Alternative paths in HIV-1 targeted human signal transduction pathways

Background Human immunodeficiency virus-1 (HIV-1) has a minimal genome of only 9 genes, which encode 15 proteins. HIV-1 thus depends on the human host for virtually every aspect of its life cycle. The universal language of communication in biological systems, including between pathogen and host, is via signal transduction pathways. The fundamental units of these pathways are protein protein interactions. Understanding the functional significance of HIV-1, human interactions requires viewing them in the context of human signal transduction pathways. Results Integration of HIV-1, human interactions with known signal transduction pathways indicates that the majority of known human pathways have the potential to be effected through at least one interaction with an HIV-1 protein at some point during the HIV-1 life cycle. For each pathway, we define simple paths between start points (i.e. no edges going into a node) and end points (i.e. no edges leaving a node). We then identify the paths that pass through human proteins that interact with HIV-1 proteins. We supplement the combined map with functional information, including which proteins are known drug targets and which proteins contribute significantly to HIV-1 function as revealed by recent siRNA screens. We find that there are often alternative paths starting and ending at the same proteins but circumventing the intermediate steps disrupted by HIV-1. Conclusion A mapping of HIV-1, human interactions to human signal transduction pathways is presented here to link interactions with functions. We proposed a new way of analyzing the virus host interactions by identifying HIV-1 targets as well as alternative paths bypassing the HIV-1 targeted steps. This approach yields numerous experimentally testable hypotheses on how HIV-1 function may be compromised and human cellular function restored by pharmacological approaches. We are making the full set of pathway analysis results available to the community. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Balakrishnan, Sivaraman [verfasserIn] Tastan, Oznur Carbonell, Jaime Klein-Seetharaman, Judith

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2009

Schlagwörter:	Acquire Immune Deficiency Syndrome Alternative Path Simple Path Start Node Acquire Immune Deficiency Syndrome Patient

Anmerkung:	© Balakrishnan et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (

Übergeordnetes Werk:	Enthalten in: BMC genomics - London : BioMed Central, 2000, 10(2009), Suppl 3 vom: 03. Dez.
Übergeordnetes Werk:	volume:10 ; year:2009 ; number:Suppl 3 ; day:03 ; month:12

Links:	Volltext

DOI / URN:	10.1186/1471-2164-10-S3-S30

Katalog-ID:	SPR027048977

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520			\|a Background Human immunodeficiency virus-1 (HIV-1) has a minimal genome of only 9 genes, which encode 15 proteins. HIV-1 thus depends on the human host for virtually every aspect of its life cycle. The universal language of communication in biological systems, including between pathogen and host, is via signal transduction pathways. The fundamental units of these pathways are protein protein interactions. Understanding the functional significance of HIV-1, human interactions requires viewing them in the context of human signal transduction pathways. Results Integration of HIV-1, human interactions with known signal transduction pathways indicates that the majority of known human pathways have the potential to be effected through at least one interaction with an HIV-1 protein at some point during the HIV-1 life cycle. For each pathway, we define simple paths between start points (i.e. no edges going into a node) and end points (i.e. no edges leaving a node). We then identify the paths that pass through human proteins that interact with HIV-1 proteins. We supplement the combined map with functional information, including which proteins are known drug targets and which proteins contribute significantly to HIV-1 function as revealed by recent siRNA screens. We find that there are often alternative paths starting and ending at the same proteins but circumventing the intermediate steps disrupted by HIV-1. Conclusion A mapping of HIV-1, human interactions to human signal transduction pathways is presented here to link interactions with functions. We proposed a new way of analyzing the virus host interactions by identifying HIV-1 targets as well as alternative paths bypassing the HIV-1 targeted steps. This approach yields numerous experimentally testable hypotheses on how HIV-1 function may be compromised and human cellular function restored by pharmacological approaches. We are making the full set of pathway analysis results available to the community.
