isoform RBCK1 undergoes efficient phosphorylation by protein kinase Cbeta. The phosphorylated RBCK1 shows no self-ubiquitination activity in vitro. Overexpression of protein kinase Cbeta leads to significant increases in the amounts of intracellular RBCK1, presumably suppressing the proteasomal degradation of RBCK1 through self-ubiquitination
the cognate E2 co-enzymes of E3 enzyme Parkin regulate the activation, translocation and enzymatic functions of Parkin during mitochondrial quality control. UBE2D family members and UBE2L3 redundantly charge the RING-HECT hybrid ligase Parkin with ubiquitin, resulting in its initial activation and translocation to mitochondria. UBE2N primarily mediates the proper clustering of mitochondria, a prerequisite for degradation. Depletion of UBE2R1 results in enhanced Parkin translocation and clustering upon mitochondrial uncoupling
essential for hypersensitive response (HR) production. The CaRING1 expression triggers the hypersensitive cell death response. Transgenic Arabidopsis plants overexpressing CaRING1 also exhibit enhanced bacterial and fungal disease resistance, accompanied by the induction of salicylic acid against pathogen infection
protein quality control and subsequent elimination of terminally misfolded proteins is mediated by the ubiquitin-proteasome system. Ubr1, the N-end rule pathway E3 ligase is responsible for targeting misfolded cytoplasmic proteons to proteasomal degradation
isoform ACRE276 RNA interference silencing in tobacco results in loss of hypersensitive response specified by Cf resistance genes. ACRE276 RNAi plants are also compromised for hypersensitive response mediated by the tobacco mosaic virus defense elicitor p50
isoform GRN1 interacts with melanocortin receptor and decreases melanocortin receptors MC1R and MC4R signaling to cAMP. Inhibition of MC1R signaling by MGRN1 is not dependent on receptor down-regulation as a result of internalization or degradation. Receptor ubiquitylation is not a requisite for inhibition of signaling
isoform TRIM25 is essential not only for retinoic-acid-inducible protein RIG-I ubiquitination but also for RIG-I-mediated interferon-beta production and antiviral activity in response to RNA virus infection
overexpression of E3 ligase Pirh2 decreases DNA polymerase PolH protein stability, whereas knockdown of Pirh2 increases it. Pirh2 knockdown leads to accumulation of PolH and, subsequently, enhances the survival of UV-irradiated cells
transient expression of isoform PUB17 in Cf-9 tobacco silenced for ubiquitin ligase ACRE276 restores hypersensitive response, while mutant PUB17 lacking E3 ligase activity fails to do so. PUB17 ligase activity is crucial for defense signaling. PUB17 knockout plants are compromised in RPM1- and RPS4-mediated resistance against Pseudomonas syringae pv tomato containing avirulence genes AvrB and AvrRPS4, respectively
C3H2C3-Type RING E3 ubiquitin ligase AIRP1-overexpressing transgenic plants (35S:AtAIRP1-sGFP) are hypersensitive to exogenous abscisic acid in terms of radicle emergence, cotyledon development, root elongation, and stomatal closure. Overexpressing transgenic plants accumulate higher amounts of hydrogen peroxide in response to exogenous abscisic acid than wild-type and mutant plants. AIRP1 overexpressors are markedly tolerant to severe drought stress, as opposed to mutant plants, which are highly susceptible. The levels of drought stress-related genes and basic leucine zipper transcription factor genes are up-regulated in overexpressing plants relative to wild-type and mutant plants in response to abscisic acid
C3HC4-type RING E3 ubiquitin ligase AIRP2-overexpressing transgenic and loss-of-function mutant plants exhibit hypersensitive and hyposensitive phenotypes, respectively, to abscisic acid in terms of seed germination, root growth, and stomatal movement. Overexpressing transgenic plants are highly tolerant to severe drought stress, and loss-of-function mutant alleles are more susceptible to water stress than are wild-type plants. Higher levels of drought-induced hydrogen peroxide production are detected in overexpressing mutant as compared with loss-of-function mutant plants. Abscisic acid-inducible drought-related genes are up-regulated in overexpressing and down-regulated in loss-of-function progeny. The positive effects of AIRP2 on abscisic acid-induced stress genes are dependent on SNF1-related protein kinases
E3 RING ligase KEG acts as an important factor in plant hormone signaling and a positive regulator of jasmonate zim-domain JAZ12 stability. JAZ12 interacts directly with KEG. Abscisic acid treatment promotes JAZ12 degradation, and KEG knockdown leads to a decrease in JAZ12 protein levels
heterogeneous overexpression of HIR1 in Arabidopsis thaliana leads to As- and Cd-insensitive phenotypes and results in decreased As and Cd accumulation in the shoots and roots
