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1 cations, such as oxidation, nitrosation, and lipidation.
2 ction, and NOX inhibition does not block LC3 lipidation.
3  low levels of apoE4 lipoprotein association/lipidation.
4 e ATG conjugation system, which mediates LC3 lipidation.
5 e generation of small vesicles active in LC3 lipidation.
6 1/ABCG1-induced apoE lipoprotein association/lipidation.
7  important for E3 interaction as well as LC3 lipidation.
8 diated autophagy in plants by promoting ATG8 lipidation.
9  as the optimal position for neoglycopeptide lipidation.
10 nd that further expansion occurs via post-ER lipidation.
11 licated in palmitoyl transfer during protein lipidation.
12  preventing or limiting the extent of apoA-I lipidation.
13 nt properties of Ha-Ras activation state and lipidation.
14 ollowed by a slower process of MTP-dependent lipidation.
15 t that apoB may interact with MTP before its lipidation.
16 ional constraint and competitive blockade of lipidation.
17 ATG3, and ATG12ATG5-ATG16L1 machinery of LC3 lipidation.
18  facilitated by hydrophobic interactions and lipidation.
19 ted in Parkinson's disease, through GABARAPs lipidation.
20 aliA and aliB, are important for lipoprotein lipidation.
21 ated proteins 1A/1B light chain 3 (ATG8/LC3) lipidation.
22 ul for investigating the function of protein lipidation.
23  ALPS has additional roles in supporting LC3 lipidation.
24 tion of ATG16L1 to the PAS and inhibited LC3 lipidation.
25 TG16L1, enzymes contributing directly to LC3 lipidation.
26 action at a level similar to that of protein lipidation.
27           STING activation also induces LC3B lipidation, a classical but equivocal marker of autophag
28 ree assay, purified PlcA protein blocked LC3 lipidation, a key step in early autophagosome biogenesis
29 artment (ERGIC) as a membrane source for LC3 lipidation, a key step of autophagosome biogenesis.
30 ck a known recognition signal for C-terminal lipidation, a modification that is generally necessary f
31 ed to be the result of the impairment of Ras lipidation, a stable modification (T1/2 approximately 20
32 istoylation is a ubiquitous class of protein lipidation across eukaryotes and N-myristoyl transferase
33  induction and flux, including synthesis and lipidation/activation of the ubiquitin-like protein LC3
34 recruitment of COPII to the ERGIC to bud LC3 lipidation-active vesicles as one potential membrane sou
35 he donor membrane in the generation of small lipidation-active vesicles.
36      When expressed in cells with endogenous lipidation activity, the substrate is intracellularly li
37 ough the motif and exhibit WDD-dependent LC3 lipidation activity.
38 orm in astrocytes, suggesting that increased lipidation acts as a folding chaperone enabling E4 to ad
39 we examined the roles of N-glycosylation and lipidation/acylation in regulating the activities of Win
40               However, in the absence of LC3 lipidation, additional factors are required including TA
41     MmcO is membrane associated, probably by lipidation after export across the inner membrane by the
42                                         ATG8 lipidation also occurs during non-canonical autophagy, a
43 ghts into the interactions among ABCA1, ApoE lipidation and aggregation, and underscores the promise
44           Recent studies have shown that the lipidation and assembly state of apolipoprotein E (apoE)
45 induced by sorafenib was validated by LC3B-I lipidation and autophagosome accumulation.
46 omises starvation- and rapamycin-induced LC3 lipidation and autophagosome formation.
47 acellular bacteria clearance by inducing LC3 lipidation and autophagosome formation.
48 pids that plays an essential role during LC3 lipidation and autophagosome maturation.
49 autophagosomes and by measuring LC3B protein lipidation and autophagy-related protein expressions.
50 ibited significantly reduced (48%; p < 0.01) lipidation and evidence of HDL biogenesis.
