{"gene":"PF3D7_0604100","run_date":"2026-09-07T10:55:52","timeline":{"discoveries":[{"year":2010,"finding":"SIP2 (PF3D7_0604100) was purified and characterized as the nuclear factor that specifically binds SPE2 motif arrays in subtelomeric domains of P. falciparum. A 60 kDa N-terminal domain (PfSIP2-N) is released during schizogony and is the active DNA-binding fragment, while the full-length protein does not bind SPE2. High-affinity binding requires both adjacent AP2 domains and a conserved bipartite SPE2 consensus motif. Genome-wide in silico mapping identified 777 putative binding sites, 94% of which cluster in heterochromatic subtelomeric domains upstream of var genes and in telomere-associated repeat elements. Immunofluorescence and ChIP assays showed co-localization of PfSIP2-N with PfHP1 at chromosome ends. Genome-wide ChIP confirmed exclusive binding of PfSIP2-N to subtelomeric SPE2 landmarks in vivo. Over-expression of PfSIP2-N had no effect on global gene transcription, indicating a structural/heterochromatin role rather than a gene-activation role.","method":"Protein purification, protein-binding assays, site-directed mutagenesis of binding motif, immunofluorescence (IFA), chromatin immunoprecipitation (ChIP), genome-wide ChIP, in silico genome mapping, over-expression with transcriptome analysis","journal":"PLoS pathogens","confidence":"High","confidence_rationale":"Tier 1–2 / Strong — multiple orthogonal methods (biochemical purification, ChIP, IFA, genome-wide mapping, mutagenesis of binding motif, overexpression + transcriptomics) in a single focused study on this exact protein","pmids":["20195509"],"is_preprint":false,"attribution":[{"species":"Plasmodium falciparum","strain":""}]},{"year":2008,"finding":"The DNA-binding specificity of PfSIP2 (PF3D7_0604100) was characterized using protein-binding microarrays (PBMs), defining its cognate DNA motif. Protein-DNA sequence specificity was shown to be conserved in orthologous ApiAP2 proteins between phylogenetically distant Apicomplexan species.","method":"Protein-binding microarrays (PBMs), computational motif analysis","journal":"Proceedings of the National Academy of Sciences of the United States of America","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — direct biochemical assay (PBMs) establishing DNA-binding specificity, single lab, two methods (PBM + computational)","pmids":["18541913"],"is_preprint":false,"attribution":[{"species":"Plasmodium falciparum","strain":""}]},{"year":2025,"finding":"In P. berghei, conditional disruption of pbsip2 (the SIP2 ortholog) resulted in developmental arrest before merozoite formation, with notable down-regulation of merozoite-related genes. ChIP-seq showed that PbSIP2 comprehensively activated merozoite-related genes by binding to cis-regulatory elements including the bipartite motif (TGCAN4-6GTGCA). SIP2 was identified as the master transcription factor for merozoite formation, establishing erythrocyte infectivity.","method":"Conditional gene disruption (loss-of-function), RNA-seq (transcriptomics), ChIP-seq","journal":"Science advances","confidence":"High","confidence_rationale":"Tier 2 / Strong — conditional KO with defined cellular phenotype (arrest before merozoite formation) plus genome-wide ChIP-seq confirming direct transcriptional targets, multiple orthogonal methods in a single focused study","pmids":["40117352"],"is_preprint":false,"attribution":[{"species":"Plasmodium berghei","strain":""}]},{"year":2025,"finding":"PfSIP2 (PF3D7_0604100) was identified as essential for sporozoite infection of human hepatocytes. This was established through functional analyses in the context of single-cell RNA sequencing of parasites in the Anopheles mosquito midgut.","method":"Single-cell RNA sequencing, functional analysis (loss-of-function)","journal":"Nature","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — functional genetic analysis with a defined phenotype (failure to infect hepatocytes), single lab, limited methodological detail in abstract","pmids":["41125888"],"is_preprint":false,"attribution":[{"species":"Plasmodium falciparum","strain":""}]},{"year":2025,"finding":"A preprint version of the mosquito-stage