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1 AIP does not affect long-term survival.
2 AIP inhibits IRF7 function by antagonizing the nuclear l
3 AIP is a rare disease whose recognition and understandin
4 AIP neurons responding to outline shapes also responded
5 AIP was also tested on induced pluripotent stem cells de
6 AIP-1 overexpression also reduced accumulation of Abeta
7 AIP-directed mitochondrial import of survivin did not af
11 and vital status of 78 patients with type 1 AIP who met the original HISORt criteria and 19 patients
13 a mutation in Caenorhabditis elegans AIPR-1 (AIP-related-1), which causes profound increases in evoke
16 type 1 AIP were older than those with type 2 AIP (62 +/- 14 vs 48 +/- 19 years; P < .0001) and had a
18 re geared toward diagnosis of type 1; type 2 AIP can be definitively diagnosed only on pancreatic his
21 IP receptors AgrC and the AIPs, as AP4-24H11.AIP-4 binding recapitulates features that have been prop
27 pon Staphylococcus lugdunensis AIP-1 (1) and AIP-2 (2) displayed respective IC50 values of 0.2 +/- 0.
32 ctrometry and discovered that the AIP-II and AIP-III signals are 12 residues in length, making them t
33 d IRF7 is enhanced upon virus infection, and AIP potently inhibits IRF7-induced type I IFN (IFNalpha/
34 al and anterior intraparietal areas (MIP and AIP), and parietal area PEip; somatosensory areas S1 and
36 t is shown to be under dorsolateral (PMv and AIP) more than dorsomedial control, and under SPL7, soma
39 rmed by macaque anterior intraparietal area (AIP) and hand area (F5) of the ventral premotor cortex i
41 tions, with the anterior intraparietal area (AIP) playing a major role in routing information about o
42 comprising the anterior intraparietal area (AIP), ventral premotor (PMv), and primary motor cortex (
45 ocated anterior to the angular gyrus such as AIP and VIP are less medially displaced relative to maca
49 s a survivin 1-141 mutant that does not bind AIP was not imported to mitochondria and failed to inhib
52 therapeutic efficacy of synthetic S. caprae AIP was evident by a dramatic reduction in both dermonec
55 led two key structural elements that control AIP-III (and non-native peptide) activity: (1) a tri-res
56 More detailed studies with the convenient AIP model indicated that CSF-1 neutralization led to a r
57 gative I-Abeta chain(-/-) (Ab0) mice develop AIP spontaneously, likely due to dysregulation of CD8(+)
58 HLA-DR*0405 transgenic Ab0 NOD mice develop AIP with high prevalence after sublethal irradiation and
59 indicate that (1)H NMR can help to diagnose AIP attacks based on the identification of ALA and PBG.
63 y, whereas patients with homozygous dominant AIP (HD-AIP) have early-onset chronic neurological impai
64 s explain the chemical principles that drive AIP production, including uncovering a hitherto unknown
66 s with SDB, which could be blocked by either AIP or KN93 (N-[2-[[[(E)-3-(4-chlorophenyl)prop-2-enyl]-
67 tructures of the three native S. epidermidis AIP signals and five non-native analogs with distinct ac
68 d analogue of the Staphylococcus epidermidis AIP-1 (3) elicited an IC50 value of 2.7 +/- 0.1 muM.
70 aration were significantly reduced following AIP cTBS without directly modifying corticospinal excita
74 tion via a thiolactone bond is essential for AIP function; therefore, recognition of the cyclic form
76 ne in the rate of operative intervention for AIP, a steroid-responsive disease with propensity for re
77 ponsive genes and suggests that a search for AIP-dependent, AHR-responsive genes may guide us to the
78 orticoids have become a standard therapy for AIP, but the indications requiring treatment as well as
81 R*0405 expression fails to protect mice from AIP, the HLA-DRB1*0405 allele appears to be an important
82 predicted well during movement planning from AIP (medial array) and F5 (lateral array), whereas M1 pr
83 tify and quantify ALA and PBG in urines from AIP patients and (2) to identify metabolites that would
88 as patients with homozygous dominant AIP (HD-AIP) have early-onset chronic neurological impairment, i
89 manifestations, knock-in mice with human HD-AIP missense mutations c.500G>A (p.Arg167Glu) or c.518_5
90 er, these studies suggest that the severe HD-AIP neurological phenotype results from decreased myelin
94 nfavorable, and therefore, it is unclear how AIP-producing bacteria produce sufficient amounts of the
97 2_844delGAG) identical to that causing human AIP and two missense mutations, c.250G>A (p.A84T) and c.
