at the 2-N-acetyl position but are not selective for one class of glycoprotein over others. To address this limitation, we are exploring additional MCRs that have bioorthogonal functionality at other positions. Here, we report the characterization of 2-azido-2-deoxy-glucose (2AzGlc). We find that 2AzGlc selectively labels intracellular O-GlcNAc modifications, which further supports a somewhat unexpected, structural flexibility in this pathway. In contrast to the endogenous modification N-acetyl-glucosamine (GlcNAc), we find that 2AzGlc is not dynamically removed from protein substrates and that treatment with higher concentrations of per-acetylated 2AzGlc is toxic to cells. Finally, we demonstrate that this toxicity is an inherent property of the small-molecule, as removal of the 6-acetyl-group renders the corresponding reporter nontoxic but still results in protein labeling.
O-GlcNAc proteins:
A2A5R8, A2A6U3, A2AF81, A2AG39, A2AIW9, A2AJ72, A2AJI1, A2AKV2, A2AL12, A2AMW0, A2AUR3, LAS1L, TRM1L, A5A4Y9, A6PWC3, B0QZF8, B1AU76, UPP, B7ZC19, B7ZP47, B8JJC1, D3YWF6, D3YWK1, D3YWS3, D3YYP4, E9PX53, E9Q066, I2BP2, E9Q4Q2, E9Q5L7, E9Q7W0, E9QP59, F8WGW3, G3UX26, G3UYZ0, G3UZ44, G3X972, H3BKW0, H7BWX9, GTPB1, AIP, ATOX1, HDAC1, GSH0, DHX15, IKBE, AKAP2, SLK, IMPCT, IF6, ACOT1, NMT1, DHB12, SRPK1, ZN326, KLC1, RPP30, IDHC, CASP8, GCR, TYSY, RIR1, S10AA, LEG1, G3P, TPIS, PRDX3, CBX3, TISD, CATA, IMDH2, NFKB1, MAP4, CEBPB, CDK4, FKBP4, HMGB2, KAP3, MP2K1, RANG, PTN11, FBRL, PTN12, FMR1, HMGCL, DYN1, CAP1, STAT1, STAT3, PURA, ALD2, SIPA1, PURA2, GSHR, FOSL2, FOSL1, GSTM5, PCY1A, VATA, HDGF, UBP10, RHOX5, HMGA2, CCHL, NUB1, FAF1, ZNRD2, TB182, PCBP1, ARL1, PFD3, TCTP, HMGB1, DYL1, UB2L3, HDAC2, ELAV1, 4EBP2, PYRG1, TCPB, SPTC2, PSME2, BOP1, WBP2, XDH, HMMR, E2AK2, CO6A1, FABP5, LARP7, CNN2, PP4R2, RM10, Q3TFP0, GUAA, FUBP2, TRADD, CTU2, Q3U4W8, SNX27, BABA1, EDC4, COBL1, SKAP2, ARH40, CSTOS, LRRF1, ZMAT1, Q45VK5, JIP4, MDC1, Q5SUW3, SRC8, SAMH1, KHDR1, SPB6, CAPR1, PAPS1, TS101, PA1B2, FNTA, IGBP1, FSCN1, FXR1, CBX5, RAI1, MELK, FOXC2, DBNL, CYTB, NDRG1, RALY, GPDM, RAB3I, F120A, NOP58, Q6DFZ1, TPM4, Q6NXL1, Q6NZD2, TNPO3, SMHD1, UGGG1, UBXN7, TXLNA, DC1L2, KI18B, JUPI2, LARP1, CAND2, ACAP2, HNRPQ, SPAG7, ATX2L, MAP6, ELP1, PJA2, PGRC2, KCMF1, Q80VB6, FA98B, WDTC1, CPPED, LPP, PEF1, IF4B, ATG4B, FTO, Q8BH80, PRUN1, AHSA1, RCC2, NCEH1, LSS, FBLN3, PPR18, SRRM2, MSRB3, PPME1, RL1D1, TBCD4, NHLC2, MAP1S, TLK1, CND2, RAE1L, SEP10, ZFP57, UBA6, UBA3, STON1, PPM1F, GNL3, PUR1, HMCS1, Q8K0C7, PDXK, ANGE2, LRC41, SDE2, DNM1L, ANLN, MATR3, CBR3, MEPCE, ERF3A, DC1L1, SPART, TDIF2, HEXI1, SNP47, UBP15, MAVS, UBXN4, ACSF2, MICU1, ZNG1, BACH, ISOC1, IPYR2, CSDE1, PIP30, GCSH, Q91X76, DUS3L, BAG2, KCC1A, TTC1, HNRLL, RIN1, PP6R3, MARC2, DBR1, ATAD3, PSIP1, NXF1, NONO, PLST, RRAGC, VMA5A, TARA, DDAH2, TADA1, GRPE1, ABD12, NU155, OGFR, NPM3, GLOD4, COPRS, DPOE4, MIEN1, TRAP1, VATG1, CHSP1, OCAD1, RANB3, MFR1L, NDUF7, TBC15, PPIL4, MPPB, CYBP, ZCHC8, CD37L, MMS19, ARPIN, HNRPM, NXP20, SPF27, TOE1, Q9D4G5, ATAD1, CF226, IPYR, ORN, CNN3, KAP0, PLIN3, AKAP8, EIF3F, IFG15, LIMA1, NEK7, RTN3, STK3, NUP50, SYSM, HSPB8, BAG3, CUL3, RABX5, CAF1A, DREB, TOM40, DNJC7, NFU1, FBX6, NUBP1, DEST, TEBP, ACOT9, NFKB2, KAD2, SKP1, PDC6I, VAPA, CARM1, RAD9A, IF2G, SAE2, TRIP6, MBD2, HNRPF
Species: Mus musculus
Download
Page 1 of 1