study also reported PfSIP2 as essential for sporozoite infection of human hepatocytes, consistent with the peer-reviewed finding.","method":"Single-cell RNA sequencing, functional analysis (loss-of-function)","journal":"bioRxiv : the preprint server for biology","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — replicates the peer-reviewed Nature finding; preprint, single lab","pmids":["39605504"],"is_preprint":true,"attribution":[{"species":"Plasmodium falciparum","strain":""}]}],"current_model":"SIP2 (PF3D7_0604100) is an ApiAP2 transcription factor whose N-terminal domain (PfSIP2-N, released during schizogony) binds bipartite SPE2 motifs exclusively at subtelomeric heterochromatin in P. falciparum, co-localizing with HP1 and contributing to chromosome end biology without globally regulating transcription; in P. berghei its ortholog PbSIP2 functions as the master transcription factor for merozoite formation by directly activating merozoite-related genes via a bipartite TGCA motif, and PfSIP2 is additionally required for sporozoite infection of human hepatocytes."},"narrative":{"mechanistic_narrative":"SIP2 (PF3D7_0604100) is an ApiAP2-family transcription factor whose function diverges markedly between Plasmodium species [PMID:20195509, PMID:40117352]. In P. falciparum, its DNA-binding specificity was defined by protein-binding microarrays and shown to be conserved across phylogenetically distant Apicomplexa [PMID:18541913], and the factor was purified as the nuclear protein that specifically recognizes bipartite SPE2 motif arrays: high-affinity binding requires both adjacent AP2 domains and is carried by a 60 kDa N-terminal fragment (PfSIP2-N) released during schizogony, whereas the full-length protein does not bind SPE2 [PMID:20195509]. Genome-wide mapping and ChIP place PfSIP2-N almost exclusively at subtelomeric heterochromatin—upstream of var genes and within telomere-associated repeats—where it co-localizes with PfHP1, and its over-expression does not perturb global transcription, indicating a structural chromosome-end/heterochromatin role rather than gene activation in this species [PMID:20195509]. PfSIP2 is also required for sporozoite infection of human hepatocytes [PMID:41125888]. In contrast, in P. berghei the ortholog PbSIP2 acts as a master transcriptional activator of merozoite formation: its conditional disruption arrests development before merozoite formation with down-regulation of merozoite genes, and ChIP-seq shows direct binding to cis-regulatory bipartite (TGCAN4-6GTGCA) motifs to activate those genes and establish erythrocyte infectivity [PMID:40117352].","teleology":[{"year":2008,"claim":"Establishing what DNA sequence PfSIP2 recognizes was the prerequisite for any functional model; protein-binding microarrays defined its cognate motif and showed the specificity is conserved across distant Apicomplexa.","evidence":"Protein-binding microarrays and computational motif analysis in P. falciparum","pmids":["18541913"],"confidence":"Medium","gaps":["In vitro motif specificity does not establish in vivo genomic occupancy","No cellular phenotype or biological role assigned"],"attribution":[{"species":"Plasmodium falciparum","strain":""}]},{"year":2010,"claim":"Whether PfSIP2 acts as a classical gene-activating transcription factor or has another role was resolved by showing it is an autoprocessed factor targeting subtelomeric heterochromatin rather than driving transcription.","evidence":"Protein purification, mutagenesis of the SPE2 motif, IFA, genome-wide ChIP, and over-expression transcriptomics in P. falciparum","pmids":["20195509"],"confidence":"High","gaps":["Mechanism and trigger of N-terminal fragment release during schizogony not defined","Functional consequence of PfHP1 co-localization for var gene silencing or chromosome-end biology not directly tested","Direct genetic loss-of-function phenotype in P. falciparum blood stages not established here"],"attribution":[{"species":"Plasmodium falciparum","strain":""}]},{"year":2025,"claim":"The in vivo biological role of the SIP2 ortholog was defined in P. berghei, revealing a species-divergent function as the master activator of merozoite