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diff --git a/gnqa/data/study1/responses/aging/experts/expert_aging_10.json b/gnqa/data/study1/responses/aging/experts/expert_aging_10.json new file mode 100644 index 0000000..d400a87 --- /dev/null +++ b/gnqa/data/study1/responses/aging/experts/expert_aging_10.json @@ -0,0 +1,148 @@ +{ + "created_at": "2024-05-31T21:59:24.668100Z", + "data": { + "amplify": false, + "answer": "The genes involved in the aging process include daf-16, daf-2, BAZ2B, HMGB4, NOC2L, RAI1, SIK1, SMARCA2, SPZ1, TBP, TRIP13, ZKSCAN1, DBH, TPO, LSS, GPER, HCRTR2, ATG2A, NEDD4L, PSMB1, UBXN4, USP6, EEF1A2, ITGB2, TUBB2C, WRN, ABCA7, AZGP1, CD36, DEGS2, PI4KA, SOAT2, APOE, LDLR, CDKN2B, RBM38, IGF1R, FOXO3, SNCA, NAP1L4, GAB2, QKI, and many others.", + "context": { + "0af83a97-18ef-47f4-9f0c-872633ca3414": [ + { + "document_id": "0af83a97-18ef-47f4-9f0c-872633ca3414", + "text": "\n\nIndicative biological pathways associated with the candidate aging genes" + }, + { + "document_id": "0af83a97-18ef-47f4-9f0c-872633ca3414", + "text": "\n\nFig. 2 Significant biological processes associated with the candidate aging genes" + }, + { + "document_id": "0af83a97-18ef-47f4-9f0c-872633ca3414", + "text": "\n\nFollowing are examples of the identified genes and experimental or GWAS link between these genes and aging.On the list of the 25 top genes, NAP1L4 encodes a member of the nucleosome assembly protein (NAP) family, which interacts with both core and linker histones, and shuttles between the cytoplasm and nucleus, suggesting a role as histone chaperone.Histone protein levels decline during aging, and dramatically affect chromatin structure.Remarkably, the lifespan can be extended by manipulations that reverse the age-dependent changes to chromatin structure, indicating the pivotal role of chromatin structure in aging [32].In another example, gene expression of NAP1L4 increases with age in the skin tissue [33].Findings of GWAS link a number of the identified genes to age-related disorders, such as GAB2 and late onset Alzheimer's disease [86], and QKI and coronary heart disease/myocardial infarction [79].Interestingly, GWAS reports also link QKI to successful aging [87]." + } + ], + "18e216d9-ea5c-4dfe-a30d-632163fcf39e": [ + { + "document_id": "18e216d9-ea5c-4dfe-a30d-632163fcf39e", + "text": "\n\nExamples of biological candidate genes with pleiotropic functions, which are involved in aging in general and in musculoskeletal aging in particular, are numerous: (a) in addition to the IGF-1 and vitamin D genes, estrogen metabolism pathway genes, including estrogen receptors and aromatase (CYP19), are associated with fat-free mass (Walsh et al. 2005) and BMD (Shearman et al. 2004), prostate and breast cancer (Gallicchio et al. 2006), and cardiovascular disease risk (Shearman et al. 2003)." + } + ], + "271236e4-60b1-4fe9-a3cc-11748e3cc718": [ + { + "document_id": "271236e4-60b1-4fe9-a3cc-11748e3cc718", + "text": "\n\nIn-depth analysis of the age-regulated genes revealed that multiple genes in the DNA damage response pathway were upregulated with age including those that function in non-homologous end-joining repair (mre11, rad50, Ku80 and mus308) and in translesion DNA synthesis (mus205 and DNApol-eta) [44][45][46].Genes that encoded enzymes with antioxidant properties, such as the thioredoxin reductase Trxr-1, and antioxidant genes involved in glutamate metabolism, such as GlnRS, isoQC and QC, were also upregulated with age [47][48][49][50].We also observed increased age-associated expression of chaperone genes (Cct1, Cct4, Cct5, Cct6, Hsc70-4) and the unfolded protein response transcription factor Xbp1, consistent with an induction of the unfolded protein response [51][52][53].Under stress conditions, there is a translational switch that favors production of stressrelated proteins while decreasing translation of other proteins [54].Paralogs of