in vivo degradation of substrates for integral endoplasmic reticulum membrane E3 ubiquitin ligase Doa10 is inhibitied by mutations in the alpha2 helix of E2 enzyme Ubc7 by preventing the conjugation of donor ubiquitin to the acceptor. Ubiquitin chain formation by mutant Ubc7 is not restored by the E3 enzyme Doa10 RING domain. alpha2 Helix mutations selectively impair the in vivo degradation of Doa10 substrates
in vivo degradation of substrates for integral endoplasmic reticulum membrane E3 ubiquitin ligase Hrd1 is not impaired by mutations within helix alpha2 of ubiquitin-conjugating enzyme Ubc7. Ubiquitin-chain formation by mutant Ubc7 is restored selectively by the E3 enzyme Hrd1 RING domain
isoform NERF is the cis-natural antisense transcript gene of NFYA5. NERF can produce siRNAs from their overlapping region and affect NFYA5 transcripts by functioning together with miR169. The NERF protein functions as an E3 ligase for ubiquitination. Overexpression of NERF or overlapping region cDNA leads to siRNA-NERF accumulation, miR169 repression, and NFYA5 transcript enhancement. Knockdown of NERF transcripts by an artificial miRNA enhances miR169 abundance and reduces NFYA5 transcripts
loss-of-function mutant line shows hyposensitivity to abscisic acid during its germination stage. AIRP3 is idetical to Loss of Gdu2, LOG2, which participates in an amino acid export system. The knockout mutant and RNAi knockdown transgenic plants display impaired abscisic acid-mediated seed germination and stomata closure. Suppression of AIRP3 results in marked hypersensitive phenotypes toward high salinity and water deficit relative to wild-type plants
loss-of-function mutant seedlings exhibit accelerated endocytosis in roots, and have altered expression of several genes involved in the membrane trafficking system. Protein trafficking inhibitor, brefeldin A, treatment leads to brefeldin A bodies in the mutant. The mutant also shows increased tolerance to salt, ionic and osmotic stresses, reduced accumulation of reactive oxygen species during salt stress, and increased expression of AtRbohD, which encodes a nicotinamide adenine dinucleotide phosphate oxidase involved in H2O2 production
mutant sugar-insensitive3, i.e. Sis3 is resistant to the inhibitory effects of high concentrations of exogenous glucose and sucrose on early seedling development. In contrast to wild-type plants, sis3 mutants develop green, expanded cotyledons and true leaves when sown on medium containing high concentrations (e.g. 270 mM) of sucrose. Mutant Sis3 exhibits wild-type responses to the inhibitory effects of abscisic acid and paclobutrazol, a gibberellic acid biosynthesis inhibitor, on seed germination
RING E3 Ligase Xbat32 mutants produce significantly more ethylene than wildtype plants and inhibition of ethylene biosynthesis or perception significantly increases Xbat32 lateral root production. Xbat32 interacts with the ethylene biosynthesis enzymes aminocyclopropane-1-carboxylic acid synthases ACS4 and ACS7 in yeast-two-hybrid assays and may negatively regulate ethylene biosynthesis by modulating the abundance of ACS proteins. Loss of Xbat32 may promote the stabilization of ACSs and lead to increased ethylene synthesis and suppression of lateral root formation. Auxin treatments only partially rescue the lateral root defect of Xbat32 mutants, but they completely restore wild-type levels of Xbat32 lateral root production when coupled with ethylene inhibition. Abscisic acid stimulates rather than inhibits mutant Xbat32 lateral root formation, and abscisic acid acts synergistically with auxin to promote mutant Xbat32 lateral root production
RING finger E3 ligase RHA2b expression is induced by abscisic acid and overexpression of RHA2b leads to abscisic acid-associated phenotypes such as abscisic acid hypersensitivity in seed germination and seedling growth, enhanced stomatal closure, reduced water loss, and, therefore, increased drought tolerance. T-DNA insertion mutant Rha2b-1 shows abscisic acid-insensitive phenotypes and reduced drought tolerance. A Rha2a Rha2b-1 double mutant generally enhances abscisic acid insensitivity of mutant Rha2b-1 in seed germination, seedling growth, and stomatal closure, suggesting that Rha2b and Rha2a act redundantly in regulating abscisic acid responses
RING finger E3 ligase RNF186 participates in the process of endoplasmic reticulum stress-mediated apoptosis. Overexpression of RNF186 stimulates upregulation of endoplasmic reticulum sensor proteins and rapid transmission of endoplasmic reticulum Ca2+ in Hela cells, while RNF186 knockdown leads to a moderate degree of resistance to endoplasmic reticulum stress. The half-life of substrate RNF186 is prolonged under endoplasmic reticulum stress, and the ubiquitination of BNip1 is greatly enhanced when endoplasmic reticulum stress occurs. Knockdown of BNip1 attenuates the stress signals at endoplasmic reticulum induced by RNF186