formation rather than a heterochromatin structural factor.","evidence":"Conditional gene disruption with RNA-seq and ChIP-seq in P. berghei","pmids":["40117352"],"confidence":"High","gaps":["Whether P. falciparum SIP2 shares this merozoite-activation role is not demonstrated","Reconciliation of the heterochromatin-associated PfSIP2 model with the activator PbSIP2 model is unresolved","Relationship between full-length protein and any processed active form in P. berghei not addressed"],"attribution":[{"species":"Plasmodium berghei","strain":""}]},{"year":2025,"claim":"A distinct life-cycle requirement was identified: PfSIP2 is essential for sporozoite infection of human hepatocytes, extending its role beyond blood-stage chromosome biology.","evidence":"Single-cell RNA sequencing of mosquito midgut parasites with loss-of-function functional analysis in P. falciparum (also reported in a bioRxiv preprint)","pmids":["41125888","39605504"],"confidence":"Medium","gaps":["Limited mechanistic detail on how PfSIP2 supports hepatocyte infection","Target genes or DNA-binding events underlying the sporozoite phenotype not defined","Relationship of this role to the subtelomeric heterochromatin function unclear"],"attribution":[{"species":"Plasmodium falciparum","strain":""}]},{"year":null,"claim":"It remains unresolved how the same ApiAP2 factor functions as a subtelomeric heterochromatin-associated protein in P. falciparum yet as a genome-wide merozoite-gene activator in P. berghei, and what mechanism unifies its blood-stage and sporozoite roles.","evidence":"No single study in the corpus reconciles the divergent P. falciparum and P. berghei models","pmids":[],"confidence":"Low","gaps":["No direct comparison of PfSIP2 and PbSIP2 activity in a shared assay","No structural or mechanistic account of N-terminal processing across species","P. falciparum blood-stage loss-of-function phenotype not directly characterized"],"attribution":[]}],"mechanism_profile":{"molecular_activity":[],"localization":[],"pathway":[],"complexes":[],"partners":["PFHP1 (CO-LOCALIZES AT SUBTELOMERIC CHROMOSOME ENDS IN P. FALCIPARUM) [#0]"],"other_free_text":["PfSIP2-N is a 60 kDa N-terminal DNA-binding fragment released during schizogony; the full-length protein does not bind SPE2, and high-affinity binding requires both adjacent AP2 domains [#0]","PfSIP2 binds bipartite SPE2 consensus motifs concentrated at subtelomeric heterochromatin (94% of 777 predicted sites), upstream of var genes and in telomere-associated repeats [#0]","Over-expression of PfSIP2-N does not alter global transcription, indicating a structural/heterochromatin role in P. falciparum [#0]","PbSIP2 binds a bipartite TGCAN4-6GTGCA motif and directly activates merozoite-related genes in P. berghei; its disruption arrests development before merozoite formation [#2]","Species-divergent function: heterochromatin-associated in P. falciparum [#0] versus master merozoite-gene activator in P. berghei [#2]","PfSIP2 is required for sporozoite infection of human hepatocytes [#3, 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A 60 kDa N-terminal domain (PfSIP2-N) is released during schizogony and is the active DNA-binding fragment, while the full-length protein does not bind SPE2. High-affinity binding requires both adjacent AP2 domains and a conserved bipartite SPE2 consensus motif. Genome-wide in silico mapping identified 777 putative binding sites, 94% of which cluster in heterochromatic subtelomeric domains upstream of var genes and in telomere-associated repeat elements. Immunofluorescence and ChIP assays showed co-localization of PfSIP2-N with PfHP1 at chromosome ends. Genome-wide ChIP confirmed exclusive binding of PfSIP2-N to subtelomeric SPE2 landmarks in vivo. Over-expression of PfSIP2-N had no effect on global gene transcription, indicating a structural/heterochromatin role rather than a gene-activation role.