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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 is steroid-responsive but maintaining remission cont
5 AIP neurons responding to outline shapes also responded
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
14 nd evaluated the inhibitory activities of 10 AIP derivatives based on a truncated AIP analogue that i
17 type 1 AIP were older than those with type 2 AIP (62 +/- 14 vs 48 +/- 19 years; P < .0001) and had a
19 re geared toward diagnosis of type 1; type 2 AIP can be definitively diagnosed only on pancreatic his
22 IP receptors AgrC and the AIPs, as AP4-24H11.AIP-4 binding recapitulates features that have been prop
25 AgrC1 loop 2 resulted in conversion of (Ala5)AIP-1 from a potent antagonist to an activator, essentia
29 while differential recognition of AIP-1 and AIP-4 depends primarily on three amino acid residues in
31 pon Staphylococcus lugdunensis AIP-1 (1) and AIP-2 (2) displayed respective IC50 values of 0.2 +/- 0.
36 ctrometry and discovered that the AIP-II and AIP-III signals are 12 residues in length, making them t
37 d IRF7 is enhanced upon virus infection, and AIP potently inhibits IRF7-induced type I IFN (IFNalpha/
38 al and anterior intraparietal areas (MIP and AIP), and parietal area PEip; somatosensory areas S1 and
39 detection of early chronic pancreatitis and AIP, risk stratification and application of risk-lowerin
44 rmed by macaque anterior intraparietal area (AIP) and hand area (F5) of the ventral premotor cortex i
46 comprising the anterior intraparietal area (AIP), ventral premotor (PMv), and primary motor cortex (
47 ocated anterior to the angular gyrus such as AIP and VIP are less medially displaced relative to maca
53 s a survivin 1-141 mutant that does not bind AIP was not imported to mitochondria and failed to inhib
54 grC-I caused the receptor to be activated by AIP-I nearly as well as the wild type AgrC-I receptor.
56 with a peptide inhibitor of calcineurin (CaN-AIP); the non-selective PP1/PP2A inhibitors okadaic acid
58 therapeutic efficacy of synthetic S. caprae AIP was evident by a dramatic reduction in both dermonec
62 led two key structural elements that control AIP-III (and non-native peptide) activity: (1) a tri-res
63 More detailed studies with the convenient AIP model indicated that CSF-1 neutralization led to a r
64 gative I-Abeta chain(-/-) (Ab0) mice develop AIP spontaneously, likely due to dysregulation of CD8(+)
65 HLA-DR*0405 transgenic Ab0 NOD mice develop AIP with high prevalence after sublethal irradiation and
67 indicate that (1)H NMR can help to diagnose AIP attacks based on the identification of ALA and PBG.
71 s explain the chemical principles that drive AIP production, including uncovering a hitherto unknown
73 d analogue of the Staphylococcus epidermidis AIP-1 (3) elicited an IC50 value of 2.7 +/- 0.1 muM.
75 aration were significantly reduced following AIP cTBS without directly modifying corticospinal excita
79 tion via a thiolactone bond is essential for AIP function; therefore, recognition of the cyclic form
82 ne in the rate of operative intervention for AIP, a steroid-responsive disease with propensity for re
83 ponsive genes and suggests that a search for AIP-dependent, AHR-responsive genes may guide us to the
84 orticoids have become a standard therapy for AIP, but the indications requiring treatment as well as
87 R*0405 expression fails to protect mice from AIP, the HLA-DRB1*0405 allele appears to be an important
88 predicted well during movement planning from AIP (medial array) and F5 (lateral array), whereas M1 pr
89 tify and quantify ALA and PBG in urines from AIP patients and (2) to identify metabolites that would
93 nfavorable, and therefore, it is unclear how AIP-producing bacteria produce sufficient amounts of the
95 2_844delGAG) identical to that causing human AIP and two missense mutations, c.250G>A (p.A84T) and c.