51 esidues is the only known reversible form of lipidation and has been implicated in protein membrane a
52  of ABCA1 in humans and mice causes abnormal lipidation and increased catabolism of HDL, resulting in
53 ed protein 1 light chain 3 beta-II (LC3B-II) lipidation and induced sequestosome 1 (SQSTM1, p62) tran
54  for morphology, Western blotting for LC3B-I lipidation and mammalian target of rapamycin signaling m
55                                              Lipidation and processing of NilC occurs by a mechanism
56 ients show reduced WIPI2 puncta, reduced LC3 lipidation and reduced autophagic flux.
57 gene into PLTP-KO hepatocytes stimulated the lipidation and secretion of apoB:1000-containing lipopro
58 lore the mechanism involved, we examined the lipidation and secretion of nascent very low-density lip
59  before adding OA and the inhibitor, apoB100 lipidation and secretion were no longer impaired.
60 nteracts with GABARAP, thus facilitating LC3 lipidation and subsequent lysosomal acidification to per
61                                  Both ligand lipidation and target field response influence the gradi
62  in the N-terminal mutation, the position of lipidation and the linkage to lipid.
63 xpected mechanisms of TFEB activation by LC3 lipidation and their physiological relevance during the
64                                 However, Wnt lipidation and Wnt-Frizzled (Fzd) cross-reactivity have
65 through a similar function for TM6SF2 in the lipidation and/or export of both hepatically and intesti
66 creased ABCA1, apoE4 lipoprotein-association/lipidation, and apoE4/Abeta complex, decreased soluble A
67 ocumented phosphorylation, glycosylation and lipidation, and resolve previously uninterpretable densi
68 0 had no detectable effect on the synthesis, lipidation, and secretion of apoB:1000-containing partic
69 ical experimental conditions, the synthesis, lipidation, and secretion of endogenous apoB100-containi
70 anterior muscles, the levels of LC3B protein lipidation, and the expression of autophagy-related gene
71 ases process inactive pro-LC3/GABARAP before lipidation, and the same proteases can also deconjugate
72 3B-ATG3 thioester intermediate formed before lipidation, and we biochemically demonstrate that ATG4B
73 e membrane as might be allowed by the normal lipidation; and (4) in order to function properly, there
74 ion of markers of autophagy (LC3 punctae and lipidation) around mitochondria in human dopaminergic ce
75 s essential for its subsequent intracellular lipidation as apoB28 synthesized in hepatoma cells under
76 ether chaperone binding is dependent on apoB lipidation as they secrete both unlipidated and lipidate
77 roduces a key autophagy initiation step, LC3 lipidation, as a biochemical readout to probe the role o
78 , the E2-like enzyme involved in LC3/GABARAP lipidation, as one target of conjugation with multiple c
79         Knockdown of HSF-1 increased the LC3 lipidation associated with formation of autophagosomal o
80 agy but essential for VPS34-independent LC3B lipidation at perturbed endosomes.
81  in intracellular traffic rather than in LC3 lipidation brings this "secondary" activity of ATG16L1 i
82                           Post-translational lipidation by prenylation of the CaaX-box C-terminal mot
83                             We conclude that lipidation can make Abeta more prone to aggregation and
84                                We review how lipidation can overcome common challenges in biologics d
85 ivity toward errant nucleophiles, while Atg8 lipidation cascade enzymes induce E2 active site remodel
86 ule-associated proteins 1A/1B light chain 3) lipidation cascade interact with curved membranes, provi
87 ption of AliA- and AliB-mediated lipoprotein lipidation caused severe growth defects, decreased motil
88  reinhardtii based on the protein abundance, lipidation, cellular distribution, and mRNA levels of th
89  total OMV proteins, suggesting that antigen lipidation could be a universal approach for OMV manipul
90 ncreased tubule length whereas expression of lipidation-defective LC3 decreased tubule length relativ
91 indings were associated with reversal of the lipidation deficiency of apoE4 and of the cognitive impa
92  suggest that this is due to reversal of the lipidation deficiency of apoE4.
