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1 ondary antibodies specific to each patterned primary antibody.
2 n blotting with a dinitrophenylated-specific primary antibody.
3 thin the retina using an anti-cGK I-specific primary antibody.
4 rmed by immunofluorescence using an anti-MCP primary antibody.
5 rmed by immunofluorescence using an antihook primary antibody.
6 econdary antibodies were added to bind these primary antibodies.
7 ng using patient sera/cerebrospinal fluid as primary antibodies.
8  secondary antibodies were then used to mark primary antibodies.
9 ific identifications and cross-reactivity of primary antibodies.
10  improve the utility of some poorly reactive primary antibodies.
11  sera of individual patients were tested for primary antibodies.
12 e stained with CTGF and TGF-beta1 polyclonal primary antibodies.
13 sis in which individual sera were tested for primary antibodies.
14 quitination than p53s with a more wild-type (primary antibody 1620+/pAb240-) conformation.
15 rved that cancer-derived p53s with a mutant (primary antibody 1620-/pAb240+) conformation localized i
16 munolabeled by incubation overnight with the primary antibodies 7G6, a cone-specific antibody; SV2, a
17 chemically by simultaneous staining with two primary antibodies: a phospho-specific primary and norma
18 he surface area to capture a large amount of primary antibodies (Ab1), thus amplifying the detection
19 ever, our optimization of cholesterol level, primary antibody affinity, and antibody-bead linkage all
20              To understand the importance of primary antibody affinity, we compared a series of point
21                                              Primary antibodies against inflammatory and proangiogeni
22 sections by using double immunolabeling with primary antibodies against Muller and other retina-speci
23  processed by immunoperoxidase staining with primary antibodies against RANTES, MCP-1, ICAM-1, and LF
24        Infected cells were also labeled with primary antibodies against the virus env surface protein
25 ucts was examined by Western blots using the primary antibody against 71-74 residues of cdLC1.
26  were sectioned, dewaxed, and incubated with primary antibody against TGF-beta(b)1 latency-associated
27 urfaces ready for covalent immobilization of primary antibodies and a strong bonding between PDMS sub
28 cultured, fixed, and incubated with specific primary antibodies and their corresponding labeled secon
29 dsorption was then assessed using a specific primary antibody and a secondary antibody conjugated wit
30 mmobilization of UPEC, bovine serum albumin, primary antibody and Horse Radish Peroxidase (HRP) tagge
31 ic antigen (CEA) was immobilized between the primary antibody and horseradish peroxidase (HRP)-conjug
32 he optimal concentration of coating antigen, primary antibody and secondary antibody.
33                    All but two patients made primary antibody and T-cell proliferative responses to a
34 the importance of the connection between the primary antibody and the magnetic bead, we compared brid
35 nker chemistries were tried for reacting the primary antibody, and its response to target and nonspec
36 LPS from various species of bacteria and, as primary antibodies, anti-murein lipoprotein (MLP), pepti
37                        The assay employing a primary antibodies arrayed on a CMC surface and detectio
38 f the particle and "intermediate" views, the primary antibody binding site is near the intersection b
39 Serine 15 (phospho-p53(15)), was captured by primary antibodies bound on magnetic Fe3O4 nanoparticles
40 formed between antigens and their respective primary antibodies by cupric ions at high pH.
41             Besides the initial screening of primary antibodies, collection of several hundreds of sa
42 lationship between cluster structure and the primary antibody-combining regions of the HA protein.
43                                              Primary antibody deficiencies represent the most prevale
44 plemented by more detailed incidence data on primary antibody deficiencies, revealing trends in diagn
45 new biomarker sets for further research into primary antibody deficiencies.
46 d conditions that lead to the development of primary antibody deficiencies.
47 knowledge on the pulmonary manifestations of primary antibody deficiency (PAD) syndromes in adults.
48 ough autoimmunity is common in patients with primary antibody deficiency (PAD), it remains unknown wh
49 n associated with infection in patients with primary antibody deficiency (PAD).
50                                          The primary antibody deficiency syndromes are a rare group o
51 ctivate PI3K signaling have been linked to a primary antibody deficiency.
52  the presence of this organism in 17 (19.3%) primary antibody-deficient (PAD) patients, 4 (5%) adults
53 ficiency (CVID) is the commonest symptomatic primary antibody disorder, with monogenic causes identif
54                                        These primary antibodies displayed evidence of diversity in al
55 agnostic antibody assay was performed with a primary antibody, double-labeled amplicons, and fluoroph
56                                The resulting primary antibody elicits an anti-antibody response or an
57 ed by immunohistochemistry and the following primary antibodies evaluation.
58 scent molecule: mouse monoclonal anti-biotin primary antibody (fluorescein), biotin (B-phycoerythrin)
59          Specifically, we used a cocktail of primary antibodies for both epithelial and mesenchymal a
60 -bound tissue sections reacted with specific primary antibodies for rat 5-HT(1B, 1D) and (1F) recepto
61 r (PCa) diagnosis are reported, in which the primary antibody for capture is replaced by a DNA aptame
62  of mouse IgG) decreased the affinity of the primary antibody for DCP-UO22+ by 4-fold.
63                 Omission or preadsorption of primary antibodies from the antisera and subsequent incu
64 probings of the same membrane with different primary antibodies (> or = 12) and retention of strong s
65 nti-immune complex (IC) antibody binding the primary antibody-HT-2 toxin complex.
