phapi Search Results


anp32a rabbit polyclonal  (Proteintech)
93
Proteintech anp32a rabbit polyclonal
Fig. 7. avANP32A transferred by avian influenza A virus accelerates the process of obtaining adaptive mutations. (A) H9N2 virus produced from HEK293T cells overexpressing Flag-tagged <t>ANP32A</t> or with an empty vector were purified by ultracentrifugation with a prior HAd step. The cell lysates and purified virions were then subjected to Western blotting. (B) Viral replication in MDCK cells or MDCK-avANP32A cells infected with H9N2 (huANP32A) virus and H9N2 (avANP32A) virus at an MOI of 0.1. Error bars represent mean ± SD from n = 3 independent biological replicates; unpaired t test; **P < 0.01 and ****P < 0.0001. (C) Model for the effect of avANP32A transferred by avian influenza A virus on viral replication and adaptive mutation acquisition when jumping from avian hosts to mammalian hosts. (D) H9N2 virus pack- aged with either avANP32A or huANP32A was blind passaged six times in MDCK cells. Viral RNAs were extracted and the C terminus of PB2 was amplified and deep- sequenced to monitor the residue phenotype of PB2 627 and 701 positions during passages in MDCK cells. Bar graph represents the percentage of adaptive mutations including PB2-E627K/V and D701N in each passage. Error bars represent mean ± SEM from n = 4 independent biological replicates, unpaired t test; *P < 0.05. (E) Sche- matic representation of the protocol for the experiments shown in (F). (F) The lungs of infected mice were collected for viral RNA extraction, and the C terminus of PB2 was amplified and cloned into T vectors. Nine molecular clones from each sample were randomly picked and sequenced for determination of the residue phenotype of PB2 627 and 701 positions. Samples with nine clone negatives for the emergence of PB2-E627K/V and D701N were recognized as no occurrence of adaptive mutations. In each group, the percentage of mice with emergence of adaptive mutations was calculated.
Anp32a Rabbit Polyclonal, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/phapi/ANP32A+Antibody/pm38295177-267-10-16
Average 93 stars, based on 1 article reviews
anp32a rabbit polyclonal - by Bioz Stars, 2026-08
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phap1  (ProSci Incorporated)
90
ProSci Incorporated phap1
Fig. 7. avANP32A transferred by avian influenza A virus accelerates the process of obtaining adaptive mutations. (A) H9N2 virus produced from HEK293T cells overexpressing Flag-tagged <t>ANP32A</t> or with an empty vector were purified by ultracentrifugation with a prior HAd step. The cell lysates and purified virions were then subjected to Western blotting. (B) Viral replication in MDCK cells or MDCK-avANP32A cells infected with H9N2 (huANP32A) virus and H9N2 (avANP32A) virus at an MOI of 0.1. Error bars represent mean ± SD from n = 3 independent biological replicates; unpaired t test; **P < 0.01 and ****P < 0.0001. (C) Model for the effect of avANP32A transferred by avian influenza A virus on viral replication and adaptive mutation acquisition when jumping from avian hosts to mammalian hosts. (D) H9N2 virus pack- aged with either avANP32A or huANP32A was blind passaged six times in MDCK cells. Viral RNAs were extracted and the C terminus of PB2 was amplified and deep- sequenced to monitor the residue phenotype of PB2 627 and 701 positions during passages in MDCK cells. Bar graph represents the percentage of adaptive mutations including PB2-E627K/V and D701N in each passage. Error bars represent mean ± SEM from n = 4 independent biological replicates, unpaired t test; *P < 0.05. (E) Sche- matic representation of the protocol for the experiments shown in (F). (F) The lungs of infected mice were collected for viral RNA extraction, and the C terminus of PB2 was amplified and cloned into T vectors. Nine molecular clones from each sample were randomly picked and sequenced for determination of the residue phenotype of PB2 627 and 701 positions. Samples with nine clone negatives for the emergence of PB2-E627K/V and D701N were recognized as no occurrence of adaptive mutations. In each group, the percentage of mice with emergence of adaptive mutations was calculated.