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allfields	10.1186/1471-2164-10-S3-S30 doi (DE-627)SPR027048977 (SPR)1471-2164-10-S3-S30-e DE-627 ger DE-627 rakwb eng Balakrishnan, Sivaraman verfasserin aut Alternative paths in HIV-1 targeted human signal transduction pathways 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Balakrishnan et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( Background Human immunodeficiency virus-1 (HIV-1) has a minimal genome of only 9 genes, which encode 15 proteins. HIV-1 thus depends on the human host for virtually every aspect of its life cycle. The universal language of communication in biological systems, including between pathogen and host, is via signal transduction pathways. The fundamental units of these pathways are protein protein interactions. Understanding the functional significance of HIV-1, human interactions requires viewing them in the context of human signal transduction pathways. Results Integration of HIV-1, human interactions with known signal transduction pathways indicates that the majority of known human pathways have the potential to be effected through at least one interaction with an HIV-1 protein at some point during the HIV-1 life cycle. For each pathway, we define simple paths between start points (i.e. no edges going into a node) and end points (i.e. no edges leaving a node). We then identify the paths that pass through human proteins that interact with HIV-1 proteins. We supplement the combined map with functional information, including which proteins are known drug targets and which proteins contribute significantly to HIV-1 function as revealed by recent siRNA screens. We find that there are often alternative paths starting and ending at the same proteins but circumventing the intermediate steps disrupted by HIV-1. Conclusion A mapping of HIV-1, human interactions to human signal transduction pathways is presented here to link interactions with functions. We proposed a new way of analyzing the virus host interactions by identifying HIV-1 targets as well as alternative paths bypassing the HIV-1 targeted steps. This approach yields numerous experimentally testable hypotheses on how HIV-1 function may be compromised and human cellular function restored by pharmacological approaches. We are making the full set of pathway analysis results available to the community. Acquire Immune Deficiency Syndrome (dpeaa)DE-He213 Alternative Path (dpeaa)DE-He213 Simple Path (dpeaa)DE-He213 Start Node (dpeaa)DE-He213 Acquire Immune Deficiency Syndrome Patient (dpeaa)DE-He213 Tastan, Oznur aut Carbonell, Jaime aut Klein-Seetharaman, Judith aut Enthalten in BMC genomics London : BioMed Central, 2000 10(2009), Suppl 3 vom: 03. Dez. (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:10 year:2009 number:Suppl 3 day:03 month:12 https://dx.doi.org/10.1186/1471-2164-10-S3-S30 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2009 Suppl 3 03 12
spelling	10.1186/1471-2164-10-S3-S30 doi (DE-627)SPR027048977 (SPR)1471-2164-10-S3-S30-e DE-627 ger DE-627 rakwb eng Balakrishnan, Sivaraman verfasserin aut Alternative paths in HIV-1 targeted human signal transduction pathways 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Balakrishnan et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( Background Human immunodeficiency virus-1 (HIV-1) has a minimal genome of only 9 genes, which encode 15 proteins. HIV-1 thus depends on the human host for virtually every aspect of its life cycle. The universal language of communication in biological systems, including between pathogen and host, is via signal transduction pathways. The fundamental units of these pathways are protein protein interactions. Understanding the functional significance of HIV-1, human interactions requires viewing them in the context of human signal transduction pathways. Results Integration of HIV-1, human interactions with known signal transduction pathways indicates that the majority of known human pathways have the potential to be effected through at least one interaction with an HIV-1 protein at some point during the HIV-1 life cycle. For each pathway, we define simple paths between start points (i.e. no edges going into a node) and end points (i.e. no edges leaving a node). We then identify the paths that pass through human proteins that interact with HIV-1 proteins. We supplement the combined map with functional information, including which proteins are known drug targets and which proteins contribute significantly to HIV-1 function as revealed by recent siRNA screens. We find that there are often alternative paths starting and ending at the same proteins but circumventing