RING-type E3 ligase KEG interacts directly with abscisic acid-responsive transcription factor ABI5 via its conserved C3 region. Interactions between KEG and ABI5 are observed in the cytoplasm and trans-Golgi network only when the RING domain of KEG is inactivated or when ABI5 is stabilized via mutations. Deletion of the C-terminal region of ABI5 or substituting lysine 344 for alanine prohibits protein turnover
suppression of expression of DAF, i.e. DEFECTIVE IN ANTHER DEHISCENCE1 (DAD1)-activating factor, causes non-dehiscence of the anthers, alters pollen development and causes sterility in 35S:DAF RNAi/antisense Arabidopsis plants. Ectopic expression of the dominant-negative C132S or H137Y mutations causes similar indehiscence of anthers and reduction in DAD1 expression in transgenic Arabidopsis thaliana
the RING-finger domain of March10a exhibits an E3 ubiquitin ligase activity along with the E2 ubiquitin-conjugating enzyme Ube2B. March10a undergoes proteasomal degradation by autoubiquitination in transfected COS7 cells, this activity is abolished upon microtubule disassembly
the enzyme activates plant defense responses by inducing proteolysis of the VpWRKY11 transcription factor. Enzyme overexpression in Arabidopsis confers enhanced resistance to the pathogens Golovinomyces cichoracearum and Pseudomonas syringae pv. tomato DC3000
the enzyme acts as a positive regulator of absisic acid-mediated drought avoidance and a negative regulator of salt tolerance in Arabidopsis. Enzyme overexpression plants are hypersensitive to salt and osmotic stresses during seed germination, and show drought avoidance
the enzyme is negatively correlated not only with phosphorus content and phosphorus utilization efficiency, but also with biomass and seed yield in Arabidopsis. Enzyme overexpression results in the delayed flowering time and decrease in seed yield in sufficient phosphate condition
AIR2 interacts with the 3-ketoacyl-CoA thiolase protein KAT1. AIR2 ubiquitinates KAT1 and promotes the degradation of KAT1 via the 26S proteasome degradation pathway. Overexpression of AIR2 in Arabidopsis improves the seed germination and increases the root length under arsenate stress conditions
cullin E3-ligase activity is necessary for entry into the terminal myogenic differentiation program and myotube formation. Cullin inhibition prevents entry into the terminal myogenic differentiation program, and satellite cells treated with inhibitor MLN4924 fail to differentiate. Protein levels of myogenic repressors Bhlhe41 and Id1, but not that of ZBTB38, are mediated through the activity of cullin E3-ligases
DIR1-silenced pepper plants display a drought-tolerant phenotype characterized by a low level of transpirational water loss via increased stomatal closure and elevated leaf temperatures. DIR1-overexpressing Arabidopsis thaliana plants exhibit an abscisic acid-hypersensitive phenotype during the germination stage, but an abscisic acid-hyposensitive phenotype characterized by decreased stomatal closure and reduced leaf temperatures at the adult stage. Adult DIR1-overexpressing plants exhibit a drought-sensitive phenotype characterized by high levels of transpirational water loss
E3 ligase MIEL1 interacts with MYB1, regulator for anthocyanin accumulation. MIEL1 ubiquitinates MYB1 protein, followed by degradation through a 26S proteasome pathway. MIEL1 negatively regulates anthocyanin accumulation by modulating the degradation of MYB1 protein. Arabidopsis thaliana MIEL1 expression lines produce much less anthocyan than wild-type
enzyme belongs to a family of E3 ligases with a RING-H2 domain related in sequence to the ATL and BTL RING-H2 domains. This family, named CTL, carries a motif YEELL that expands 21 amino acids next to the RING-H2 domain. E3 ubiquitin ligase BIG BROTHER is a plant CTL that regulates organ size
enzyme belongs to a family of E3 ligases with a RING-H2 domain related in sequence to the ATL and BTL RING-H2 domains. This family, named CTL, carries a motif YEELL that expands 21 amino acids next to the RING-H2 domain. RNF111 is a SUMO-targeted ubiquitin ligase
enzyme is an E3 ubiquitin ligase and the RING finger conserved region is required for its activity. Silencing of Ring leads to increased sensitivity to salt stress in wild tomato. Overexpression of Ring in Arabidopsis thaliana results in enhanced salt tolerance during seed germination and early seedling development
in Arabidopsis thaliana overexpressing AIR1, the percentage of seedlings with expanded cotyledons is significantly higher in transgenic plants than in control plants in the presence of As-containing media. The root lengths of transgenic plants are significantly greater than those of the control wild-type plants when grown on 150 and 200 microM As-containing mediums, no differences are observed between the plants grown on the control medium
