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1                                              SUMO conjugation activity alone was sufficient to target
2                                              SUMO E3 ligases enhance transfer of SUMO from the charge
3                                              SUMO homeostasis is important for many cellular processe
4                                              SUMO post-translational modification of proteins or SUMO
5                                              SUMO protease can rapidly reverse SUMO conjugation makin
6                                              SUMO(Eu) fusions therefore remain stable in eukaryotic c
7                                              SUMO-PKD2 recycles, whereas unmodified PKD2 is surface-r
8                                              SUMO-protein conjugation regulates transcription, but th
9 teract with small ubiquitin-like modifier 1 (SUMO-1) and Ubc9, and function as an intramolecular E3 l
10 itched; the red circle should identify 1CARD-SUMO (TEV) and the blue triangle should identify 1CARD-S
11  and the blue triangle should identify 1CARD-SUMO + SERPINB1 (TEV).
12                                            A SUMO E1 inhibitor, ginkgolic acid, decreases alpha-synuc
13                                            A SUMO-specific protease 4 (SUSP4) was shown to rescue p53
14  in addition to SUMO conjugation activity, a SUMO acceptor site in COP1 and the SUMO E3 ligase SAP an
15 the Rhes's serine 33, C-terminal CAAX, and a SUMO E3-like domain.
16 pposing actions of a STUbL (Slx5:Slx8) and a SUMO isopeptidase (Ulp2).
17 nd proteomic analysis identified KLP-19 as a SUMO substrate in vivo.
18                              MMS21 encodes a SUMO E3 ligase and an essential component of the Smc5/6
19 presence of SIMs in RC components generate a SUMO-SIM network that facilitates assembly of the RC.
20                                  Defect in a SUMO protease protein, suppressor of mat3 7 (SMT7), has
21 g that Tof2 is targeted for degradation in a SUMO- and STUbL-dependent manner.
22 that affect key protein regions, including a SUMO acceptor site, a central disordered alanine-rich mo
23 d structural studies disclosed that IE2 is a SUMO cis-E3 ligase.
24                            ICP0 depends on a SUMO-interaction motif located at residues 362 to 364 (S
25 Ubc9 (a SUMO-conjugating enzyme E2), PIAS (a SUMO-protein ligase E3), and Smt3 (the SUMO isoform in D
26                              We found that a SUMO interaction motif in ZIKV and DENV NS5 proteins dir
27                These findings suggest that a SUMO-driven feedback inhibition mechanism is an intrinsi
28 d modifier (SUMO) pathway components Ubc9 (a SUMO-conjugating enzyme E2), PIAS (a SUMO-protein ligase
29 coding and noncoding RNA (ncRNA) genes via a SUMO-interacting motif in the HDAC Cpr1 subunit.
30 dy reveals a novel mechanism through which a SUMO protease regulates cell division in the mat3-4 muta
31                                 Accordingly, SUMO activity ameliorated C9ORF72-ALS-related neurodegen
32 strate that intravascular pressure activates SUMO-PKD2, not PKD2, channels, as desumoylation leads to
33                     Anchorage to NPCs allows SUMO removal by the SENP SUMO protease Ulp1 and the prot
34 , we show that the chromatin association and SUMO ligase activity of Smc5-Smc6 require the Nse5-Nse6
35 eveal that SIZ1 physically connects COP1 and SUMO conjugation activity in the same NBs that can also
36        The strong colocalization of COP1 and SUMO in these NBs might also explain why many COP1 subst
37 lts suggest sequential ubiquitin-histone and SUMO-histone modifications recruit Ulp2, which removes p
38 /6 exhibits DNA-dependent ATP hydrolysis and SUMO E3 ligase activity.
39 hat SUMO (Small Ubiquitin-like Modifier) and SUMO ligase Ubc9 are required for efficient repression o
40  salt bridges between the phosphoserines and SUMO accounted for the increased IE2-SUMO affinity.
41 demonstrate that flavivirus-specific SIM and SUMO sites determine the assembly of NS5 proteins into d
42           Moreover, the presence of SIZ1 and SUMO in these NBs explains how both the timing and ampli
43  be applied to any SUMOylation substrate and SUMO isoform.