66            The detection of measles-specific primary antibodies (IgG) using electrochemical impedimet
67 or combined with carbon nanotubes (CNTs) for primary antibody immobilization to develop a simple and
68 ombinant human immunoglobulin G1 and used as primary antibodies in enzyme-linked immunosorbent assays
69                                              Primary antibodies included rabbit anti-mouse iNOS combi
70 ryosectioning and were stained using various primary antibodies, including anti-Lewis MHC class II (O
71  isolated compartments: (1) sample well, (2) primary antibody labeling well, (3) secondary antibody l
72              The recent development of large primary antibody libraries enables selection of antibodi
73    Control experiments involved omitting the primary antibodies; no labelling was visible under these
74    Protein target was sandwiched between the primary antibody of HBs (Ab1) immobilized on the MNPs an
75                                   First, the primary antibody of HBs (Ab1) was immobilized on the sur
76 -decorated universal quantum dots and intact primary antibodies, offers a fast, simple and purificati
77  easily and homogeneously coats the specific primary antibody on the polyvinylidene fluoride (PVDF) m
78                         Profiles correlating primary antibody-producing cells with the molecular char
79     Furthermore, mixed BMT reconstituted the primary antibody production in BXSB recipients impressiv
80            Moreover, mixed BMT reconstituted primary antibody production in BXSB recipients, so that
81 atic hypermutation in the diversification of primary antibody repertoire in these animals.
82         In the bone marrow, diversity in the primary antibody repertoire is created by the combinator
83                       In most vertebrates, a primary antibody repertoire is created through the recom
84 ts suggest that the binding potential of the primary antibody repertoire may be significantly expande
85                                  The limited primary antibody repertoire uses multiple mechanisms to
86 ugments the recombinational diversity of the primary antibody repertoire.
87 ociated with the structural diversity of the primary antibody repertoire.
88  to drive GALT development and diversify the primary antibody repertoire; however, the molecular mech
89 proaches to evaluate in depth the content of primary antibody repertoires and, ultimately, to study h
90 xons from germline gene segments to generate primary antibody repertoires.
91  to support the development both of a potent primary antibody response and of the germinal center res
92 c T-lymphocyte responses but does affect the primary antibody response and the generation of memory B
93  HIV-1 Envelope (Env) and characterizing the primary antibody response for HIV-1 neutralization.
94 odel of the early events that occur during a primary antibody response to a T cell-dependent antigen.
95 T cell help is selective and limiting to the primary antibody response to influenza virus infection a
96                        At the same time, the primary antibody response to the H3N2 challenge virus wa
97                                 Although the primary antibody response to the PPS14-OVA conjugate exc
98 owing MZ B-cell reconstitution resulted in a primary antibody response, demonstrating that MZ B-cell
99 o provide help to wild-type B cells during a primary antibody response.
100 r efficacy, especially in eliciting a strong primary antibody response.
101 ion of Atg7 (B/Atg7(-/-) mice) showed normal primary antibody responses after immunization against in
102  find that IKKalpha(AA) B cells mount normal primary antibody responses but do not enter germinal cen
103 -70 varied over time, including increases in primary antibody responses late in the disease course.
104                   Although BLPs enhanced the primary antibody responses seen in some children with no
105 ith the fusion protein gave rise to enhanced primary antibody responses to gp120, particularly of the
106 Although HIV-1-infected children showed good primary antibody responses to measles vaccine, their rap
107 immunized with NS3-FL developed high-titered primary antibody responses to the NS3 ATPase/ helicase d
108 with azithromycin led to significantly lower primary antibody responses, decreased recall proliferati
109  either cross-reactive antibodies to SV40 or primary antibodies resulting from SV40 infection.
110          Western blot analysis with the same primary antibody showed a specific positive band for iNO
111 ed with 2,4-dinitrophenylhydrazine (DNPH), a primary antibody specific for the 2,4-dinitrophenol grou
112 ue and its function in altered and humanized primary antibody structures.
113 ditionally, the FLISA utilizes 100-fold less primary antibody than the conventional immunoassay.
114 d to Sepharose beads, is used to capture the primary antibody (the antibody of interest).
115               Using a highly affine anti-DCF primary antibody, the optimized ULISA reached a detectio
116 hile conventional WB requires 0.4 mug of the primary antibody, the proposed technique only uses 4 x 1
117 hemistry with double immunolabeling, using a primary antibody to amino acids 1-10 of VEGF, together w
118 ctions between MCMV, a glycoprotein-specific primary antibody to MCMV, and polystyrene bead "anchors,
119 -1)) reducing at the same time the amount of primary antibody used (30,000 vs. 1000 dilution factor).
120 etecting a specific protein of interest with primary antibodies using automated fluorescence microsco
121 of the antigens recognized by the monoclonal primary antibodies was further confirmed by Western immu
122 le electrodes on a microfabricated chip, the primary antibody was selectively and covalently attached
123                                              Primary antibodies were immobilized on a solid substrate
124                                     Anti-SEB primary antibodies were immobilized onto the CNT surface
125 uidic channel, microarrays of five different primary antibodies were patterned onto a single channel
126                              First, specific primary antibodies were separately bound to enzymes in c
127                                    After all primary antibodies were tested in positive and negative
128                  PG21 anti-AR and anti-c-fos primary antibodies were visualized by fluorescence micro
129 ry antibody specific to the Fc region of the primary antibody, were used to affect virus mobility.
130 escribed was blocked by preabsorption of the primary antibodies with antigen.
131 ecificity was tested by preadsorption of the primary antibody with a peptide corresponding to sst2A(3
132 nvolves binding of the target protein with a primary antibody with high affinity and specificity, fol
133 ilized estrogen for the binding sites of the primary antibody, with subsequent revelation using alkal

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