93 (o)G204A, RGS-insensitive alpha(o)G184S, and lipidation-deficient alpha(o)G2A were all defective in t
94 virus type 1 (HIV-1) matrix (MA) protein and lipidation-deficient mutants of the fibroblast growth fa
95 ence of WIPI2 is insufficient to support LC3 lipidation, demonstrating that WIPI2 allosterically acti
96 is the E2-like enzyme necessary for ATG8/LC3 lipidation during autophagy.
97 an compensate for WIPI2 depletion to sustain lipidation during starvation.
98 ative analysis of dynamic changes in protein lipidation during vertebrate embryonic development.
99                                              Lipidation enhanced membrane affinity for most Legionell
100 gt have been identified, suggesting distinct lipidation enzymes evolved in archaea to accommodate the
101 ide is able to reverse ATG8 accumulation and lipidation, even in wild-type plants when autophagy is i
102                N-myristoylation is a protein lipidation event in which myristate is covalently linked
103 e necessary only for early translocation and lipidation events.
104 ng LC3-associated phagocytosis and other LC3-lipidation events.
105 nsity lipoproteins depends on lipid binding (lipidation) for its secretion.
106  protein that requires assembly with lipids (lipidation) for its secretion.
107 odified peptides (e.g. amidation, oxidation, lipidation, glycosylation or d-amino acids), and peptide
108 owever, little is known about how N-terminal lipidation governs membrane compartmentalization of prot
109                  However, PORCN-mediated Wnt lipidation has not been reconstituted in vitro with puri
110 mation of ATG16L1 aggregates and impairs LC3 lipidation, hence altering lysosomal fusion and degradat
111 is but also strongly suppressed hepatic VLDL lipidation, hence promoting the storage of "old fat." In
112 of both a substrate and a product of protein lipidation in a biologically relevant context.
113 alysis is required to study roles of protein lipidation in cellular regulation.
114 PLTP expression significantly increases VLDL lipidation in hepatocyte microsomal lumina, and also VLD
115 ac reduces APOE aggregation and enhances its lipidation in human brains, as well as in cellular and b
116 exploration of five major classes of protein lipidation in living cells, through the use of specific
117 omplex interplay between phosphorylation and lipidation in mediating the localization of GAP43 in neu
118 ced by stress and uncover a function for LC3 lipidation in regulating lysosome size and activity thro
119                Our data show a novel role of lipidation in targeting a checkpoint protein to KTs thro
120 asmic reticulum (ER), followed by subsequent lipidation in the ER and Golgi compartment.
121                 DC-LC3in-D5 compromises LC3B lipidation in vitro and in HeLa cells, leading to defici
122 nformationally activate Atg3 and elicit Atg8 lipidation in vitro and in vivo.
123 both necessary and sufficient to trigger LC3 lipidation in vitro.
124  and show its essential role in LC3B/GABARAP lipidation in vitro.
125 pared with ApoE3, but whether enhancing ApoE lipidation in vivo can reverse ApoE aggregation is not k
126 hagy mediator that specifies the site of LC3 lipidation, includes a C-terminal domain formed by 7 WD4
127 nding cassette transporter A1-mediated apoAI lipidation increases HDL biogenesis, thus stabilizing ci
128 assage B. burgdorferi spirochetes of a novel lipidation-independent activity capable of inducing cyto
129 s B. burgdorferi spirochetes express a novel lipidation-independent activity which induces secretion
130             However, how phosphorylation and lipidation interplay to mediate sorting of GAP43 is uncl
131                                         LC3B lipidation inversely correlates with thigh cross-section
132                                              Lipidation is a clinically-proven post-translational mod
133                                         ApoE lipidation is controlled by the activity of the ATP bind
134 eps of the macroautophagy pathway, and their lipidation is essential for autophagosome formation.
