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1 125I-CPT-L2-BA3 was rapidly internalized by cells expres
2 125I-Cry4Ba toxin bound AgCad1 from S2 cells in a compet
3 125I-f-Alb could not be completely inhibited by MAA-Alb.
4 125I-HA binding to both the 175-kDa and 300-kDa HARE pro
5 125I-HA was taken up and degraded by excised rat livers
6 125I-Hst 5 binding assays showed saturable binding (Kd =
7 125I-Labeled annexin II binding assays with PSV10 cells
8 125I-labeled rh-FcgammaRIA was cleared from mouse blood
9 125I-mAb 30B3 uptake in IPL was rapid (T1/2 15 min), sat
10 125I-ox-LDL exhibited high affinity, saturable binding t
11 125I-Relaxin-3 binds GPCR135 at high affinity with a Kd
12 125I-TGF-beta1 affinity labeling analysis of cell-surfac
13 [125I]A-312110 is a useful tool for investigation of the
14 [125I]BDNF release was also modulated by 5HT(3) receptor
15 [125I]IAmF photolabeling of recombinant VMAT2, expressed
16 [125I]TID photoincorporated into both alpha4 and beta2 su
18 -insoluble 2-(2',4'-dihydroxyphenyl)-6-[127I/125I]iodo-4-(3H)-quinazolinone (127IQ2-OH,4-OH (2)/125IQ
20 e dissociation of the agonist N6-(4-amino-3-[125I]iodobenzyl)-5'-N-methylcarboxamidoadenosine from hu
21 cocaine analog 2beta-carbomethoxy-3beta-(4-[125I]iodophenyl)tropane (beta-CIT) in intact cells expre
30 inding assays, 125I-N6-aminobenzyladenosine (125I-ABA) binds to two affinity states of A1AR with KD-h
31 hotoactivatable irreversible cocaine analog [125I]3beta-(p-chlorophenyl)tropane-2beta-carboxylic acid
32 ave developed the novel radiolabeled analog [125I]-DNP and used this to localize high-affinity (K(D)=
38 nist, inhibits binding of 125I-TGF-beta1 and 125I-IGFBP-3 to TbetaR-V and diminishes IGFBP-3-induced
40 -N-propylamine] tetralin (3H-8-OH-DPAT), and 125I-RTI-55 was used to map the distribution and develop
43 tive binding experiments using unlabeled and 125I-M12A generated an IC50 of 0.71 nm and indicated tha
44 tibodies immunoprecipitated 125I-VEGF165 and 125I-PlGF-2 in the presence of the b1b2 but not of the a
45 nhanced the binding of both 125I-VEGF165 and 125I-PlGF-2 to the b1b2 domain by 20- and 4-fold, respec
47 ." Two radioiodinated probes, [125I]10a and [125I]10b, and two radiofluorinated probes, [18F]17a and
48 the brain showed that both [(125)I]18a and [125I]18b labeled these brain sections, but [125I]13, sel
49 inhibition of striatal 125I-epibatidine and [125I]A-85380 binding with alpha-CtxMII suggest that ther
50 2 weeks decreased both 125I-epibatidine and [125I]iodo-3-[2(S)-azetidinylmethoxy]pyridine (A-85380) b
51 ography shows cell nuclear [3H]estrogen and [125I]estrogen uptake according to a distribution that pr
52 ese data indicate that [125I]IAPEGlyMER and [125I]TBZ-AIPP are effective photoaffinity labels for VMA
53 er-free radioiodinated [125I]IAPEGlyMER and [125I]TBZ-AIPP were synthesized and used to photoaffinity
57 Cholesterol is found in the same fraction as 125I-Tf on sucrose density gradients, and this fraction
58 led binding of 5-HT(1a) receptors as well as 125I-LSD-labeled binding of 5-HT(2a) receptors were eval
61 photoaffinity label 3-iodo-4-azidococaine ([125I]IACoc) binds to the sigma-1 receptor with an affini
62 determinant for AppBp1-Uba3 binding because 125I-UbR72L undergoes heterodimer-catalyzed hyperbolic H
70 M cholesterol: (1) a pool accessible to bind 125I-PFO*, a mutant form of bacterial Perfringolysin O,
72 phingomyelin(SM)-sequestered pool that binds 125I-PFO* only after SM is destroyed by sphingomyelinase
74 tered twice daily for 2 weeks decreased both 125I-epibatidine and [125I]iodo-3-[2(S)-azetidinylmethox
77 ibitable rapid degradation of receptor-bound 125I-TGF-beta1), treatment with heparitinase or a hepara
82 [125I]18b labeled these brain sections, but [125I]13, selective for Abeta(1-40) aggregates, exhibited
83 sity in monocyte progenitors was assessed by 125I macrophage colony-stimulating factor binding assay.