the intermediate steps disrupted by HIV-1. Conclusion A mapping of HIV-1, human interactions to human signal transduction pathways is presented here to link interactions with functions. We proposed a new way of analyzing the virus host interactions by identifying HIV-1 targets as well as alternative paths bypassing the HIV-1 targeted steps. This approach yields numerous experimentally testable hypotheses on how HIV-1 function may be compromised and human cellular function restored by pharmacological approaches. We are making the full set of pathway analysis results available to the community. Acquire Immune Deficiency Syndrome (dpeaa)DE-He213 Alternative Path (dpeaa)DE-He213 Simple Path (dpeaa)DE-He213 Start Node (dpeaa)DE-He213 Acquire Immune Deficiency Syndrome Patient (dpeaa)DE-He213 Tastan, Oznur aut Carbonell, Jaime aut Klein-Seetharaman, Judith aut Enthalten in BMC genomics London : BioMed Central, 2000 10(2009), Suppl 3 vom: 03. Dez. (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:10 year:2009 number:Suppl 3 day:03 month:12 https://dx.doi.org/10.1186/1471-2164-10-S3-S30 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2009 Suppl 3 03 12
allfields_unstemmed	10.1186/1471-2164-10-S3-S30 doi (DE-627)SPR027048977 (SPR)1471-2164-10-S3-S30-e DE-627 ger DE-627 rakwb eng Balakrishnan, Sivaraman verfasserin aut Alternative paths in HIV-1 targeted human signal transduction pathways 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Balakrishnan et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( Background Human immunodeficiency virus-1 (HIV-1) has a minimal genome of only 9 genes, which encode 15 proteins. HIV-1 thus depends on the human host for virtually every aspect of its life cycle. The universal language of communication in biological systems, including between pathogen and host, is via signal transduction pathways. The fundamental units of these pathways are protein protein interactions. Understanding the functional significance of HIV-1, human interactions requires viewing them in the context of human signal transduction pathways. Results Integration of HIV-1, human interactions with known signal transduction pathways indicates that the majority of known human pathways have the potential to be effected through at least one interaction with an HIV-1 protein at some point during the HIV-1 life cycle. For each pathway, we define simple paths between start points (i.e. no edges going into a node) and end points (i.e. no edges leaving a node). We then identify the paths that pass through human proteins that interact with HIV-1 proteins. We supplement the combined map with functional information, including which proteins are known drug targets and which proteins contribute significantly to HIV-1 function as revealed by recent siRNA screens. We find that there are often alternative paths starting and ending at the same proteins but circumventing the intermediate steps disrupted by HIV-1. Conclusion A mapping of HIV-1, human interactions to human signal transduction pathways is presented here to link interactions with functions. We proposed a new way of analyzing the virus host interactions by identifying HIV-1 targets as well as alternative paths bypassing the HIV-1 targeted steps. This approach yields numerous experimentally testable hypotheses on how HIV-1 function may be compromised and human cellular function restored by pharmacological approaches. We are making the full set of pathway analysis results available to the community. Acquire Immune Deficiency Syndrome (dpeaa)DE-He213 Alternative Path (dpeaa)DE-He213 Simple Path (dpeaa)DE-He213 Start Node (dpeaa)DE-He213 Acquire Immune Deficiency Syndrome Patient (dpeaa)DE-He213 Tastan, Oznur aut Carbonell, Jaime aut Klein-Seetharaman, Judith aut Enthalten in BMC genomics London : BioMed Central, 2000 10(2009), Suppl 3 vom: 03. Dez. (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:10 year:2009 number:Suppl 3 day:03 month:12 https://dx.doi.org/10.1186/1471-2164-10-S3-S30 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2009 Suppl 3 03 12