44 een small ubiquitin-like modifier (SUMO) and SUMO interaction motif (SIM), and that APB coalescence d
45                Removal of both ubiquitin and SUMO from histones is needed to overcome the impediment
46 ct of proteasome inhibition on ubiquitin and SUMO-modified proteomes using parallel quantitation of u
47 ck side binding site of Ubc9 and function as SUMO-based Ubc9 inhibitors (SUBINs).
48 lymers with ubiquitin-like modifiers such as SUMO (small ubiquitin-related modifier) or NEDD8 (neural
49 s for potential SUMOylation sites as well as SUMO interacting motifs in CPEB3.
50 ay are not efficiently degraded, many become SUMO-modified and accumulate in PML bodies.
51 uronal activity adjusted the balance between SUMO conjugation and deconjugation to continuously and b
52  Interactions Motifs (SIMs) required to bind SUMO modified substrates.
53 opy, we demonstrate that the RAP80 SIM binds SUMO-2, and that both specificity and affinity are enhan
54                       Once covalently bound, SUMO conjugation can change the stability or functionali
55 on and thioester bond formation exhibited by SUMO E1 is indeed conserved in Ub E1.
56           Post-translational modification by SUMO (small ubiquitin-like modifier) plays important but
57 on-self" nucleic acids) is also modulated by SUMO, but the underlying mechanisms are incompletely und
58  by controlling the stability of OsbZIP23 by SUMO conjugation through manipulating specific SUMO prot
59 ion and thioester bond formation revealed by SUMO E1 structures are thought to be conserved in Ub E1,
60                  This linkage is reversed by SUMO proteases, of which there are two in Saccharomyces
61 tible to extraction from DNA damage sites by SUMO-targeted ubiquitin ligase (STUbL) activity.
62  including as a signal for ubiquitination by SUMO targeted ubiquitin ligases (STUbLs).
63  septin groups can be covalently modified by SUMOs.
64 bstrate, and thus differs from the canonical SUMO-targeted substrate entry.
65  ROS triggering the evolutionarily conserved SUMO stress response, specifically depleting chromatin-a
66 lated proteins generates peptides containing SUMO-remnant diglycyl-lysine (KGG) at the site of SUMO m
67  and disordered N-terminal region containing SUMO Interactions Motifs (SIMs) required to bind SUMO mo
68           DAXX has two functionally critical SUMO-interacting motifs.
69 re particularly prominent nutrient-dependent SUMO targets.
70                             RNF212-dependent SUMO conjugation effected a checkpointlike process that
71       These findings indicate that different SUMO paralogues determine the fates of WT and mutant CFT
72 r proteins important for regulating discrete SUMO-regulated pathways.
73 ut the cell cycle, suggesting that a dynamic SUMO cycle underlies a continuous surveillance of the ce
74                                Thus, dynamic SUMO modification and the presence of SIMs in RC compone
75 ion inhibition; blocking formation of the E1-SUMO intermediate; inhibition of fatty acid synthase; no
76                    To test this, the sole E2 SUMO-conjugating enzyme, Ube2i, was ablated in mouse ooc
77  mosaic virus (TGMV) to interact with the E2 SUMO-conjugating enzyme (SCE1).
78           Specifically, BCA2 serves as an E3 SUMO ligase in the SUMOylation of IkappaBalpha, which in
79 /6 complex, including the activity of the E3 SUMO ligase NSE2, as non-redundant players that control
80                                       The E3 SUMO ligase Pli1 acts at arrested forks to safeguard int
81 inker and the SP-RING domain of PIAS3, an E3-SUMO (small ubiquitin-related modifier) ligase.
82                                         Each SUMO shifts the half-maximal activation voltage (V1/2) o
83 ometry, we identified 1209 unique endogenous SUMO modification sites.
84 also inhibited a purified, E. coli expressed SUMO protease, SENP1, in vitro, indicating the increase
85 to provide evidence that SMT7 is a bona fide SUMO protease.
86 ompany Cys-domain rotation are conserved for SUMO and Ub E1s, but changes in Ub E1 involve additional
87 e, we delineate the molecular mechanisms for SUMO-dependent control of ribosomal DNA (rDNA) silencing
88 ins a compact global architecture primed for SUMO interaction.