Phap1, supplied by ProSci Incorporated, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/phapi/PHAP+Peptide/pmc03770270-256-84-85
Average 90 stars, based on 1 article reviews
phap1 - by Bioz Stars, 2026-08
90/100 stars
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anp32a  (Boster Bio)
90
Boster Bio anp32a
Fig. 7. avANP32A transferred by avian influenza A virus accelerates the process of obtaining adaptive mutations. (A) H9N2 virus produced from HEK293T cells overexpressing Flag-tagged <t>ANP32A</t> or with an empty vector were purified by ultracentrifugation with a prior HAd step. The cell lysates and purified virions were then subjected to Western blotting. (B) Viral replication in MDCK cells or MDCK-avANP32A cells infected with H9N2 (huANP32A) virus and H9N2 (avANP32A) virus at an MOI of 0.1. Error bars represent mean ± SD from n = 3 independent biological replicates; unpaired t test; **P < 0.01 and ****P < 0.0001. (C) Model for the effect of avANP32A transferred by avian influenza A virus on viral replication and adaptive mutation acquisition when jumping from avian hosts to mammalian hosts. (D) H9N2 virus pack- aged with either avANP32A or huANP32A was blind passaged six times in MDCK cells. Viral RNAs were extracted and the C terminus of PB2 was amplified and deep- sequenced to monitor the residue phenotype of PB2 627 and 701 positions during passages in MDCK cells. Bar graph represents the percentage of adaptive mutations including PB2-E627K/V and D701N in each passage. Error bars represent mean ± SEM from n = 4 independent biological replicates, unpaired t test; *P < 0.05. (E) Sche- matic representation of the protocol for the experiments shown in (F). (F) The lungs of infected mice were collected for viral RNA extraction, and the C terminus of PB2 was amplified and cloned into T vectors. Nine molecular clones from each sample were randomly picked and sequenced for determination of the residue phenotype of PB2 627 and 701 positions. Samples with nine clone negatives for the emergence of PB2-E627K/V and D701N were recognized as no occurrence of adaptive mutations. In each group, the percentage of mice with emergence of adaptive mutations was calculated.
Anp32a, supplied by Boster Bio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/phapi/Anti-PHAP+ANP32A+Antibody/pmc06551499-45-12-13
Average 90 stars, based on 1 article reviews
anp32a - by Bioz Stars, 2026-08
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polyclonal antibody against phap1  (Boster Bio)
91
Boster Bio polyclonal antibody against phap1
Fig. 7. avANP32A transferred by avian influenza A virus accelerates the process of obtaining adaptive mutations. (A) H9N2 virus produced from HEK293T cells overexpressing Flag-tagged <t>ANP32A</t> or with an empty vector were purified by ultracentrifugation with a prior HAd step. The cell lysates and purified virions were then subjected to Western blotting. (B) Viral replication in MDCK cells or MDCK-avANP32A cells infected with H9N2 (huANP32A) virus and H9N2 (avANP32A) virus at an MOI of 0.1. Error bars represent mean ± SD from n = 3 independent biological replicates; unpaired t test; **P < 0.01 and ****P < 0.0001. (C) Model for the effect of avANP32A transferred by avian influenza A virus on viral replication and adaptive mutation acquisition when jumping from avian hosts to mammalian hosts. (D) H9N2 virus pack- aged with either avANP32A or huANP32A was blind passaged six times in MDCK cells. Viral RNAs were extracted and the C terminus of PB2 was amplified and deep- sequenced to monitor the residue phenotype of PB2 627 and 701 positions during passages in MDCK cells. Bar graph represents the percentage of adaptive mutations including PB2-E627K/V and D701N in each passage. Error bars represent mean ± SEM from n = 4 independent biological replicates, unpaired t test; *P < 0.05. (E) Sche- matic representation of the protocol for the experiments shown in (F). (F) The lungs of infected mice were collected for viral RNA extraction, and the C terminus of PB2 was amplified and cloned into T vectors. Nine molecular clones from each sample were randomly picked and sequenced for determination of the residue phenotype of PB2 627 and 701 positions. Samples with nine clone negatives for the emergence of PB2-E627K/V and D701N were recognized as no occurrence of adaptive mutations. In each group, the percentage of mice with emergence of adaptive mutations was calculated.