\",\n      \"method\": \"Protein purification, protein-binding assays, site-directed mutagenesis of binding motif, immunofluorescence (IFA), chromatin immunoprecipitation (ChIP), genome-wide ChIP, in silico genome mapping, over-expression with transcriptome analysis\",\n      \"journal\": \"PLoS pathogens\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1–2 / Strong — multiple orthogonal methods (biochemical purification, ChIP, IFA, genome-wide mapping, mutagenesis of binding motif, overexpression + transcriptomics) in a single focused study on this exact protein\",\n      \"pmids\": [\"20195509\"],\n      \"is_preprint\": false,\n      \"attribution\": [{\"species\": \"Plasmodium falciparum\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": 2008,\n      \"finding\": \"The DNA-binding specificity of PfSIP2 (PF3D7_0604100) was characterized using protein-binding microarrays (PBMs), defining its cognate DNA motif. Protein-DNA sequence specificity was shown to be conserved in orthologous ApiAP2 proteins between phylogenetically distant Apicomplexan species.\",\n      \"method\": \"Protein-binding microarrays (PBMs), computational motif analysis\",\n      \"journal\": \"Proceedings of the National Academy of Sciences of the United States of America\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — direct biochemical assay (PBMs) establishing DNA-binding specificity, single lab, two methods (PBM + computational)\",\n      \"pmids\": [\"18541913\"],\n      \"is_preprint\": false,\n      \"attribution\": [{\"species\": \"Plasmodium falciparum\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": 2025,\n      \"finding\": \"In P. berghei, conditional disruption of pbsip2 (the SIP2 ortholog) resulted in developmental arrest before merozoite formation, with notable down-regulation of merozoite-related genes. ChIP-seq showed that PbSIP2 comprehensively activated merozoite-related genes by binding to cis-regulatory elements including the bipartite motif (TGCAN4-6GTGCA). SIP2 was identified as the master transcription factor for merozoite formation, establishing erythrocyte infectivity.\",\n      \"method\": \"Conditional gene disruption (loss-of-function), RNA-seq (transcriptomics), ChIP-seq\",\n      \"journal\": \"Science advances\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Strong — conditional KO with defined cellular phenotype (arrest before merozoite formation) plus genome-wide ChIP-seq confirming direct transcriptional targets, multiple orthogonal methods in a single focused study\",\n      \"pmids\": [\"40117352\"],\n      \"is_preprint\": false,\n      \"attribution\": [{\"species\": \"Plasmodium berghei\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": 2025,\n      \"finding\": \"PfSIP2 (PF3D7_0604100) was identified as essential for sporozoite infection of human hepatocytes. This was established through functional analyses in the context of single-cell RNA sequencing of parasites in the Anopheles mosquito midgut.\",\n      \"method\": \"Single-cell RNA sequencing, functional analysis (loss-of-function)\",\n      \"journal\": \"Nature\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — functional genetic analysis with a defined phenotype (failure to infect hepatocytes), single lab, limited methodological detail in abstract\",\n      \"pmids\": [\"41125888\"],\n      \"is_preprint\": false,\n      \"attribution\": [{\"species\": \"Plasmodium falciparum\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": 2025,\n      \"finding\": \"A preprint version of the mosquito-stage study also reported PfSIP2 as essential for sporozoite infection of human hepatocytes, consistent with the peer-reviewed finding.\",\n      \"method\": \"Single-cell RNA sequencing, functional analysis (loss-of-function)\",\n      \"journal\": \"bioRxiv : the preprint server for biology\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — replicates the peer-reviewed Nature finding; preprint, single lab\",\n      \"pmids\": [\"39605504\"],\n      \"is_preprint\": true,\n      \"attribution\": [{\"species\": \"Plasmodium falciparum\", \"strain\": \"\"}]\n    }\n  ],\n  \"current_model\": \"SIP2 (PF3D7_0604100) is an ApiAP2 transcription factor whose N-terminal domain (PfSIP2-N, released during schizogony) binds bipartite SPE2 motifs exclusively at subtelomeric heterochromatin in P. falciparum, co-localizing with HP1 and contributing to chromosome end biology without globally regulating transcription; in P. berghei its ortholog PbSIP2 functions as the master transcription factor for merozoite formation by directly activating merozoite-related genes via a bipartite TGCA motif, and PfSIP2 is additionally required for sporozoite infection of human hepatocytes.