allfieldsGer	10.1186/1471-2164-10-S3-S30 doi (DE-627)SPR027048977 (SPR)1471-2164-10-S3-S30-e DE-627 ger DE-627 rakwb eng Balakrishnan, Sivaraman verfasserin aut Alternative paths in HIV-1 targeted human signal transduction pathways 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Balakrishnan et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( Background Human immunodeficiency virus-1 (HIV-1) has a minimal genome of only 9 genes, which encode 15 proteins. HIV-1 thus depends on the human host for virtually every aspect of its life cycle. The universal language of communication in biological systems, including between pathogen and host, is via signal transduction pathways. The fundamental units of these pathways are protein protein interactions. Understanding the functional significance of HIV-1, human interactions requires viewing them in the context of human signal transduction pathways. Results Integration of HIV-1, human interactions with known signal transduction pathways indicates that the majority of known human pathways have the potential to be effected through at least one interaction with an HIV-1 protein at some point during the HIV-1 life cycle. For each pathway, we define simple paths between start points (i.e. no edges going into a node) and end points (i.e. no edges leaving a node). We then identify the paths that pass through human proteins that interact with HIV-1 proteins. We supplement the combined map with functional information, including which proteins are known drug targets and which proteins contribute significantly to HIV-1 function as revealed by recent siRNA screens. We find that there are often alternative paths starting and ending at the same proteins but circumventing the intermediate steps disrupted by HIV-1. Conclusion A mapping of HIV-1, human interactions to human signal transduction pathways is presented here to link interactions with functions. We proposed a new way of analyzing the virus host interactions by identifying HIV-1 targets as well as alternative paths bypassing the HIV-1 targeted steps. This approach yields numerous experimentally testable hypotheses on how HIV-1 function may be compromised and human cellular function restored by pharmacological approaches. We are making the full set of pathway analysis results available to the community. Acquire Immune Deficiency Syndrome (dpeaa)DE-He213 Alternative Path (dpeaa)DE-He213 Simple Path (dpeaa)DE-He213 Start Node (dpeaa)DE-He213 Acquire Immune Deficiency Syndrome Patient (dpeaa)DE-He213 Tastan, Oznur aut Carbonell, Jaime aut Klein-Seetharaman, Judith aut Enthalten in BMC genomics London : BioMed Central, 2000 10(2009), Suppl 3 vom: 03. Dez. (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:10 year:2009 number:Suppl 3 day:03 month:12 https://dx.doi.org/10.1186/1471-2164-10-S3-S30 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2009 Suppl 3 03 12
allfieldsSound	10.1186/1471-2164-10-S3-S30 doi (DE-627)SPR027048977 (SPR)1471-2164-10-S3-S30-e DE-627 ger DE-627 rakwb eng Balakrishnan, Sivaraman verfasserin aut Alternative paths in HIV-1 targeted human signal transduction pathways 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Balakrishnan et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( Background Human immunodeficiency virus-1 (HIV-1) has a minimal genome of only 9 genes, which encode 15 proteins. HIV-1 thus depends on the human host for virtually every aspect of its life cycle. The universal language of communication in biological systems, including between pathogen and host, is via signal transduction pathways. The fundamental units of these pathways are protein protein interactions. Understanding the functional significance of HIV-1, human interactions requires viewing them in the context of human signal transduction pathways. Results Integration of HIV-1, human interactions with known signal transduction pathways indicates that the majority of known human pathways have the potential to be effected through at least one interaction with an HIV-1 protein at some point during the HIV-1 life cycle. For each pathway, we define simple paths between start points (i.e. no edges going into a node) and end points (i.e. no edges leaving a node). We then identify the paths that pass through human proteins that interact with HIV-1 proteins. We supplement the combined map with functional information, including which proteins are known drug targets and which proteins contribute significantly to HIV-1 function as revealed by recent siRNA screens. We find that there are often alternative paths starting and ending at the same proteins but circumventing the intermediate steps disrupted by HIV-1. Conclusion A mapping of HIV-1, human interactions to human signal transduction pathways is presented here to link interactions with functions. We proposed a new way of analyzing the virus host interactions by identifying HIV-1 targets as well as alternative paths bypassing the HIV-1 targeted steps. This approach yields numerous experimentally testable hypotheses on how HIV-1 function may be compromised and human cellular function restored by pharmacological approaches. We are making the full set of pathway analysis results available to the community. Acquire Immune Deficiency Syndrome (dpeaa)DE-He213 Alternative Path (dpeaa)DE-He213 Simple Path (dpeaa)DE-He213 Start Node (dpeaa)DE-He213 Acquire Immune Deficiency Syndrome Patient (dpeaa)DE-He213 Tastan, Oznur aut Carbonell, Jaime aut Klein-Seetharaman, Judith aut Enthalten in BMC genomics London : BioMed Central, 2000 10(2009), Suppl 3 vom: 03. Dez. (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:10 year:2009 number:Suppl 3 day:03 month:12 https://dx.doi.org/10.1186/1471-2164-10-S3-S30 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2009 Suppl 3 03 12