97 thologue of BC058385 was methylated in human AIP but not in primary androgen-stimulated prostate canc
101 Preliminary characterization of the AgrC-I-AIP-I interaction suggests that ligand specificity may b
103 g peptide (AIP) signals has been identified (AIP-I), and cross talk between agr systems has not been
105 reported a set of analogues of the group-III AIP that are capable of strongly modulating the activity
107 reversible mislocalization of ductal CFTR in AIP, the association of asymptomatic pancreatic hyperenz
109 ral other antibodies have been identified in AIP against pancreas-specific antigens like trypsinogens
110 of grasp-related and spatial information in AIP and F5 suggests at least a supportive role of these
112 activity from many electrodes in parallel in AIP and F5 while three macaque monkeys (Macaca mulatta)
116 k-lowering strategies to prevent relapses in AIP or the development of recurrent (and possibly chroni
118 aze and target positions were represented in AIP and F5 and could be readily decoded from single unit
120 1 residues were defective in a later step in AIP biosynthesis, separating the peptidase function from
122 expressing the SR-targeted CaMKII inhibitor AIP, without any significant enhancement of apoptosis vs
123 , and the selective CaMKII peptide inhibitor AIP (autocamtide-2-related inhibitory peptide) (2 microm
125 Non-native ligands capable of intercepting AIP:AgrC binding, and thereby QS, in S. aureus have attr
127 e we report that the anterior intraparietal (AIP) and the rostral ventral premotor area (F5) in the m
129 ng activity from the anterior intraparietal (AIP), ventral premotor (F5), and primary motor (M1) cort
131 2 stoichiometry, while an antagonist ligand, AIP-II, functions as an inverse agonist of the kinase ac
133 logues based upon Staphylococcus lugdunensis AIP-1 (1) and AIP-2 (2) displayed respective IC50 values
134 n the AIP-encoding gene (agrD) that modifies AIP structure must be accompanied by corresponding chang
136 e rescued by presynaptic expression of mouse AIP, demonstrating that a conserved function of AIP prot
137 utocamtide-2-related inhibitory peptide (myr-AIP)--but not by inhibition of the activity of protein p
138 ) blockers applied by bath (KN-93, myristoyl-AIP) or expressed selectively in the sensory neurons (AI
139 onal structural analysis of the known native AIP signals (AIPs-I-IV) and several AIP-III analogues wi
143 levations (>140 mg/dl) are seen in 70-80% of AIP patients and also in 5% of normal population and 10%
144 utable to higher-than-normal accumulation of AIP-III in a codY mutant strain, as determined using ult
145 emistry for the diagnosis of acute attack of AIP and identify urinary glycin as a potential marker of
147 ed as a hub that shared the visual coding of AIP only temporarily and switched to highly dominant mot
149 dressed this by studying the consequences of AIP "virtual lesions" on physiological interactions betw
150 have previously localized the determinant of AIP receptor specificity to the C-terminal half of the A
154 identify recent advances in the diagnosis of AIP and evaluate outcomes with various diagnostic strate
156 tural insights may enable the engineering of AIP cross-reactive antibodies or quorum quenching vaccin
159 owever, when combined with other features of AIP, it can be of great diagnostic value though its util
163 , demonstrating that a conserved function of AIP proteins is to inhibit calcium release from ryanodin
166 leading us to hypothesize that induction of AIP-1 may be a protective cellular response directed tow
167 uced activation of IFN, whereas knockdown of AIP by siRNA potentiates virally activated IFN productio
170 strong structural support for a mechanism of AIP-mediated AgrC activation and inhibition in S. aureus
173 he first naturally occurring animal model of AIP in four unrelated cat lines who presented phenotypic
175 sgenic model, we show that overexpression of AIP-1 protected against, while RNAi knockdown of AIP-1 e
181 ealed that while differential recognition of AIP-1 and AIP-4 depends primarily on three amino acid re
194 G4) is a feature of autoimmune pancreatitis (AIP) and IgG4-associated cholangitis (IAC); a >2-fold in
195 isting knowledge of autoimmune pancreatitis (AIP) and to review the progress made in the diagnosis an
196 e concentrations in autoimmune pancreatitis (AIP) by restoring mislocalized CFTR protein to the apica
204 or the diagnosis of autoimmune pancreatitis (AIP) with the objective of establishing a strategy to di
205 genic mechanisms of autoimmune pancreatitis (AIP), an increasingly recognized, immune-mediated form o
206 es of patients with autoimmune pancreatitis (AIP), and follow-up periods have generally been short.