Polyclonal Antibody Against Phap1, supplied by Boster Bio, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/phapi/Anti-ANP32A+Monoclonal+Antibody/ppr0132453-57-6-14
Average 91 stars, based on 1 article reviews
polyclonal antibody against phap1 - by Bioz Stars, 2026-08
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anti anp32a mab dc63  (ProSci Incorporated)
90
ProSci Incorporated anti anp32a mab dc63
Fig. 7. avANP32A transferred by avian influenza A virus accelerates the process of obtaining adaptive mutations. (A) H9N2 virus produced from HEK293T cells overexpressing Flag-tagged <t>ANP32A</t> or with an empty vector were purified by ultracentrifugation with a prior HAd step. The cell lysates and purified virions were then subjected to Western blotting. (B) Viral replication in MDCK cells or MDCK-avANP32A cells infected with H9N2 (huANP32A) virus and H9N2 (avANP32A) virus at an MOI of 0.1. Error bars represent mean ± SD from n = 3 independent biological replicates; unpaired t test; **P < 0.01 and ****P < 0.0001. (C) Model for the effect of avANP32A transferred by avian influenza A virus on viral replication and adaptive mutation acquisition when jumping from avian hosts to mammalian hosts. (D) H9N2 virus pack- aged with either avANP32A or huANP32A was blind passaged six times in MDCK cells. Viral RNAs were extracted and the C terminus of PB2 was amplified and deep- sequenced to monitor the residue phenotype of PB2 627 and 701 positions during passages in MDCK cells. Bar graph represents the percentage of adaptive mutations including PB2-E627K/V and D701N in each passage. Error bars represent mean ± SEM from n = 4 independent biological replicates, unpaired t test; *P < 0.05. (E) Sche- matic representation of the protocol for the experiments shown in (F). (F) The lungs of infected mice were collected for viral RNA extraction, and the C terminus of PB2 was amplified and cloned into T vectors. Nine molecular clones from each sample were randomly picked and sequenced for determination of the residue phenotype of PB2 627 and 701 positions. Samples with nine clone negatives for the emergence of PB2-E627K/V and D701N were recognized as no occurrence of adaptive mutations. In each group, the percentage of mice with emergence of adaptive mutations was calculated.
Anti Anp32a Mab Dc63, supplied by ProSci Incorporated, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/phapi/ANP32A+Antibody/pmc06592432-342-65-85
Average 90 stars, based on 1 article reviews
anti anp32a mab dc63 - by Bioz Stars, 2026-08
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anti phap1 antibody  (ProSci Incorporated)
90
ProSci Incorporated anti phap1 antibody
Fig. 7. avANP32A transferred by avian influenza A virus accelerates the process of obtaining adaptive mutations. (A) H9N2 virus produced from HEK293T cells overexpressing Flag-tagged <t>ANP32A</t> or with an empty vector were purified by ultracentrifugation with a prior HAd step. The cell lysates and purified virions were then subjected to Western blotting. (B) Viral replication in MDCK cells or MDCK-avANP32A cells infected with H9N2 (huANP32A) virus and H9N2 (avANP32A) virus at an MOI of 0.1. Error bars represent mean ± SD from n = 3 independent biological replicates; unpaired t test; **P < 0.01 and ****P < 0.0001. (C) Model for the effect of avANP32A transferred by avian influenza A virus on viral replication and adaptive mutation acquisition when jumping from avian hosts to mammalian hosts. (D) H9N2 virus pack- aged with either avANP32A or huANP32A was blind passaged six times in MDCK cells. Viral RNAs were extracted and the C terminus of PB2 was amplified and deep- sequenced to monitor the residue phenotype of PB2 627 and 701 positions during passages in MDCK cells. Bar graph represents the percentage of adaptive mutations including PB2-E627K/V and D701N in each passage. Error bars represent mean ± SEM from n = 4 independent biological replicates, unpaired t test; *P < 0.05. (E) Sche- matic representation of the protocol for the experiments shown in (F). (F) The lungs of infected mice were collected for viral RNA extraction, and the C terminus of PB2 was amplified and cloned into T vectors. Nine molecular clones from each sample were randomly picked and sequenced for determination of the residue phenotype of PB2 627 and 701 positions. Samples with nine clone negatives for the emergence of PB2-E627K/V and D701N were recognized as no occurrence of adaptive mutations. In each group, the percentage of mice with emergence of adaptive mutations was calculated.
