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Results: 7

1.
FIG. 7

FIG. 7. From: Characterization of Determinants for Envelope Binding and Infection in Tva, the Subgroup A Avian Sarcoma and Leukosis Virus Receptor.

Effect of titration of selected Tva DEW mutants on EnvA binding. Various amounts of lysates from 293T cells expressing DEW mutants of Tva (0.1 to 10 μl) were used in the blocking ELISA. Percent inhibition of sTva binding to captured EnvA for each sample is the average from three independent experiments, each performed in triplicate. Bars indicate standard deviation.

Lijun Rong, et al. J Virol. 1998 June;72(6):4552-4559.
2.
FIG. 6

FIG. 6. From: Characterization of Determinants for Envelope Binding and Infection in Tva, the Subgroup A Avian Sarcoma and Leukosis Virus Receptor.

Analysis of Trp48 mutants of Tva. (A) Expression of Tva Trp48 mutants in 293T cells analyzed by Western blotting with antiserum to Tva. Sizes are indicated in kilodaltons. (B) Blocking ELISA (10 μl of each cell lysate) was performed to assess the EnvA binding activity of Tva Trp48 mutants, expressed as percent inhibition. Percent inhibition for each sample is the average from three independent experiments, each performed in triplicate. Bars indicate standard deviation.

Lijun Rong, et al. J Virol. 1998 June;72(6):4552-4559.
3.
FIG. 5

FIG. 5. From: Characterization of Determinants for Envelope Binding and Infection in Tva, the Subgroup A Avian Sarcoma and Leukosis Virus Receptor.

Analysis of Glu47 mutants of Tva. (A) Expression of Tva Glu47 mutants in 293T cells analyzed by Western blotting with antiserum to Tva. Sizes are indicated in kilodaltons. (B) Blocking ELISA (10 μl of each cell lysate) was performed to assess the EnvA binding activity of Tva Glu47 mutants, expressed as percent inhibition. Percent inhibition for each sample is the average from three experiments, each performed in triplicate. Bars indicate standard deviation.

Lijun Rong, et al. J Virol. 1998 June;72(6):4552-4559.
4.
FIG. 4

FIG. 4. From: Characterization of Determinants for Envelope Binding and Infection in Tva, the Subgroup A Avian Sarcoma and Leukosis Virus Receptor.

Analysis of Asp46 mutants of Tva. (A) Expression of Tva Asp46 mutants in 293T cells analyzed by Western blotting with polyclonal serum to Tva. Sizes are indicated in kilodaltons. (B) Blocking ELISA (10 μl of each cell lysate) was performed to measure the EnvA binding activity of Tva Asp46 mutants, expressed as percent inhibition of labeled sTva binding. Percent inhibition for each sample is the average from three experiments, each performed in triplicate. Bars indicate standard deviation.

Lijun Rong, et al. J Virol. 1998 June;72(6):4552-4559.
5.
FIG. 3

FIG. 3. From: Characterization of Determinants for Envelope Binding and Infection in Tva, the Subgroup A Avian Sarcoma and Leukosis Virus Receptor.

Analysis of EnvA binding by wt Tva by using a blocking ELISA. The ability of Tva in a cell lysate to bind EnvA was indirectly analyzed by determining the level of inhibition of labeled sTva binding. Increasing amounts of lysate from 293T cells expressing wt Tva were incubated with captured gD-EnvA before biotin-labeled sTva was added in the blocking ELISA protocol as described in Materials and Methods. Each experiment was performed in triplicate, and the standard deviation was less than 10% of the mean optical density reading.

Lijun Rong, et al. J Virol. 1998 June;72(6):4552-4559.
6.
FIG. 1

FIG. 1. From: Characterization of Determinants for Envelope Binding and Infection in Tva, the Subgroup A Avian Sarcoma and Leukosis Virus Receptor.

Tva LDLR module and effects of homolog substitutions and deletions on viral receptor function. (A) Cartoon of the Tva LDLR module. Amino acids of the Tva LDLR module are labeled, and the proposed three disulfide bonds based on human LDLR repeats 1, 2, and 5 are indicated. The highly conserved residues found in most LDLR modules are shaded. (B) Sequences of the Tva LDLR module homolog substitution and deletion mutants. The functions of these mutants as viral receptors as assayed by infection with RCAS(A)AP are shown at the right. Values represent positive AP-staining cells per milliliter of viral stock [RCAS(A)-AP vector] used.

Lijun Rong, et al. J Virol. 1998 June;72(6):4552-4559.
7.
FIG. 2

FIG. 2. From: Characterization of Determinants for Envelope Binding and Infection in Tva, the Subgroup A Avian Sarcoma and Leukosis Virus Receptor.

Expression and EnvA binding properties of Tva LDLR module homolog substitution and deletion mutants. (A) Transient expression of Tva mutants in 293T cells. Cell lysates from 293T cells transiently transfected with Tva mutant plasmids were analyzed by SDS-PAGE and Western blot analysis using a polyclonal antiserum against Tva protein. 293T, mock-transfected cells. Sizes are indicated in kilodaltons. (B) EnvA binding activity of Tva mutants measured by blocking ELISA. Cell lysates (10 μl) from 293T cells transiently expressing the mutant Tva proteins were used in the blocking ELISA as described in Materials and Methods. Percent inhibition of labeled sTva binding was calculated as described in Materials and Methods. Percent inhibition for each sample is the average from three experiments, each performed in triplicate. Bars indicate standard deviation. (C) Relative envelope binding activities of Tva mutants ΔC1C3, ΔC3C5, and C45/ΔC1C3 with increasing amount of cell lysates measured by blocking ELISA, expressed as percent inhibition. Percent inhibition for each sample is the average from three experiments, each performed in triplicate. Bars indicate standard deviation.

Lijun Rong, et al. J Virol. 1998 June;72(6):4552-4559.

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