isoform RCHY1 is an interacting partner of the viral SARS-unique domain (SUD) and papain-like protease (PLpro). Residues 95-144 of RCHY1 and 389-652 of SUD (SUD-NM) are crucial for interaction. Association with SUD increases the stability of RCHY1 and augments RCHY1-mediated ubiquitination as well as degradation of p53. The calcium/calmodulin-dependent protein kinase II delta (CAMK2D) also binds to SUD. The PLpros from SARSCoV, MERS-CoV, and HCoV-NL63 also physically interact with and stabilize RCHY1, and thus trigger degradation of endogenous p53. A SUD-PLpro fusion interacts with RCHY1 more intensively and causes stronger p53 degradation than SARS-CoV PLpro alone. p53 inhibits replication of infectious SARS-CoV as well as of replicons and human coronavirus NL63
RFP1 is a functional RING E3 ubiquitin ligase that mediates ubiquitination of protein betaC1 from Tomato yellow leaf curl China virus-associated betasatellite. betaC1 is ubiquitinated in vivo and degraded by the plant 26S proteasome. After viral infection, plants overexpressing RFP1 develop attenuated symptoms, whereas plants with silenced expression of RFP1 show severe symptoms
RING E3 ligase PIR2 interacts with protein phosphatase PP2CA. A PIR2 knockout mutant does not display altered response to abscisic acid, the PIR1-1/PIR2 double mutant becomes more insensitive to abscisic acid than the wild-type or PIR1-1 and PIR2 single mutants
splicing isoform PIR1.2 exhibits E3 ligase activity and determines protein phosphatase PP2CA's stability in the presence of abscisic acid. The PIR1 knockout mutant displays an abscisic acid-hyposensitive phenotype. A PIR1-1/PIR2 double mutant becomes more insensitive to abscisic acid than the wild-type or PIR1-1 and PIR2 single mutants
the expression of transcription factor WRKY22 and RING-type ubiquitin ligase HOS1 is upregulated in the priming resistance of peach fruit against Rhizopus stolonifer. The two proteins physically interact in vivo
the identity of residues at specific positions in the RING domain can tune activity levels up or down. Substitutions may create a structurally intact BRCA1/BARD1 heterodimer that is inactive in vitro with all E2 enzymes. Substitutions in BRCA1 or BARD1 RING domains may result in hyperactivity, as both proteins have evolved attenuated activity. Loss of attenuation results in decreased product specificity
the RING domain of E3 ligase ZNRF1 binds Ube2N with a Kd of about 50 nM. ZNRF1 interacts with Ube2D2 with a Kd of about 1 mM. The ubiquitination efficiency of ZNRF1:E2 pairs correlates with their affinity. An excess of ZNRF1 inhibits Ube2N-mediated ubiquitination at concentrations at or above 500 nM instead of showing enhanced ubiquitination
tobacco leaf-produced EMR mediates mildew resistance locus O-12 degradation in a proteasome-dependent manner. EMR forms a complex with ubiquitin-conjugating enzyme UBC32. Mutation of EMR and RNAi increase the tolerance of plants to endoplasmic reticulum stress. EMR RNAi in a brassinosteroid signaling mutant protein background, leads to partial recovery of the brassinosteroid insensitive phenotypes as compared with the original mutant plants and increased ER stress tolerance
Ube4A is required for complete assembly of specific DNA damage repair factors at double-strand break sites and proper internal organization of double-strand break-associated protein foci. UBE4A's recruitment to sites of DNA damage is dependent on primary E3 ligases in the DNA damage repair and promotes enhancement and sustainment of K48- and K63-linked ubiquitin chains at these sites. This step is required for timely recruitment of the RAP80 and BRCA1 proteins and proper organization of RAP80- and BRCA1-associated protein complexes at double-strand break sites. The pathway is required for optimal end-resection at double-strand breaks, and its abrogation leads to up-regulation of the highly mutagenic alternative end-joining repair at the expense of error-free homologous recombination repair
UFD-2 is a mediator of DNA-damage-induced apoptosis. After initiation of homologous recombination by RAD-51, UFD-2 forms foci that contain substrate-processivity factors including the ubiquitin-selective segregase CDC-48 (p97), the deubiquitination enzyme ATX-3 (Ataxin-3) and the proteasome. In the absence of UFD-2, RAD-51 foci persist, and DNA damage-induced apoptosis is prevented. UFD-2 foci are retained until recombination intermediates are removed by the Holliday-junction-processing enzymes GEN-1, MUS-81 or XPF-1. Formation of UFD-2 foci also requires proapoptotic CEP-1 (p53) signaling
enzyme is an E3 ubiquitin ligase and the RING finger conserved region is required for its activity. Silencing of Ring leads to increased sensitivity to salt stress in wild tomato. Overexpression of Ring in Arabidopsis thaliana results in enhanced salt tolerance during seed germination and early seedling development