Anti Phap1 Antibody, supplied by ProSci Incorporated, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/phapi/PHAP+Antibody/us09937178-316-102-104
Average 90 stars, based on 1 article reviews
anti phap1 antibody - by Bioz Stars, 2026-08
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pp32/phapi  (Biesterfeld Spezialchemie)
90
Biesterfeld Spezialchemie pp32/phapi
Fig. 7. avANP32A transferred by avian influenza A virus accelerates the process of obtaining adaptive mutations. (A) H9N2 virus produced from HEK293T cells overexpressing Flag-tagged <t>ANP32A</t> or with an empty vector were purified by ultracentrifugation with a prior HAd step. The cell lysates and purified virions were then subjected to Western blotting. (B) Viral replication in MDCK cells or MDCK-avANP32A cells infected with H9N2 (huANP32A) virus and H9N2 (avANP32A) virus at an MOI of 0.1. Error bars represent mean ± SD from n = 3 independent biological replicates; unpaired t test; **P < 0.01 and ****P < 0.0001. (C) Model for the effect of avANP32A transferred by avian influenza A virus on viral replication and adaptive mutation acquisition when jumping from avian hosts to mammalian hosts. (D) H9N2 virus pack- aged with either avANP32A or huANP32A was blind passaged six times in MDCK cells. Viral RNAs were extracted and the C terminus of PB2 was amplified and deep- sequenced to monitor the residue phenotype of PB2 627 and 701 positions during passages in MDCK cells. Bar graph represents the percentage of adaptive mutations including PB2-E627K/V and D701N in each passage. Error bars represent mean ± SEM from n = 4 independent biological replicates, unpaired t test; *P < 0.05. (E) Sche- matic representation of the protocol for the experiments shown in (F). (F) The lungs of infected mice were collected for viral RNA extraction, and the C terminus of PB2 was amplified and cloned into T vectors. Nine molecular clones from each sample were randomly picked and sequenced for determination of the residue phenotype of PB2 627 and 701 positions. Samples with nine clone negatives for the emergence of PB2-E627K/V and D701N were recognized as no occurrence of adaptive mutations. In each group, the percentage of mice with emergence of adaptive mutations was calculated.
Pp32/Phapi, supplied by Biesterfeld Spezialchemie, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/phapi/pp32+phapi/pmc03753705-437-26-24
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phapi antibody - c-terminal region (oaqa00140)  (Aviva Systems)
N/A
The PHAP proteins (tumor suppressor putative HLA-DR associated proteins) are important regulators of mitochondrial apoptosis. PHAP facilitates apoptosomemediated caspase-9 activation to stimulate the mitochondrial apoptosis pathway. In addition, PHAP opposes both Ras- and myc- mediated
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phapi antibody - middle region (oaqa00137)  (Aviva Systems)
N/A
The PHAP proteins (tumor suppressor putative HLA-DR associated proteins) are important regulators of mitochondrial apoptosis. PHAP facilitates apoptosomemediated caspase-9 activation to stimulate the mitochondrial apoptosis pathway. In addition, PHAP opposes both Ras- and myc- mediated
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Image Search Results


Fig. 7. avANP32A transferred by avian influenza A virus accelerates the process of obtaining adaptive mutations. (A) H9N2 virus produced from HEK293T cells overexpressing Flag-tagged ANP32A or with an empty vector were purified by ultracentrifugation with a prior HAd step. The cell lysates and purified virions were then subjected to Western blotting. (B) Viral replication in MDCK cells or MDCK-avANP32A cells infected with H9N2 (huANP32A) virus and H9N2 (avANP32A) virus at an MOI of 0.1. Error bars represent mean ± SD from n = 3 independent biological replicates; unpaired t test; **P < 0.01 and ****P < 0.0001. (C) Model for the effect of avANP32A transferred by avian influenza A virus on viral replication and adaptive mutation acquisition when jumping from avian hosts to mammalian hosts. (D) H9N2 virus pack- aged with either avANP32A or huANP32A was blind passaged six times in MDCK cells. Viral RNAs were extracted and the C terminus of PB2 was amplified and deep- sequenced to monitor the residue phenotype of PB2 627 and 701 positions during passages in MDCK cells. Bar graph represents the percentage of adaptive mutations including PB2-E627K/V and D701N in each passage. Error bars represent mean ± SEM from n = 4 independent biological replicates, unpaired t test; *P < 0.05. (E) Sche- matic representation of the protocol for the experiments shown in (F). (F) The lungs of infected mice were collected for viral RNA extraction, and the C terminus of PB2 was amplified and cloned into T vectors. Nine molecular clones from each sample were randomly picked and sequenced for determination of the residue phenotype of PB2 627 and 701 positions. Samples with nine clone negatives for the emergence of PB2-E627K/V and D701N were recognized as no occurrence of adaptive mutations. In each group, the percentage of mice with emergence of adaptive mutations was calculated.