135        In the vastus lateralis, LC3B protein lipidation is increased by COPD and the expression of au
136 's disease, ABCA1 role as a modifier of APOE lipidation is of significance for this disease.
137                  Although post-translational lipidation is prevalent in eukaryotes, its impact on the
138    On giant unilamellar vesicles (GUVs), LC3 lipidation is strictly dependent on the recruitment of W
139 ranslational modification whereby C-terminal lipidation leads to protein localization to membranes.
140 rmore, the Ca(2+) leakage-dependent ATG8/LC3 lipidation limited Mtb phagosome damage and restricted M
141 ion strategies, others hijack the eukaryotic lipidation machinery to ensure plasma membrane localizat
142 king ATG5, an essential component of the LC3 lipidation machinery, show reduced ability to regulate l
143  of selective autophagy in cells lacking the lipidation machinery, wherein receptor-mediated clusteri
144 ence of several core ATGs, including the LC3 lipidation machinery.
145 ked glycosylation site insertion and protein lipidation mapping in conjunction with cellular fraction
146 ivity was shown to be dependent upon protein lipidation, mast cell TNF-alpha release was not induced
147 teins in cellular membranes via differential lipidation may be more subtle than previously thought.
148  studies suggest that both N-methylation and lipidation may contribute to antibiotic activity, wherea
149 substrate for Lpcat1 and reveal that histone lipidation may occur through its O-palmitoylation as a n
150 istically distinguish between different LC3B lipidation mechanisms under different cellular condition
151  or mammalian proteins that commonly undergo lipidation might also function as antigens.
152 at the nature and regiochemistry of glycosyl lipidation modulated vancomycin-resistent Enterococci po
153 s have been discovered, including acylation, lipidation, monoaminylation, and glycation, many of whic
154 RrgA, an ancillary pilus subunit devoid of a lipidation motif, particularly when presented as part of
155 ractions, we engineered probes consisting of lipidation motifs attached to fluorescent proteins by va
156                                   Thus, dual lipidation motifs on Gpa1p and Ste18p are required for a
157                      This type of reversible lipidation occurs in both plasma and organellar membrane
158                                              Lipidation occurs in the endoplasmic reticulum and is de
159 oteins reside in secretory vesicles, or full lipidation occurs post-ER.
160 n the folding of apoB before any substantial lipidation occurs.
161                GGTase-I catalyzes C-terminal lipidation of >100 proteins, including many GTP- binding
162 nvolved in delivery of TLR2 agonists such as lipidation of antigen, conjugation to polymers, phosphon
163 f ABCA1, thereby allowing the second step of lipidation of apoA-I and formation of nascent high densi
164                                              Lipidation of apoA-I by ABCA1 increases its potential fo
165                                      Initial lipidation of apoA-I by hepatic ABCA1 is critical for pl
166 ways than lipid-free apoA-I in vitro and (2) lipidation of apoA-I prevents it from rapidly associatin
167 est that ABCA1 is necessary for the adequate lipidation of apoAI, which enables the interaction with
168 eride transfer protein (MTP), which mediates lipidation of apoB in HepG2 cells.
169 ational assembly pathway, post-translational lipidation of apoB28 displayed a strict dependence upon
170 tative functional role of MTP in the initial lipidation of apoB:1000 in stable transformants of McA-R
171 trate that Abca1 is essential for the proper lipidation of ApoE and mediates the effects of T0 on Abe
172  found to have markedly decreased levels and lipidation of apoE in the central nervous system.
173 he conclusions that increased ABCA1-mediated lipidation of apoE in the CNS can reduce amyloid burden
174 sing ABCA1 in the brain would have increased lipidation of apoE-containing lipoproteins and decreased
175 Tg primary astrocytes demonstrated increased lipidation of apoE-containing particles.
176 containing lipoproteins, suggesting abnormal lipidation of apoE.