\"\n}\n```","stage2_raw":"{\n  \"mechanistic_narrative\": \"SIP2 (PF3D7_0604100) is an ApiAP2-family transcription factor whose function diverges markedly between Plasmodium species [#0, #2]. In P. falciparum, its DNA-binding specificity was defined by protein-binding microarrays and shown to be conserved across phylogenetically distant Apicomplexa [#1], and the factor was purified as the nuclear protein that specifically recognizes bipartite SPE2 motif arrays: high-affinity binding requires both adjacent AP2 domains and is carried by a 60 kDa N-terminal fragment (PfSIP2-N) released during schizogony, whereas the full-length protein does not bind SPE2 [#0]. Genome-wide mapping and ChIP place PfSIP2-N almost exclusively at subtelomeric heterochromatin—upstream of var genes and within telomere-associated repeats—where it co-localizes with PfHP1, and its over-expression does not perturb global transcription, indicating a structural chromosome-end/heterochromatin role rather than gene activation in this species [#0]. PfSIP2 is also required for sporozoite infection of human hepatocytes [#3]. In contrast, in P. berghei the ortholog PbSIP2 acts as a master transcriptional activator of merozoite formation: its conditional disruption arrests development before merozoite formation with down-regulation of merozoite genes, and ChIP-seq shows direct binding to cis-regulatory bipartite (TGCAN4-6GTGCA) motifs to activate those genes and establish erythrocyte infectivity [#2].\",\n  \"teleology\": [\n    {\n      \"year\": 2008,\n      \"claim\": \"Establishing what DNA sequence PfSIP2 recognizes was the prerequisite for any functional model; protein-binding microarrays defined its cognate motif and showed the specificity is conserved across distant Apicomplexa.\",\n      \"evidence\": \"Protein-binding microarrays and computational motif analysis in P. falciparum\",\n      \"pmids\": [\"18541913\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"In vitro motif specificity does not establish in vivo genomic occupancy\",\n        \"No cellular phenotype or biological role assigned\"\n      ],\n      \"attribution\": [{\"species\": \"Plasmodium falciparum\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": 2010,\n      \"claim\": \"Whether PfSIP2 acts as a classical gene-activating transcription factor or has another role was resolved by showing it is an autoprocessed factor targeting subtelomeric heterochromatin rather than driving transcription.\",\n      \"evidence\": \"Protein purification, mutagenesis of the SPE2 motif, IFA, genome-wide ChIP, and over-expression transcriptomics in P. falciparum\",\n      \"pmids\": [\"20195509\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\n        \"Mechanism and trigger of N-terminal fragment release during schizogony not defined\",\n        \"Functional consequence of PfHP1 co-localization for var gene silencing or chromosome-end biology not directly tested\",\n        \"Direct genetic loss-of-function phenotype in P. falciparum blood stages not established here\"\n      ],\n      \"attribution\": [{\"species\": \"Plasmodium falciparum\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": 2025,\n      \"claim\": \"The in vivo biological role of the SIP2 ortholog was defined in P. berghei, revealing a species-divergent function as the master activator of merozoite formation rather than a heterochromatin structural factor.\",\n      \"evidence\": \"Conditional gene disruption with RNA-seq and ChIP-seq in P. berghei\",\n      \"pmids\": [\"40117352\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\n        \"Whether P. falciparum SIP2 shares this merozoite-activation role is not demonstrated\",\n        \"Reconciliation of the heterochromatin-associated PfSIP2 model with the activator PbSIP2 model is unresolved\",\n        \"Relationship between full-length protein and any processed active form in P. berghei not addressed\"\n      ],\n      \"attribution\": [{\"species\": \"Plasmodium berghei\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": 2025,\n      \"claim\": \"A distinct life-cycle requirement was identified: PfSIP2 is essential for sporozoite infection of human hepatocytes, extending its role beyond blood-stage chromosome biology.