89 ith genetic data showing the requirement for SUMO and PCNA binding for the SDSA role of Srs2, Srs2 di
90  Here, we characterized the requirements for SUMO NB formation and for their subsequent colocalizatio
91 two KCNE1 accessory subunits, and up to four SUMOs, one on Lys424 of each KCNQ1 subunit.
92 ponent, the kinase BUB-1, contain functional SUMO interaction motifs (SIMs), allowing them to recruit
93 ely few known/effective inhibitors of global SUMO-conjugation.
94 however the mechanisms regulating the global SUMO balance remain poorly defined.
95 re, we report, Rhes, a brain-enriched GTPase/SUMO E3-like protein, induces the biogenesis of TNT-like
96   Like other SENP family members, SENP7S has SUMO isopeptidase activity but unlike full-length SENP7L
97 graphy, we solved the structure of the human SUMO E1 ubiquitin fold domain in complex with the E2, Ub
98 he phosphorylation drastically increased IE2-SUMO affinity, IE2 SUMOylation, and cis-E3 activity of I
99 nes and SUMO accounted for the increased IE2-SUMO affinity.
100 upts several long-range tertiary contacts in SUMO, leading to a heterogeneous and dynamic protein wit
101 st of malignancies associated with increased SUMO expression.
102         However, the roles of the individual SUMOs in modulating cognition and the mechanisms that li
103 n functionally co-opted via a stress-induced SUMO switch to augment antiviral immunity.
104  binding the piRNA/Piwi complex and inducing SUMO-dependent recruitment of the SetDB1/Wde histone met
105 anner, so we hypothesized that LMP1 inhibits SUMO-protease activity, resulting in reduced de-sumoylat
106 x that stimulates the return of internalized SUMO-PKD2 channels to the plasma membrane.
107 ads to lysosomal degradation of internalized SUMO-PKD2 protein, which reduces surface channel abundan
108 n stress and for activation of the intrinsic SUMO ligase activity of the complex by collapsed replica
109 es the cell-cell transport of mHTT involving SUMO-mediated mechanisms.
110 etion of the STUbL SLX5 or disruption of its SUMO-interacting motifs, confirming that Tof2 is targete
111 es SUMOylated TopoIIalpha activity using its SUMO-binding ability.
112        The burden of deSUMOylating the large SUMO-proteome rests on 6 full-length mammalian SUMO-prot
113 rate how the opposing actions of a localized SUMO isopeptidase and a STUbL regulate rDNA silencing by
114 MO-proteome rests on 6 full-length mammalian SUMO-proteases or SENP.
115                     Preventing Pli1-mediated SUMO chains was sufficient to bypass the need for anchor
116 onsumoylated (PKD2) or triple SUMO1-modifed (SUMO-PKD2) proteins.
117 both ubiquitin (Ub) and the Ub-like modifier SUMO.
118 n of all steps of HR by the protein modifier SUMO, which has been increasingly recognized for its bro
119 oforms of the small ubiquitin-like modifier (SUMO) affects thousands of proteins in the human proteom
120 dified by the small ubiquitin-like modifier (SUMO) and functionally interacts with the PIAS3 SUMO E3
121 tions between small ubiquitin-like modifier (SUMO) and SUMO interaction motif (SIM), and that APB coa
122 ly, including small ubiquitin-like modifier (SUMO) conjugating enzymes.
123               Small ubiquitin-like modifier (SUMO) conjugation is a reversible post-translational mod
124 , such as the small ubiquitin-like modifier (SUMO) domain, phospholipase A2 and PrsW-family protease
125               Small ubiquitin-like modifier (SUMO) is a common post-translational modifier that affec
126               Small ubiquitin-like modifier (SUMO) is a peptide that can be post-translationally conj
127 gation to the small ubiquitin-like modifier (SUMO) is emerging as an important mechanism to transduce
128       Dynamic small ubiquitin-like modifier (SUMO) linkages to diverse cellular protein groups are cr
129               Small ubiquitin-like modifier (SUMO) modification regulates numerous cellular processes
130  cells by the Small ubiquitin-like modifier (SUMO) on two independent sites: K169, within a consensus
131 attachment of small ubiquitin-like modifier (SUMO) proteins to a lysine (Lys) residue on target prote
132 dification by small ubiquitin-like modifier (SUMO) proteins.