84 on AP/BL AT1R distribution as determined by 125I-angiotensin II binding in LLCPK(Cl4) cells transfec
85 of proteasome chymotrypsin-like subunits by 125I-YL3-VS demonstrates that REGgamma(K188E)'s activati
91 here present a method in which conventional 125I-labeled RIA ([125I] RIA) is adapted to a microtiter
93 on of P-gp substrate verapamil increased CSF 125I-T4 recovery to 51.4+/-2.8%, although mrp1 and oatp
97 10 or 30 mg/kg) inhibited dose-dependently [125I]sauvagine binding selectively at brain sites of CRF
99 rifluoromethyl)-3-(m-iodophenyl) diazirine ([125I]TID) and exposed to agonist for either 0 ms (closed
104 When purified, it competitively displaced 125I-Cry11Ba binding to An. gambiae BBMV and bound Cry11
105 talytic domain of factor XIa also displaced [125I]factor XIa from the surface of activated platelets
106 human CCR1 with a Kd of 9.2 nm and displaces 125I-labeled CCL3 from CCR1-transfected cells with an IC
110 Cla-1-associated 3H-LPS uptake exceeded 125I-apolipoprotein uptake by 5-fold indicating a select
111 re cortical AT1 and AT2 receptor expression, 125I-Ang II glomerular binding, tissue renin activity, t
115 atriuretic peptide had greater affinity for [125I]-DNP binding sites than C-type natriuretic peptide
119 which can reset the high affinity state for [125I]IAAP binding without any further nucleotide hydroly
122 ignificantly increased pulmonary and hepatic 125I albumin leak compared with enteral feeding without
126 CCK-2 receptor mRNA abundance and increased 125I-gastrin binding was demonstrated in IEC-6 cells fol
127 ut not indomethacin) significantly increased 125I-T4 accumulation, implicating a role for P-gp and oa
128 oral administration to rats, MTIP inhibited 125I-sauvagine binding to rat cerebellar membranes ex vi
129 l-imidazo [1,2-b]pyridazine (MTIP) inhibited 125I-sauvagine binding to rat pituitary membranes and cl
131 port substrate [125I]iodoarylazidoprazosin ([125I]IAAP), resulting in dissociation of the latter.