177             If the APOE4 loss-of-function is lipidation of apoE4, then induction of ABCA1/ABCG1 may b
178                            This implies that lipidation of apolipoprotein A-I by the ABCA1 pathway is
179 phospholipid transfer activity of MTP in the lipidation of apolipoprotein B and CD1d has been indicat
180 epithelial cells (IECs) and is essential for lipidation of apolipoprotein B, associates with CD1d in
181 use models by inducing the transcription and lipidation of apolipoprotein E (apoE).
182  inhibited under stress conditions to ensure lipidation of ATG8 and thus autophagy progression in C.
183    ATG5 is a part of the E3 ligase directing lipidation of ATG8 proteins, a process central to membra
184 ed E1-E2-E3 trienzyme cascade that catalyzes lipidation of Atg8-family ubiquitin-like proteins (UBLs)
185 tidylinositol-3-phosphate, as well as on the lipidation of Atg8/LC3-like proteins, this area of resea
186                                 However, the lipidation of Atg8p and assembly of the micropexophagic
187 e palmitoylation, a common posttranslational lipidation of cysteine residues.
188 nsporter, which plays a critical role in the lipidation of extracellular apolipoprotein acceptors, tr
189                   Mutagenesis of the site of lipidation of FlgP (C18G) prevented [3H]palmitate incorp
190 o complement this defect, demonstrating that lipidation of FlgP is essential for its role in intestin
191                                              Lipidation of FXYD1 was shown to critically modulate inh
192 idence that overexpression of Bcl-2 inhibits lipidation of GABARAP, a key step in autophagosome forma
193 lipoprotein A-I provides the scaffolding for lipidation of HDL and has an important role in reverse c
194 -/- mice to ask whether ABCA1 is involved in lipidation of HDL in the central nervous system (CNS).
195 irculation of mature HDL particles by direct lipidation of hepatic lipid-poor apoA-I, slowing its cat
196   However, a role for adipose in cholesterol lipidation of high-density lipoprotein (HDL) in vivo is
197 sferase (FTase) catalyzes post-translational lipidation of key signal transduction proteins and is es
198 h its effect on ATG5, HuD contributed to the lipidation of LC3 and the formation of LC3-positive auto
199                                              Lipidation of LC3 is required for its coclustering with
200            Autophagy results in the covalent lipidation of LC3, conferring the property of membrane a
201 e proteolytic cleavage of pro-LC3 and the de-lipidation of LC3-PE from autophagosomes, both executed
202                                              Lipidation of methionine sulfoxide reductase A occurs in
203 elated genes Atg4c and Atg7 (involved in the lipidation of microtubule-associated protein 1 light cha
204 iciently suppressed a key step in autophagy, lipidation of microtubule-associated protein 1 light cha
205 formation of autophagosomes by promoting the lipidation of microtubule-associated protein LC3 (light
206                 Although CASM results in the lipidation of multiple ATG8 protein family members, we e
207                 Our results demonstrate that lipidation of N/OFQ(1-13)-NH(2) is a useful strategy for
208 ansfer protein (MTP) plays a key role in the lipidation of nascent apoB and the secretion of apoB-con
209  of the endoplasmic reticulum and in the net lipidation of nascent apoB, and may be essential for lip
210      Here, we report that post-translational lipidation of newly synthesized proteins in axonal compa
211                      Hence, we reasoned that lipidation of peptidomimetic ligands could promote membr
212 rase (FTase) catalyzes the carboxyl-terminal lipidation of Ras and several other cellular signal tran
213  not the glycine-rich motif, is required for lipidation of TbpB and tethering to the outer membrane.