133 1 for the Ubl small ubiquitin-like modifier (SUMO) revealed a single active site that is transformed
134 chment of the small ubiquitin-like modifier (SUMO) to substrate proteins modulates their turnover, ac
135  the Ub-like family, small Ub-like modifier (SUMO), has also been recognised as integral for efficien
136 onstrate that small ubiquitin-like modifier (SUMO)- and folate-dependent nuclear de novo thymidylate
137  required the small ubiquitin-like modifier (SUMO)-conjugating enzyme, UBC9, and the promyelocytic le
138    A scan for small ubiquitin-like modifier (SUMO)-interacting motifs (SIMs) revealed two SIMs in IE2
139 gen (PCNA), a small ubiquitin-like modifier (SUMO)-targeted substrate, and thus differs from the cano
140 -like protein small ubiquitin-like modifier (SUMO).
141 dified by the small ubiquitin-like modifier (SUMO).
142 controlled by small ubiquitin-like modifier (SUMO)ylation.
143 ugation of small ubiquitin-related modifier (SUMO) and comprises an important regulator of protein fu
144 own of the small ubiquitin-related modifier (SUMO) pathway components Ubc9 (a SUMO-conjugating enzyme
145 achment of small ubiquitin-related modifier (SUMO) proteins to lysine side chains to produce branched
146  modified by small ubiquitin-like modifiers (SUMOs) and what roles this modification may have in sept
147 fications by small ubiquitin-like modifiers (SUMOs) regulate many cellular processes, including genom
148 ically requires ectopic expression of mutant SUMOs with introduced tryptic sites.
149 mapping and mutagenesis, we identified a new SUMO-interacting motif (SIM) in PIASy.
150 in (PML) and thus was not due to nonspecific SUMO conjugation by ubiquitination enzymes.
151                   Yet, mutating one DENV NS5 SUMO site (K546R) localized the NS5 mutant to discrete N
152                          Our data reveal NS5 SUMO motifs as novel NB coordinating factors that distin
153 discrete NBs, and NBs formed by the ZIKV NS5 SUMO mutant (K252R) were restructured into discrete prot
154                      Expressing the ZIKV NS5 SUMO site mutant (K252R) resulted in NS5/STAT2/PML NBs t
155                                     ZIKV NS5 SUMO sites also transcriptionally regulate cell cycle an
156                      We reveal that ZIKV NS5 SUMO sites direct NS5 binding to STAT2, disrupt the form
157                                Attachment of SUMO moieties to internal lysines in Ubc9 itself can fur
158                               The binding of SUMO to SUMO interacting motifs (SIMs) can translate the
159         Moreover, the noncovalent binding of SUMO-interacting motif (SIM) at the SUMO surface was cri
160                               Conjugation of SUMO (Small Ubiquitin-like Modifier) protein to cellular
161 ar pressure regulates the surface density of SUMO-PKD2-mediated Na(+) currents (I(Na)) in myocytes to
162                                Disruption of SUMO dynamics prompts various pathophysiological conditi
163                  However, direct evidence of SUMO modification in ErbB4 signaling has remained elusiv
164 evious study has shown that re-expression of SUMO-modified MeCP2 in Mecp2-null neurons rescues synapt
165 itor of activated STAT (PIAS) RING family of SUMO E3 ligases, as essential for mitotic chromosomal SU
166     Our findings demonstrate the function of SUMO sites in ZIKV NS5 NB formation and their importance
167      Our results highlight the importance of SUMO-SIM networks in regulating the assembly of dynamic
168 how that ageing elicits a marked increase of SUMO levels in C. elegans.
169 Cas9-mediated depletion of three isoforms of SUMO diminishes Rhes-mediated mHTT transport.
170            PIASy adds to the growing list of SUMO E3 ligases containing multiple SIMs that play impor
171               Interdependent localization of SUMO, ubiquitin, and proteasomes along chromosome axes w
172 hese proteins, which is reflected by loss of SUMO at tRNA genes.