language	English
source	Enthalten in BMC genomics 10(2009), Suppl 3 vom: 03. Dez. volume:10 year:2009 number:Suppl 3 day:03 month:12
sourceStr	Enthalten in BMC genomics 10(2009), Suppl 3 vom: 03. Dez. volume:10 year:2009 number:Suppl 3 day:03 month:12
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Acquire Immune Deficiency Syndrome Alternative Path Simple Path Start Node Acquire Immune Deficiency Syndrome Patient
isfreeaccess_bool	false
container_title	BMC genomics
authorswithroles_txt_mv	Balakrishnan, Sivaraman @@aut@@ Tastan, Oznur @@aut@@ Carbonell, Jaime @@aut@@ Klein-Seetharaman, Judith @@aut@@
publishDateDaySort_date	2009-12-03T00:00:00Z
hierarchy_top_id	326644954
id	SPR027048977
language_de	englisch
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author	Balakrishnan, Sivaraman
spellingShingle	Balakrishnan, Sivaraman misc Acquire Immune Deficiency Syndrome misc Alternative Path misc Simple Path misc Start Node misc Acquire Immune Deficiency Syndrome Patient Alternative paths in HIV-1 targeted human signal transduction pathways
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topic_title	Alternative paths in HIV-1 targeted human signal transduction pathways Acquire Immune Deficiency Syndrome (dpeaa)DE-He213 Alternative Path (dpeaa)DE-He213 Simple Path (dpeaa)DE-He213 Start Node (dpeaa)DE-He213 Acquire Immune Deficiency Syndrome Patient (dpeaa)DE-He213
topic	misc Acquire Immune Deficiency Syndrome misc Alternative Path misc Simple Path misc Start Node misc Acquire Immune Deficiency Syndrome Patient
topic_unstemmed	misc Acquire Immune Deficiency Syndrome misc Alternative Path misc Simple Path misc Start Node misc Acquire Immune Deficiency Syndrome Patient
topic_browse	misc Acquire Immune Deficiency Syndrome misc Alternative Path misc Simple Path misc Start Node misc Acquire Immune Deficiency Syndrome Patient
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title	Alternative paths in HIV-1 targeted human signal transduction pathways
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title_full	Alternative paths in HIV-1 targeted human signal transduction pathways
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title_sort	alternative paths in hiv-1 targeted human signal transduction pathways
title_auth	Alternative paths in HIV-1 targeted human signal transduction pathways
abstract	Background Human immunodeficiency virus-1 (HIV-1) has a minimal genome of only 9 genes, which encode 15 proteins. HIV-1 thus depends on the human host for virtually every aspect of its life cycle. The universal language of communication in biological systems, including between pathogen and host, is via signal transduction pathways. The fundamental units of these pathways are protein protein interactions. Understanding the functional significance of HIV-1, human interactions requires viewing them in the context of human signal transduction pathways. Results Integration of HIV-1, human interactions with known signal transduction pathways indicates that the majority of known human pathways have the potential to be effected through at least one interaction with an HIV-1 protein at some point during the HIV-1 life cycle. For each pathway, we define simple paths between start points (i.e. no edges going into a node) and end points (i.e. no edges leaving a node). We then identify the paths that pass through human proteins that interact with HIV-1 proteins. We supplement the combined map with functional information, including which proteins are known drug targets and which proteins contribute significantly to HIV-1 function as revealed by recent siRNA screens. We find that there are often alternative paths starting and ending at the same proteins but circumventing the intermediate steps disrupted by HIV-1. Conclusion A mapping of HIV-1, human interactions to human signal transduction pathways is presented here to link interactions with functions. We proposed a new way of analyzing the virus host interactions by identifying HIV-1 targets as well as alternative paths bypassing the HIV-1 targeted steps. This approach yields numerous experimentally testable hypotheses on how HIV-1 function may be compromised and human cellular function restored by pharmacological approaches. We are making the full set of pathway analysis results available to the community. © Balakrishnan et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (
abstractGer	Background Human immunodeficiency virus-1 (HIV-1) has a minimal genome of only 9 genes, which encode 15 proteins. HIV-1 thus depends on the human host for virtually every aspect of its life cycle. The universal language of communication in biological systems, including between pathogen and host, is via signal transduction pathways. The fundamental units of these pathways are protein protein interactions. Understanding the functional significance of HIV-1, human interactions requires viewing them in the context of human signal transduction pathways. Results Integration of HIV-1, human interactions with known signal transduction pathways indicates that the majority of known human pathways have the potential to be effected through at least one interaction with an HIV-1 protein at some point during the HIV-1 life cycle. For each pathway, we define simple paths between start points (i.e. no edges going into a node) and end points (i.e. no edges leaving a node). We then identify the paths that pass through human proteins that interact with HIV-1 proteins. We supplement the combined map with functional information, including which proteins are known drug targets and which proteins contribute significantly to HIV-1 function as revealed by recent siRNA screens. We find that there are often alternative paths starting and ending at the same proteins but circumventing the intermediate steps disrupted by HIV-1. Conclusion A mapping of HIV-1, human interactions to human signal transduction pathways is presented here to link interactions with functions. We proposed a new way of analyzing the virus host interactions by identifying HIV-1 targets as well as alternative paths bypassing the HIV-1 targeted steps. This approach yields numerous experimentally testable hypotheses on how HIV-1 function may be compromised and human cellular function restored by pharmacological approaches. We are making the full set of pathway analysis results available to the community. © Balakrishnan et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (
abstract_unstemmed	Background Human immunodeficiency virus-1 (HIV-1) has a minimal genome of only 9 genes, which encode 15 proteins. HIV-1 thus depends on the human host for virtually every aspect of its life cycle. The universal language of communication in biological systems, including between pathogen and host, is via signal transduction pathways. The fundamental units of these pathways are protein protein interactions. Understanding the functional significance of HIV-1, human interactions requires viewing them in the context of human signal transduction pathways. Results Integration of HIV-1, human interactions with known signal transduction pathways indicates that the majority of known human pathways have the potential to be effected through at least one interaction with an HIV-1 protein at some point during the HIV-1 life cycle. For each pathway, we define simple paths between start points (i.e. no edges going into a node) and end points (i.e. no edges leaving a node). We then identify the paths that pass through human proteins that interact with HIV-1 proteins. We supplement the combined map with functional information, including which proteins are known drug targets and which proteins contribute significantly to HIV-1 function as revealed by recent siRNA screens. We find that there are often alternative paths starting and ending at the same proteins but circumventing the intermediate steps disrupted by HIV-1. Conclusion A mapping of HIV-1, human interactions to human signal transduction pathways is presented here to link interactions with functions. We proposed a new way of analyzing the virus host interactions by identifying HIV-1 targets as well as alternative paths bypassing the HIV-1 targeted steps. This approach yields numerous experimentally testable hypotheses on how HIV-1 function may be compromised and human cellular function restored by pharmacological approaches. We are making the full set of pathway analysis results available to the community. © Balakrishnan et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (
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title_short	Alternative paths in HIV-1 targeted human signal transduction pathways
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Alternative paths in HIV-1 targeted human signal transduction pathways

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