214 alysts that exhibit site-selectivity for the lipidation of the aliphatic hydroxyls on vancomycin, gen
215 ES1 deficiency promotes the accumulation and lipidation of the ATG8 protein, which is associated with
216 ion of WHAMM in healthy cell lines inhibited lipidation of the autophagosomal protein LC3 and clearan
217 hanism of membrane degradation that involves lipidation of the autophagy protein LC3 onto lysosomal m
218 to the peripheral cytoplasm, contributing to lipidation of the autophagy protein LC3B and maturation
219 totic cell death that is associated with the lipidation of the autophagy protein microtubule-associat
220  ATG16L1 is mostly known for its role in the lipidation of the human homologs of ATG8 (i.e., LC3 and
221 geranyltransferase were both involved in the lipidation of the Legionella CAAX motif proteins.
222 man embryonic kidney 293 cells that measures lipidation of the marker protein GFP-LC3 following amino
223 PR signaling pathways suppressed HCV-induced lipidation of the microtubule-associated protein light c
224 ein B output and (ii) changing the degree of lipidation of the particles with triacylglycerol so that
225                               Host-dependent lipidation of these three effectors directs plasma membr
226  (FTase) catalyzes the biologically relevant lipidation of up to several hundred cellular proteins.
227 luding reduced triglyceride secretion, lower lipidation of very-low-density lipoproteins, and increas
228                                              Lipidation of Vtg occurs at its site of synthesis in ver
229       Although it is generally accepted that lipidation of WNTs by the acyltransferase Porcupine (POR
230 hree cargo receptors potently stimulated LC3 lipidation on GUVs.
231 in of ATG16L1 and specifically mediates ATG8 lipidation on single membranes.
232 t gaps in our understanding of the effect of lipidation on therapeutic efficacy, where increased rese
233 cipated mechanism that is distinct from LC3B lipidation onto double-membrane autophagosomes.
234 We report that STING activation induces LC3B lipidation onto single-membrane perinuclear vesicles med
235        Deleting Atg7 or Atg5 or blocking LC3 lipidation or ATG5-ATG12 conjugation decreases ERK phosp
236 s without the need for modifications such as lipidation or chemical stapling.
237 dependent of its length, its requirement for lipidation or microsomal triglyceride transfer protein e
238                                  In the dual lipidation pathway, bCdc42 was prenylated, but it bypass
239 Ras constructs, including key changes to the lipidation pattern of the hypervariable region, suggest
240 ts derived from peptides already modified by lipidation, PEGylation, and Fc fusion could produce ultr
241      First, we discuss the current status of lipidation, PEGylation, and Fc fusion technologies to ob
242 n, Lys/Arg post-translational modifications, lipidation, peptide stapling, and improved parameterizat
243 g the three modified peptides, the degree of lipidation positively correlated with increased intestin
244 ith a ChREBP-dependent induction of the VLDL lipidation proteins microsomal TG transfer protein and t
245  post-translational modifications, including lipidation, proteolysis, and carboxyl methylation.
246                          Phosphorylation and lipidation provide posttranslational mechanisms that con
247                            Posttranslational lipidation provides critical modulation of the functions
248                   We have utilized a natural lipidation PTM (hedgehog-mediated cholesterol modificati
249                   Here, we introduce protein-lipidation quantitation (PLQ)-the first method for quant
250                                              Lipidation, raft targeting, and secretion can be blocked
251   Previously, we established a cell-free LC3 lipidation reaction to identify the ER-Golgi intermediat
252                When both PI 3-kinase and LC3 lipidation reactions were performed simultaneously, posi
253                        Unexpectedly, the LC3-lipidation-related functions of ATG16L1 are not required
254 ssential step of this process in yeast, Atg8 lipidation, relies on the presence of Atg16, a subunit o
255         Molecular mechanisms underlying Atg8 lipidation remain poorly understood despite association
256                 Despite its great potential, lipidation remains an underutilized strategy in the clin
257                                 In vitro LC3 lipidation requires energy and is subject to regulation
258 s the ATG8-PE adduct, we also show that ATG8 lipidation requires the ATG12-ATG5 conjugate.