Journal: Science advances

Article Title: Avian ANP32A incorporated in avian influenza A virions promotes interspecies transmission by priming early viral replication in mammals.

doi: 10.1126/sciadv.adj4163

Figure Lengend Snippet: Fig. 7. avANP32A transferred by avian influenza A virus accelerates the process of obtaining adaptive mutations. (A) H9N2 virus produced from HEK293T cells overexpressing Flag-tagged ANP32A or with an empty vector were purified by ultracentrifugation with a prior HAd step. The cell lysates and purified virions were then subjected to Western blotting. (B) Viral replication in MDCK cells or MDCK-avANP32A cells infected with H9N2 (huANP32A) virus and H9N2 (avANP32A) virus at an MOI of 0.1. Error bars represent mean ± SD from n = 3 independent biological replicates; unpaired t test; **P < 0.01 and ****P < 0.0001. (C) Model for the effect of avANP32A transferred by avian influenza A virus on viral replication and adaptive mutation acquisition when jumping from avian hosts to mammalian hosts. (D) H9N2 virus pack- aged with either avANP32A or huANP32A was blind passaged six times in MDCK cells. Viral RNAs were extracted and the C terminus of PB2 was amplified and deep- sequenced to monitor the residue phenotype of PB2 627 and 701 positions during passages in MDCK cells. Bar graph represents the percentage of adaptive mutations including PB2-E627K/V and D701N in each passage. Error bars represent mean ± SEM from n = 4 independent biological replicates, unpaired t test; *P < 0.05. (E) Sche- matic representation of the protocol for the experiments shown in (F). (F) The lungs of infected mice were collected for viral RNA extraction, and the C terminus of PB2 was amplified and cloned into T vectors. Nine molecular clones from each sample were randomly picked and sequenced for determination of the residue phenotype of PB2 627 and 701 positions. Samples with nine clone negatives for the emergence of PB2-E627K/V and D701N were recognized as no occurrence of adaptive mutations. In each group, the percentage of mice with emergence of adaptive mutations was calculated.

Article Snippet: Immunoblotting analysis was carried out using the following primary antibodies: ANP32A rabbit polyclonal (15810- 1- AP, Proteintech), ANP32B mouse monoclonal (66160- 1- Ig, Proteintech), ANP32E rabbit polyclonal (A17220, Abclonal), Flag mouse monoclonal (F1804, SigmaAldrich), Flag rabbit polyclonal (F7425, Sigma- Aldrich), HA mouse monoclonal (H9658, Sigma- Aldrich), ACTB rabbit monoclonal (AC026, Abclonal), His mouse monoclonal (66005- 1, Proteintech), V5 mouse monoclonal (ab27671, Abcam), glutathione S- transferase (GST) rabbit polyclonal (10000- 0- AP, Proteintech), CD81 mouse monoclonal (66866- 1- Ig, Proteintech), and IBV NP rabbit polyclonal (GTX128538, GeneTex).

Techniques: Virus, Produced, Plasmid Preparation, Purification, Western Blot, Infection, Mutagenesis, Amplification, Residue, RNA Extraction, Clone Assay