102 g peptide (AIP) signals has been identified (AIP-I), and cross talk between agr systems has not been
104 reported a set of analogues of the group-III AIP that are capable of strongly modulating the activity
105 reversible mislocalization of ductal CFTR in AIP, the association of asymptomatic pancreatic hyperenz
107 ral other antibodies have been identified in AIP against pancreas-specific antigens like trypsinogens
108 of grasp-related and spatial information in AIP and F5 suggests at least a supportive role of these
109 activity from many electrodes in parallel in AIP and F5 while three macaque monkeys (Macaca mulatta)
112 aze and target positions were represented in AIP and F5 and could be readily decoded from single unit
114 1 residues were defective in a later step in AIP biosynthesis, separating the peptidase function from
116 CACS were markedly elevated with increasing AIP quartile in participants with baseline CACSs of 0 an
119 expressing the SR-targeted CaMKII inhibitor AIP, without any significant enhancement of apoptosis vs
120 Non-native ligands capable of intercepting AIP:AgrC binding, and thereby QS, in S. aureus have attr
122 e we report that the anterior intraparietal (AIP) and the rostral ventral premotor area (F5) in the m
124 ng activity from the anterior intraparietal (AIP), ventral premotor (F5), and primary motor (M1) cort
126 2 stoichiometry, while an antagonist ligand, AIP-II, functions as an inverse agonist of the kinase ac
128 logues based upon Staphylococcus lugdunensis AIP-1 (1) and AIP-2 (2) displayed respective IC50 values
129 e rescued by presynaptic expression of mouse AIP, demonstrating that a conserved function of AIP prot
130 utocamtide-2-related inhibitory peptide (myr-AIP)--but not by inhibition of the activity of protein p
131 ) blockers applied by bath (KN-93, myristoyl-AIP) or expressed selectively in the sensory neurons (AI
132 onal structural analysis of the known native AIP signals (AIPs-I-IV) and several AIP-III analogues wi
136 levations (>140 mg/dl) are seen in 70-80% of AIP patients and also in 5% of normal population and 10%
137 in S. aureus by sensing the accumulation of AIP via the histidine kinase AgrC and the response regul
138 utable to higher-than-normal accumulation of AIP-III in a codY mutant strain, as determined using ult
139 emistry for the diagnosis of acute attack of AIP and identify urinary glycin as a potential marker of
141 ed as a hub that shared the visual coding of AIP only temporarily and switched to highly dominant mot
143 dressed this by studying the consequences of AIP "virtual lesions" on physiological interactions betw
146 identify recent advances in the diagnosis of AIP and evaluate outcomes with various diagnostic strate
148 tural insights may enable the engineering of AIP cross-reactive antibodies or quorum quenching vaccin
149 cilitate the optimal processing or export of AIP for signal amplification through AgrC/A and inductio
152 owever, when combined with other features of AIP, it can be of great diagnostic value though its util
157 , demonstrating that a conserved function of AIP proteins is to inhibit calcium release from ryanodin
158 uced activation of IFN, whereas knockdown of AIP by siRNA potentiates virally activated IFN productio
161 strong structural support for a mechanism of AIP-mediated AgrC activation and inhibition in S. aureus
165 he first naturally occurring animal model of AIP in four unrelated cat lines who presented phenotypic
166 t plays a key role in the invasive nature of AIP-mutation-positive tumors and the CCL5/CCR5 pathway i
168 sgenic model, we show that overexpression of AIP-1 protected against, while RNAi knockdown of AIP-1 e
183 G4) is a feature of autoimmune pancreatitis (AIP) and IgG4-associated cholangitis (IAC); a >2-fold in
184 isting knowledge of autoimmune pancreatitis (AIP) and to review the progress made in the diagnosis an
185 e concentrations in autoimmune pancreatitis (AIP) by restoring mislocalized CFTR protein to the apica
191 or the diagnosis of autoimmune pancreatitis (AIP) with the objective of establishing a strategy to di
192 genic mechanisms of autoimmune pancreatitis (AIP), an increasingly recognized, immune-mediated form o
193 es of patients with autoimmune pancreatitis (AIP), and follow-up periods have generally been short.