259  but not Lsp engineered to lack its putative lipidation residue.
260                  In conclusion, apoB100 bulk lipidation, resulting in conversion of LDL/HDL to VLDL,
261          Further systematic analysis of Rheb lipidation revealed that weak, nonselective, membrane in
262  any known recognition signal for C-terminal lipidation, Rit-transformed cell growth and survival in
263                     However, mutation of the lipidation site did not affect the oxidase activity or t
264 gement, an aromatic belt in proximity to its lipidation site positions the highly electronegative sur
265 thin the C-terminal tail, serve as important lipidation sites and are differentially conjugated to pa
266 to increase apoE levels without altering its lipidation state may actually worsen Abeta amyloidosis,
267  as the number of phospholipid molecules or "lipidation state" of apoA-I increases.
268                                          The lipidation states of apolipoproteins and Abeta peptides
269 n is dependent upon the ApoE isoform and its lipidation status.
270 gh both regulated translocation and an early lipidation step of the nascent particle with cholesterol
271 s must undergo a series of posttranslational lipidation steps before they become biologically functio
272                                      GABARAP lipidation, stimulated by the channel of STING, is key f
273  peptide efficacy using two distinct peptide lipidation strategies.
274 modified dendrimer platform with and without lipidation strategy.
275  of LC3 or Atg7, a protein that mediates LC3 lipidation, suppressed HCV replication, indicating a pos
276  on these results we propose a model whereby lipidation targets Wnt-1 to secretory vesicles that deli
277 ppression of G9a induces LC3B expression and lipidation that is dependent on RNA synthesis, protein t
278 TING pathway induces V-ATPase-dependent LC3B lipidation that may mediate cell-autonomous host defense
279                                          LC3-lipidation, the signature of autophagosome formation, re
280  oleic acid (OA) was added to stimulate apoB lipidation; therefore, either large apoB100-lipoproteins
281                            cGAMP induced LC3 lipidation through a pathway that is dependent on WIPI2
282        However, only complex C1 supports LC3 lipidation through the curvature-targeting amphipathic l
283  we establish a cell-free assay based on LC3 lipidation to define the organelle membrane supporting e
284 of single domains into multidomain proteins, lipidation to mimic posttranslational modifications, and
285  that all ATG8s can also undergo alternative lipidation to phosphatidylserine (PS) during CASM, induc
286 ic phospholipid, 15-HpETE-PE, promoted LC3-I lipidation to stimulate autophagy.
287 nding amphipathic helix is required for LC3B lipidation under all conditions tested.
288 nt in ATG8 function is ATG12, which promotes lipidation upon its attachment to ATG5.
289 ically modifies the V-ATPase to inhibit LC3B lipidation via ATG16L1.
290                                 When apoB100 lipidation was blocked by an inhibitor of MTP (MTPI), re
291 ophagosomal and autophagosomal membranes via lipidation, was analyzed in the CCL-136 muscle cell line
292 ein-lipid conjugation reaction, the ATG8/LC3 lipidation, we show how the membrane association of the
293 ng ERGIC serves as a membrane source for LC3 lipidation, which is a key step in autophagosome biogene
294 or localizing ATG12-5-16 L1 and driving ATG8 lipidation, whilst WIPI3 and 4 belong to a second W34IR-
295 creased markers of autophagy, including LC3B lipidation with further accumulation following bafilomyc
296 between PI3KC3-C1 and WIPI2 led to rapid LC3 lipidation with kinetics similar to that seen in cellula
297                          This unique form of lipidation with palmitoleic acid is a vital step in the
298     A second conjugation reaction, Aut7/Atg8 lipidation with phosphatidylethanolamine, as well as a p
299  protein-protein interaction prevents PfAtg8 lipidation with phosphatidylethanolamine.
300                         We reconstituted LC3 lipidation with recombinant PI3KC3-C1, -C2, or various m

 
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