173 dence that influenza virus-triggered loss of SUMO-modified TRIM28 leads to derepression of endogenous
174                        Consequently, loss of SUMO-modified TRIM28 potentiates canonical cytosolic dsR
175 athway has co-opted a conserved mechanism of SUMO-dependent recruitment of the SetDB1/Wde chromatin m
176 , our findings provide support for a role of SUMO in the cytosolic response to aberrant proteins.
177 on regulates transcription, but the roles of SUMO proteases in transcription remain unclear.
178  review aims to connect established roles of SUMO with its newly identified effects on recombinationa
179 remnant diglycyl-lysine (KGG) at the site of SUMO modification.
180 matics is vital to the fold and stability of SUMO.
181 ing protease sites in the C-terminal tail of SUMO proteins.
182          SUMO E3 ligases enhance transfer of SUMO from the charged E2 enzyme to the substrate.
183           A major factor in the variation of SUMO-target function is the balance between the conjugat
184 ing enzyme Ubc9 catalyzes the conjugation of SUMOs to -amino groups of lysine residues in target prot
185 ition of most of the H3K9me3 mark depends on SUMO and the SUMO ligase Su(var)2-10, which recruits the
186 g correlation between LMP1 and sumo-1/2/3 or SUMO-1/2/3 levels, and show that LMP1-induced sumo expre
187 tate, a single-unoccupied molecular orbital (SUMO), which turns rectification off and drops R to 6.
188                        We reveal that OsOTS1 SUMO protease directly targets the ABA and drought respo
189      SAP domains are common among many other SUMO E3s, and are implicated in substrate recognition an
190 O) and functionally interacts with the PIAS3 SUMO E3 ligase.
191  that distinct SUBINs primarily inhibit poly-SUMO chain formation, whereas mono-SUMOylation was not i
192 will enable a thorough investigation of poly-SUMO-mediated cellular processes, such as DNA damage res
193 n further lead to the formation of polymeric SUMO chains.
194 (small ubiquitin-like modification)/polySIM (SUMO-interacting motif) condensates, analogous to PML bo
195   Modification by the ubiquitin-like protein SUMO affects hundreds of cellular substrate proteins and
196  Drosophila the small ubiquitin-like protein SUMO and the SUMO E3 ligase Su(var)2-10 are required for
197 lity and SENP2 activity is needed to provide SUMO.
198 to be the most important motifs to recognize SUMO chains.
199 tion motifs (SIMs), allowing them to recruit SUMO modified proteins, including KLP-19, into the RC.
200 and this enhancement was mediated by reduced SUMO-specific protease 1 (SENP1) and SENP3 expression, t
201     The mechanistic role of these regulatory SUMO proteases in mediating stress responses has not bee
202 me is targeted to the nucleolus for removing SUMO from specific substrates and how curtailing sumoyla
203            SUMO protease can rapidly reverse SUMO conjugation making this modification system highly
204 ess tolerance and overexpression of the rice SUMO E3 ligase gene OsSIZ1 improves heat and water defic
205  the availability of the new chain-selective SUMO inhibitors reported here will enable a thorough inv
206 rage to NPCs allows SUMO removal by the SENP SUMO protease Ulp1 and the proteasome, promoting timely
207 tational determination of the individual SIM-SUMO affinities based on these structural arrangements y
208 opportunities to characterize individual SIM-SUMO complexes and suggests that further studies will be
209                    However, the study of SIM-SUMO complexes is complicated by their typically low aff
210 l results regarding the structure of the SIM-SUMO interface.
211                       We noticed unusual SIM-SUMO interfaces in a previously reported NMR structure (
212                         Mutation of a single SUMO-targeted lysine residue perturbs telomere dynamics.
213 MO conjugation through manipulating specific SUMO protease levels.
214 stitution significantly decreased stability, SUMO/SIM affinity, and the rate of SUMOylation.
215 tif described here and a globular-structured SUMO-binding catalytic domain, to stabilize p53.
216 oting the accumulation of the BZR1 targeting SUMO protease, ULP1a.