195 allel in macaque premotor (F5) and parietal (AIP) cortices during a delayed grasping task revealed th
196 tive inhibitors of the autoinducing peptide (AIP) activated AgrC receptor, by altering the activation
197 ine kinase detects its autoinducing peptide (AIP) ligand and generates an intracellular signal result
199 and the binding of an autoinducing peptide (AIP) signal to its cognate transmembrane receptor (AgrC)
200 s, but only one of the autoinducing peptide (AIP) signals has been identified (AIP-I), and cross talk
201 pathogen that utilizes autoinducing peptide (AIP) signals to mediate QS and thereby regulate virulenc
202 ning peptide called an autoinducing peptide (AIP) that is biosynthesized from the AgrD precursor by t
203 ted that the S. caprae autoinducing peptide (AIP) was responsible, and mass spectrometric analysis id
204 analogues of a native autoinducing peptide (AIP-III) signal that can inhibit AgrC-type QS receptors
205 sed in FRD-SR-autocamide inhibitory peptide (AIP) mice, expressing the SR-targeted CaMKII inhibitor A
206 or autocamtide-2-related inhibitory peptide (AIP) normalized the increased amplitude of NMDAR-EPSCs a
208 e, autocamtide-2-related inhibitory peptide [AIP], is fused to green fluorescent protein (GFP) and ex
211 ls with aggregation-induced phosphorescence (AIP) is designed, which exhibits two distinctly differen
213 ion between the atherogenic index of plasma (AIP), which has been suggested as a novel marker for ath
216 patients with acute intermittent porphyria (AIP), an inherited metabolic disorder of heme biosynthes
221 nvaginations-the anterior intestinal portal (AIP) towards the rostral end of the embryo and the cauda
223 tios of aqueous-inlet to oil-inlet pressure (AIP/OIP), yielding a linear relationship between muaq an
227 yl hydrocarbon receptor interacting protein (AIP) mutation-induced aggressive, young-onset growth hor
228 yl hydrocarbon receptor-interacting protein (AIP) mutations lead to somatotroph tumorigenesis in mice
229 yl hydrocarbon receptor-interacting protein (AIP), a co-chaperone protein, as required for response t
230 yl hydrocarbon receptor-interacting protein (AIP), a survivin-associated immunophilin, causes embryon
233 uitin ligase atrophin-1 interacting protein (AIP)4 to bind, ubiquitinate, and stabilize Amot130.
234 In import assays using recombinant proteins, AIP directly mediated the import of survivin to mitochon
240 n native AIP signals (AIPs-I-IV) and several AIP-III analogues with varied biological activities usin
245 be a signature of healthy muscle whereas SHG-AIP with one centered spot in pathological mdx muscle is
247 esults demonstrated that binding of a single AIP molecule was sufficient to enhance filament severing
249 oxidative stress but not apoptosis in FRD-SR-AIP mice, in which a CaMKII inhibitor is targeted to the
250 eractions between the cognate staphylococcal AIP receptors AgrC and the AIPs, as AP4-24H11.AIP-4 bind
259 onal structure, although it is possible that AIP needs more training time to learn to generate novel
262 that active endodermal shortening around the AIP accounts for most of the heart field motion towards
266 adjusting for traditional risk factors, the AIP was significantly associated with CAC progression in
267 Taking advantage of the AIE feature, the AIP molecules are fabricated into OLEDs as a homogeneous
269 n December 2011 proposed a structure for the AIP to provide a framework for the minimal components of
271 We now invite broader participation in the AIP development process so that the resource can be impl
272 frequently associated with mutations in the AIP gene and are sometimes associated with hypersecretio
273 wered inflammatory macrophage number; in the AIP model, this reduced number was not due to suppressed
275 these studies provide new insights into the AIP:AgrC interactions crucial for QS activation in S. ep
276 s challenge the current understanding of the AIP area as a critical stage in the dorsal stream for th
284 ng mass spectrometry and discovered that the AIP-II and AIP-III signals are 12 residues in length, ma
286 d into four groups (I-IV) according to their AIP signal and cognate extracellular receptor, AgrC.
287 We structurally characterized all three AIP types using mass spectrometry and discovered that th
288 ere stratified into four groups according to AIP quartiles, which were determined by the log of (trig
289 tabolites that would predict the response to AIP crisis treatment and reflect differential metabolic
290 T cells; we compared their susceptibility to AIP with HLA-DQ8 or HLA-DR*0401 (single) transgenic, or
291 transgenic mice can also develop unprovoked AIP, whereas HLA-DR*0401, HLA-DQ8, and HLA-DR*0405/DQ8 t
292 ial variability and movement timing, whereas AIP might be more closely linked to overall movement int
293 ructure of the AP4-24H11 Fab in complex with AIP-4 at 2.5 A resolution to determine its mechanism of
295 We analyzed data from 122 individuals with AIP who were followed from 2003 to 2013 and genotyped fo
297 sed in pancreatic tissues from patients with AIP, compared with controls, and expression of chemokine