\",\n      \"evidence\": \"Single-cell RNA sequencing of mosquito midgut parasites with loss-of-function functional analysis in P. falciparum (also reported in a bioRxiv preprint)\",\n      \"pmids\": [\"41125888\", \"39605504\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"Limited mechanistic detail on how PfSIP2 supports hepatocyte infection\",\n        \"Target genes or DNA-binding events underlying the sporozoite phenotype not defined\",\n        \"Relationship of this role to the subtelomeric heterochromatin function unclear\"\n      ],\n      \"attribution\": [{\"species\": \"Plasmodium falciparum\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"It remains unresolved how the same ApiAP2 factor functions as a subtelomeric heterochromatin-associated protein in P. falciparum yet as a genome-wide merozoite-gene activator in P. berghei, and what mechanism unifies its blood-stage and sporozoite roles.\",\n      \"evidence\": \"No single study in the corpus reconciles the divergent P. falciparum and P. berghei models\",\n      \"pmids\": [],\n      \"confidence\": \"Low\",\n      \"gaps\": [\n        \"No direct comparison of PfSIP2 and PbSIP2 activity in a shared assay\",\n        \"No structural or mechanistic account of N-terminal processing across species\",\n        \"P. falciparum blood-stage loss-of-function phenotype not directly characterized\"\n      ],\n      \"attribution\": []\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0003700\", \"supporting_discovery_ids\": [0, 1, 2]},\n      {\"term_id\": \"GO:0043565\", \"supporting_discovery_ids\": [0, 1, 2]},\n      {\"term_id\": \"GO:0000981\", \"supporting_discovery_ids\": [2]}\n    ],\n    \"localization\": [\n      {\"term_id\": \"GO:0005634\", \"supporting_discovery_ids\": [0]},\n      {\"term_id\": \"GO:0000781\", \"supporting_discovery_ids\": [0]},\n      {\"term_id\": \"GO:0000792\", \"supporting_discovery_ids\": [0]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"GO:0006355\", \"supporting_discovery_ids\": [2]},\n      {\"term_id\": \"GO:0006338\", \"supporting_discovery_ids\": [0]},\n      {\"term_id\": \"GO:0044409\", \"supporting_discovery_ids\": [3, 4]}\n    ],\n    \"complexes\": [],\n    \"partners\": [\n      \"PfHP1 (co-localizes at subtelomeric chromosome ends in P. falciparum) [#0]\"\n    ],\n    \"other_free_text\": [\n      \"PfSIP2-N is a 60 kDa N-terminal DNA-binding fragment released during schizogony; the full-length protein does not bind SPE2, and high-affinity binding requires both adjacent AP2 domains [#0]\",\n      \"PfSIP2 binds bipartite SPE2 consensus motifs concentrated at subtelomeric heterochromatin (94% of 777 predicted sites), upstream of var genes and in telomere-associated repeats [#0]\",\n      \"Over-expression of PfSIP2-N does not alter global transcription, indicating a structural/heterochromatin role in P. falciparum [#0]\",\n      \"PbSIP2 binds a bipartite TGCAN4-6GTGCA motif and directly activates merozoite-related genes in P. berghei; its disruption arrests development before merozoite formation [#2]\",\n      \"Species-divergent function: heterochromatin-associated in P. falciparum [#0] versus master merozoite-gene activator in P. berghei [#2]\",\n      \"PfSIP2 is required for sporozoite infection of human hepatocytes [#3, #4]\"\n    ]\n  }\n}","audit_flag":null,"strains":[{"strain":"Pf3D7","gene_id":"PF3D7_0604100","name":null,"product":"AP2 domain transcription factor","uniprot_acc":null,"chromosome":null,"start_pos":null},{"strain":"PbANKA","gene_id":"PBANKA_0102900","name":null,"product":"AP2 domain transcription factor, putative","uniprot_acc":null,"chromosome":null,"start_pos":null},{"strain":"PkH","gene_id":"PKNH_1146400","name":null,"product":"AP2 domain transcription factor, putative","uniprot_acc":null,"chromosome":null,"start_pos":null}],"gene_symbol":"SIP2","evaluation":null}