132 '-dimethylaminophenyl)-6-iodobenzothiazole, [125I]7(TZDM), a known ligand for A beta aggregates, with
135 g photolabeling with 3-trifluoromethyl-3-(m-[125I]iodophenyl)diazirine ([125I]TID) to determine funct
137 pophilic reagent, 3'-(trifluoromethyl)-3-(m-[125I]iodophenyl)diazirine, to label proteins in the oute
139 reater than those of 99mTc-sestamibi, making 125I-iodorotenone the superior flow tracer in the isolat
141 given 1 ml NTS and 12.5, 6.25, and 3.125 mg [125I]AHIgG/100 g body wt had increased glomerular uptake
142 lding Km values for ATP (103 +/- 12 microm), 125I-Nedd8 (0.95 +/- 0.18 microm), and HsUbc12 (43 +/- 1
143 e C5a receptor (C5aR), the binding of murine 125I-C5a to murine neutrophils was reduced, the in vitro
144 hRs are pharmacologically similar to native [125I]alpha-conotoxin MII (alpha-CtxMII)-binding and 3-(2
146 caveolin-1 cDNA did not alter the amount of 125I-labeled HDL that associated with the cells, althoug
151 Cross-linking studies measuring binding of 125I-activin-A to the ALK4-trunc mutants in the presence
152 ncreased C5L2 protein (defined by binding of 125I-anti-C5L2 IgG) occurred in lung, liver, heart, and
156 ls showed significantly increased binding of 125I-labeled anti-C5aR to organs when compared to either
157 (Cpd 1), a compound that inhibits binding of 125I-labeled glucagon to the human glucagon receptor wit
158 ctable by flow cytometry, and the binding of 125I-labeled IP-10/CXCL10 to these cells was not compete
162 factor-BB and reduced by 40% the binding of 125I-platelet-derived growth factor-BB to fibroblast cel
163 AP, an LRP-1 antagonist, inhibits binding of 125I-TGF-beta1 and 125I-IGFBP-3 to TbetaR-V and diminish
167 probability of DNA breaks caused by decay of 125I is inversely related to the distance between the ra
169 was determined either by the degradation of 125I-labeled OS to trichloroacetic acid-soluble label or
172 oautoradiographic studies show expression of 125I-labeled iodo-deschloroepibatidine binding sites in
173 r Kv1.6 antibodies by immunoprecipitation of 125I-alpha-dendrotoxin-labelled rabbit brain K+ channels
174 77 cells resulted in 3-4.4-fold increases of 125I-low density lipoprotein (LDL) and 125I-high density
176 xpressing LRP mediate the internalization of 125I-labeled MMP-9.TIMP-1 complexes, whereas cell lines
177 reporter function to probe the mechanism of 125I-ubiquitin transfer between activation and ligation
178 n had a specific activity of 3.9 micromol of 125I-alpha-bungarotoxin binding sites/g of protein.
180 s including decreasing polyubiquitylation of 125I-lysozyme by removing ubiquitin from polyubiquitin c
182 ange from a low (<1) to a high (>1) ratio of 125I-TGF-beta1 binding to TbetaR-II and TbetaR-I and enh
183 lls exhibit low (<1) and high (>1) ratios of 125I-TGF-beta1 binding to TbetaR-II and TbetaR-I, respec
185 P-gp and oatps contribute to the transfer of 125I-T4 between the CSF, CP and brain, hence regulating
187 nd completely blocked the specific uptake of 125I-HA at 37 degrees C by rat liver sinusoidal endothel
190 lysis of nAChR currents, autoradiography of [125I]-alpha-bungarotoxin binding, and in situ hybridizat
194 in (Ile370-Val607) inhibited the binding of [125I]factor XIa to the platelets (Ki approximately 3.5 n
195 vo autoradiography revealed that binding of [125I]sauvagine, a mixed CRH1/CRH2 agonist, was prevented
199 tribution after an intravenous injection of [125I]16(IMPY) in normal mice showed a high initial brain
202 affect expression of the great majority of [125I]alpha-CtxMII-binding sites, indicating that they do
203 ely related analogs, induce regeneration of [125I]IAAP binding to vanadate-trapped (or fluoroaluminat
204 ts indicate that this stimulated release of [125I]BDNF is not regulated by a feedback mechanism media
209 ed 1,4-dihydropyridine KATP channel opener, [125I]A-312110 [(9R)-9-(4-fluoro-3-125iodophenyl)-2,3,5,9
211 formaldehyde-bovine serum albumin (f-Alb) or 125I-malondialdehyde-acetaldehyde-bovine serum albumin (
212 ubated with 125I-labeled FVIII C2 domain, or 125I-FVIIIa, or 125I-FVIII((LC)), or peptides from the C
213 active (IR) binding of either labeled Epb or 125I-alpha-conotoxin MII increased to a much greater ext
214 -labeled FVIII C2 domain, or 125I-FVIIIa, or 125I-FVIII((LC)), or peptides from the C2 domain region,
217 f CaGC to native and recombinant paramyosin, 125I-CaGC was used as a binding tracer in SDS-PAGE analy
220 n of the SPECT and PET probes with preformed 125I-labeled thrombi and with a nonbinding control probe
222 An angiotensin analog, photoaffinity probe 125I-SBpa-Ang II, was used to specifically label the non
223 lick chemistry." Two radioiodinated probes, [125I]10a and [125I]10b, and two radiofluorinated probes,
224 hroughput screening methods for quantitating 125I-SS14 binding to human somatostatin receptor 2 (hSST
227 fold less potent at human 5-HT2A receptors ([125I]DOI) with a derived Ki value of 18 nM and 20-fold l
229 pyridine dihydrochloride (A85380)-resistant [125I]epibatidine-binding nAChR subtypes, respectively.