208 allel in macaque premotor (F5) and parietal (AIP) cortices during a delayed grasping task revealed th
209 eria, agr encodes an autoactivating peptide (AIP) that is the inducing ligand for AgrC, the agr signa
210 tive inhibitors of the autoinducing peptide (AIP) activated AgrC receptor, by altering the activation
212 ine kinase detects its autoinducing peptide (AIP) ligand and generates an intracellular signal result
214 s, but only one of the autoinducing peptide (AIP) signals has been identified (AIP-I), and cross talk
215 pathogen that utilizes autoinducing peptide (AIP) signals to mediate QS and thereby regulate virulenc
216 ning peptide called an autoinducing peptide (AIP) that is biosynthesized from the AgrD precursor by t
217 ted that the S. caprae autoinducing peptide (AIP) was responsible, and mass spectrometric analysis id
218 e synthesizes a cyclic autoinducing peptide (AIP) with a distinct sequence that activates its cognate
220 analogues of a native autoinducing peptide (AIP-III) signal that can inhibit AgrC-type QS receptors
222 sed in FRD-SR-autocamide inhibitory peptide (AIP) mice, expressing the SR-targeted CaMKII inhibitor A
223 or autocamtide-2-related inhibitory peptide (AIP) normalized the increased amplitude of NMDAR-EPSCs a
224 ed autocamtide-2-related inhibitory peptide (AIP) was used in a rat in vivo model of retinal toxicity
229 patients with acute intermittent porphyria (AIP), an inherited metabolic disorder of heme biosynthes
236 tios of aqueous-inlet to oil-inlet pressure (AIP/OIP), yielding a linear relationship between muaq an
240 yl hydrocarbon receptor-interacting protein (AIP), a survivin-associated immunophilin, causes embryon
243 uitin ligase atrophin-1 interacting protein (AIP)4 to bind, ubiquitinate, and stabilize Amot130.
244 In import assays using recombinant proteins, AIP directly mediated the import of survivin to mitochon
247 n native AIP signals (AIPs-I-IV) and several AIP-III analogues with varied biological activities usin
252 be a signature of healthy muscle whereas SHG-AIP with one centered spot in pathological mdx muscle is
255 this spontaneous pancreatic amylase-specific AIP in regulatory T cell-deficient NOD.CD28KO mice provi
257 oxidative stress but not apoptosis in FRD-SR-AIP mice, in which a CaMKII inhibitor is targeted to the
258 eractions between the cognate staphylococcal AIP receptors AgrC and the AIPs, as AP4-24H11.AIP-4 bind
265 a lead-in to this study, we discovered that AIP type I could be generated in Escherichia coli throug
266 that active endodermal shortening around the AIP accounts for most of the heart field motion towards
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 to retain functionality, any changes in the AIP-encoding gene (agrD) that modifies AIP structure mus
276 s challenge the current understanding of the AIP area as a critical stage in the dorsal stream for th
283 ng mass spectrometry and discovered that the AIP-II and AIP-III signals are 12 residues in length, ma
284 d into four groups (I-IV) according to their AIP signal and cognate extracellular receptor, AgrC.
285 We structurally characterized all three AIP types using mass spectrometry and discovered that th
286 tabolites that would predict the response to AIP crisis treatment and reflect differential metabolic
287 T cells; we compared their susceptibility to AIP with HLA-DQ8 or HLA-DR*0401 (single) transgenic, or
289 AMP tumors (PRIM, late-stage primary tumors; AIP, androgen-independent primary tumors; and MET, metas
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
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