217 quired for NS5 nuclear localization and that SUMO sites regulate NS5 NB complex constituents, assembl
218                                We found that SUMO (Small Ubiquitin-like Modifier) and SUMO ligase Ubc
219                       Results indicated that SUMO-protease activity decreased in a LMP1-dependent man
220 egradation of OsOTS1 protein indicating that SUMO conjugation is an important response to drought str
221                              We propose that SUMO conjugation establishes a precondition for designat
222                    We therefore propose that SUMO serves as a mark for nonfunctional mitochondrial pr
223                     Our findings reveal that SUMO is an important determinant of lifespan, and provid
224                                 We show that SUMO E3 ligase GEI-17/PIAS is required for KLP-19 recrui
225                                 We show that SUMO modification of mitochondrial proteins does not rel
226              Together, our data suggest that SUMO modification is essential to restrain pathogenic ba
227                     Our results suggest that SUMO-based modulation of a DNA damage sensor positively
228                                          The SUMO/SENP1 system is the most efficient for such applica
229 tivity, a SUMO acceptor site in COP1 and the SUMO E3 ligase SAP and Miz 1 (SIZ1).
230 he small ubiquitin-like protein SUMO and the SUMO E3 ligase Su(var)2-10 are required for piRNA-guided
231  of the H3K9me3 mark depends on SUMO and the SUMO ligase Su(var)2-10, which recruits the histone meth
232 d interaction with host factors, such as the SUMO E2-conjugating enzyme.
233 lecular mechanism of a novel mutation at the SUMO motif on signal transducer and activator of transcr
234 nding of SUMO-interacting motif (SIM) at the SUMO surface was critically dependent on the paired arom
235                                 To date, the SUMO E3 ligase that provides substrate specificity for S
236            Phosphorylation also enhanced the SUMO-dependent transactivation activity and auto-repress
237 lencing factor Sir4, NE-associated Esc1, the SUMO E3 ligase Siz2, and the nuclear pore complex (NPC)
238  novel selection system, we have evolved the SUMO(Eu)/SENP1(Eu) pair to orthogonality with the yeast
239                                 Finally, the SUMO acceptor lysine was functionally required for ErbB4
240       In this study, we investigated how the SUMO-SIM interaction regulates the degradation of PML II
241 hyper-methylation mutants, we identified the SUMO E3 ligase SIZ1 as a critical regulator of active DN
242  Here, protein array analysis identified the SUMO E3, protein inhibitor of activated STAT 4 (PIAS4),
243                      We further identify the SUMO-protease SENP6 as a key factor, not only controllin
244 e will focus on conjugation machinery in the SUMO, NEDD8, ATG8, ATG12, URM1, UFM1, FAT10, and ISG15 p
245 vation of specific aromatic pairs inside the SUMO protein core has a role in its stability and functi
246 DNA breaks, thus providing insights into the SUMO and ubiquitin interplay in genome maintenance.
247                               By mapping the SUMO proteome in Saccharomyces cerevisiae, we discovered
248  preventing Drp1 SUMOylation by mutating the SUMO acceptor sites enhances binding to Mff.
249               Histones are substrates of the SUMO (small ubiquitin-like modifier) conjugation pathway
250 by a calcium/calpain-induced cleavage of the SUMO E1 enzyme SAE2, thus leading to sumoylation inhibit
251 ave previously shown that acetylation of the SUMO E2 conjugase enzyme, Ubc9, at K65 downregulates its
252  here we identified an important role of the SUMO modification pathway in limiting Pol eta interactio
253                            Disruption of the SUMO pathway abolishes discrimination of interrupted and
254  mitochondrial proteins as substrates of the SUMO pathway in yeast.
255     In this study, we reveal the role of the SUMO protease, OsOTS1 in mediating tolerance to drought
256                      Either knockdown of the SUMO-activating enzyme SAE2 or pharmacologic inhibition
257 ed on a common infection-induced loss of the SUMO-modified form of TRIM28/KAP1, a host transcriptiona
258 on delineating the regulatory effects of the SUMO-SIM interaction on ICP0 E3 ubiquitin ligase activit
259 d degradation of PIM1 via recruitment of the SUMO-targeted ubiquitin ligase, RNF4.