232 hod in which conventional 125I-labeled RIA ([125I] RIA) is adapted to a microtiter plate format, term
235 horesis (SDS-PAGE) analysis showed specific [125I]IAPEGlyMER labeling of a polypeptide that migrated
237 affinity of Pgp for its transport substrate [125I]iodoarylazidoprazosin ([125I]IAAP), resulting in di
241 ollectively, these results demonstrate that [125I]A-312110 binds with high affinity and has an improv
243 Taken together, these results indicate that [125I]BDNF release is activity dependent, and is modulate
245 also demonstrated, for the first time, that [125I]iodoarylazidoprazosin, a photoaffinity analog of th
249 tering proximal to the DSB resulted from the 125I decays responsible for DSB formation and was not du
250 internal control fragment recovered from the 125I linearized plasmid did not exhibit endo IV sensitiv
252 4Cu-D-Cys-FBP8, detected the location of the 125I-labeled thrombus, confirming high target specificit
253 ed a 3-fold increase in sequestration of the 125I-PNA/8D3 antisense radiopharmaceutical in the brains
257 a2-Cys445, which are also homologous to the [125I]TID-labeled residues alpha1-Cys418 and beta1-Cys447
258 Cys226 and Cys231, which correspond to the [125I]TID-labeled residues Cys222 and Phe227 at the lipid
259 d, the substrate site remains accessible to [125I]IAAP even after removal of the modulator from the m
262 ect expression of nAChRs in monkeys, we used 125I-epibatidine, an agonist at nAChRs containing alpha2
270 type or mutant AChR subunits, we show, using 125I-alpha-bungarotoxin binding and immunofluorescence t
272 g kg(-1), pentobarbitone 10 mg kg(-1) i.v.), 125I-T4 was perfused continuously into ventricular CSF w
278 ide, SFLLRN (25 microM), were incubated with 125I-labeled FVIII C2 domain, or 125I-FVIIIa, or 125I-FV
280 homologous (normal) fibrinogen, labeled with 125I and 121I, respectively, were performed in two affec
283 s, acute hyperpermeability was measured with 125I-albumin, and cytokines and myeloperoxidase activity
284 s used as the other competition partner with 125I-[MePhe7]NKB as the radioligand, indicating competit
288 udies, rat livers were perfused in situ with 125I-formaldehyde-bovine serum albumin (f-Alb) or 125I-m
291 3H]EB) is approximately 30% higher than with 125I-3-(2(S)-azetidinylmethoxy)pyridine (A-85380) and mo
293 ic kinetics for HsUbc12 transthiolation with 125I-Nedd8 (kcat = 3.5 +/- 0.2 s-1), yielding Km values
294 ein (Ki approximately 2.7 nM) competed with [125I]factor XIa for binding sites on activated platelets
295 onist high affinity state was examined with [125I]-para-iodoclonidine autoradiography and alpha2-AR f
297 ion of brainstem sections preincubated with [125I]p-iodoclonidine revealed no inter-strain difference
299 ections of a transgenic mouse (Tg2576) with [125I]16(IMPY) displayed high selective binding to amyloi
300 HTB-81 cells with the same construct yielded 125I-hUG binding with high affinity (Kd=18 nM) and speci
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