260 nds on Cdc13 localization at DSBs and on the SUMO ligase Siz1, which is required for de novo telomere
261 AS (a SUMO-protein ligase E3), and Smt3 (the SUMO isoform in Drosophila) by RNAi prevents Smo accumul
262  activity alone was sufficient to target the SUMO machinery into NBs.
263                            We found that the SUMO (small ubiquitin-like modifier)-modification and ub
264                            We found that the SUMO (small ubiquitin-related modifier) ligase ZATT (ZNF
265                      We demonstrate that the SUMO (Small Ubiquitin-related Modifier) pathway crosstal
266                       We also found that the SUMO acceptor site mutant PIF3(K13R) binds more strongly
267 n in different contexts, suggesting that the SUMO pathway functions as an important module in gene si
268                 Our results suggest that the SUMO pathway is responsible for both repression of inter
269              We further demonstrate that the SUMO protease activity is required for supernumerous mit
270                     Our data reveal that the SUMO protease, HEARTBREAK (HTB), from Capsella rubella c
271                             We have used the SUMO(Eu) system in an affinity-capture-proteolytic-relea
272                                    While the SUMO system appears to predominantly target nuclear prot
273 membrane protein-1 (LMP1) interacts with the SUMO-conjugating enzyme Ubc9, which induces protein sumo
274 AT1 mutation (c.2114A>T, p.E705V) within the SUMO motif ((702)IKTE(705)) in a patient with disseminat
275                                        These SUMO paralogue-specific effects of PIAS4 were reproduced
276                                        These SUMO paralogues form polychains, which are recognized by
277 ite SUMOylation, and that collectively these SUMO modifications are essential for PIAS1- and STUbL-me
278                            However, how this SUMO conjugation activity concentrates the proteins invo
279 ype influenza A virus robustly triggers this SUMO switch in TRIM28, the induction of IFN-stimulated g
280 se bodies with COP1 required, in addition to SUMO conjugation activity, a SUMO acceptor site in COP1
281 UMO-1 in vivo and reduced its conjugation to SUMO-2/3.
282  SfPER-C1 peritrophin A-type domain fused to SUMO/His-tag confirmed that SfPER binds to chitin.
283  show that HR is differentially sensitive to SUMO availability and SENP2 activity is needed to provid
284                       The binding of SUMO to SUMO interacting motifs (SIMs) can translate the SUMOyla
285                              Taken together, SUMO regulates ICP0 substrate recognition via multiple f
286                                     In turn, SUMO fine-tunes DAF-16 and SKN-1 activity in specific C.
287 nnels formed without KCNE1 carry at most two SUMOs despite having four available KCNQ1-Lys424 sites.
288  interaction between the RanBP2-RanGAP1-UBC9 SUMO E3 ligase complex and NUSAP1.
289 ysine residue 714 in the ErbB4 ICD undergoes SUMO modification, which was reversed by sentrin-specifi
290  acids, Phe(36)-Tyr(51)-Phe(64), is a unique SUMO signature that is absent in other ubiquitin-like ho
291 g a resource of almost 600 common and unique SUMO remodeling events that are mounted during influenza
292             We also identified a yet-unknown SUMO-interacting motif (SIM) in YAP and TAZ required for
293 al. (2017) report how a DNA translocase uses SUMO as a cue to save Top2 from ubiquitin-mediated degra
294                  Rhes interacts with Nix via SUMO E3-ligase domain, and Nix depletion totally abrogat
295  axes are hubs for regulated proteolysis via SUMO-dependent control of the ubiquitin-proteasome syste
296       These findings suggest a model whereby SUMO regulates the distribution, oligomerization, and ac
297             PIAS4 modified F508del CFTR with SUMO-1 in vivo and reduced its conjugation to SUMO-2/3.
298  with Rac1 and inhibits its interaction with SUMO-specific protease 1 (SENP1), which in turn inhibits
299  the common F508del mutant to modify it with SUMO-2/3.
300                                     The ZATT SUMO ligase activity further promotes TDP2 interactions

 
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