canonical translation factors such as NAT1 and Rack1, which were both upregulated, promote this switch to cap-independent translation [55,56].Notably, Rheb, which is downregulated with age, positively regulates ribosome production and capdependent translation by activating the mechanistic target of rapamycin (mTOR) kinase pathway [57].Thus, decreased Rheb levels during aging could decrease mTOR pathway activity, which extends lifespan and is protective against age-related pathology [58].Together, these data suggest that multiple genes are induced in aging photoreceptors to mitigate the effects of oxidative stress, protein misfolding and DNA damage." + } + ], + "3a9e80fc-b20d-4828-aaed-1a6ad490020a": [ + { + "document_id": "3a9e80fc-b20d-4828-aaed-1a6ad490020a", + "text": "CellAge vs human orthologues of longevity-associated model organism genes\n\nTo understand how senescence is linked to the genetics of aging processes, we looked at the intersection of CellAge genes and the 869 genes in the human orthologues of model organisms' longevity-associated genes (LAGs) dataset, collected based on quantitative changes in lifespan [34].Like CellAge, where genes are classified based on whether their upregulation induces, inhibits, or has an unknown impact on CS, the longevity orthologues dataset also provides information on the effect of upregulation of its genes, namely whether it promotes (pro, 421) or inhibits (anti, 448) longevity (Additional file 1: Table S7; Additional file 2: Fig. S2)." + }, + { + "document_id": "3a9e80fc-b20d-4828-aaed-1a6ad490020a", + "text": "\n\nUsing network biology, we implicated the CellAge genes in various processes, particularly cell division and immune system processes.We used network topology to identify potential regulators of CS and bottlenecks that could impact various downstream processes if deregulated.Indeed, we identified 11 genes that have already been shown to contribute towards CS, which will be added to future versions of CellAge.Finally, we experimentally verified 26 genes that induce CS morphology or biomarkers when knocked down in human mammary fibroblasts.Of these, 13 genes (C9orf40, CDC25A, CDCA4, CKAP2, GTF3C4, HAUS4, IMMT, MCM7, MTHFD2, MYBL2, NEK2, NIPA2, and TCEB3) were strong hits in inducing a senescent phenotype." + }, + { + "document_id": "3a9e80fc-b20d-4828-aaed-1a6ad490020a", + "text": "\n\nResults: We develop CellAge (http://genomics.senescence.info/cells),a manually curated database of 279 human genes driving cellular senescence, and perform various integrative analyses.Genes inducing cellular senescence tend to be overexpressed with age in human tissues and are significantly overrepresented in anti-longevity and tumor-suppressor genes, while genes inhibiting cellular senescence overlap with pro-longevity and oncogenes.Furthermore, cellular senescence genes are strongly conserved in mammals but not in invertebrates.We also build cellular senescence protein-protein interaction and co-expression networks.Clusters in the networks are enriched for cell cycle and immunological processes.Network topological parameters also reveal novel potential cellular senescence regulators.Using siRNAs, we observe that all 26 candidates tested induce at least one marker of senescence with 13 genes (C9orf40, CDC25A, CDCA4, CKAP2, GTF3C4, HAUS4, IMMT, MCM7, MTHFD2, MYBL2, NEK2, NIPA2, and TCEB3) decreasing cell number, activating p16/p21, and undergoing morphological changes that resemble cellular senescence.Conclusions: Overall, our work provides a benchmark resource for researchers to study cellular senescence, and our systems biology analyses reveal new insights and gene regulators of cellular senescence." + } + ], + "42cbc297-d57c-4c1f-8d3f-f9e52748b823": [ + { + "document_id": "42cbc297-d57c-4c1f-8d3f-f9e52748b823", + "text": "Genomics-a fundamental basis for understanding skin aging\n\nIn the last decade, genomic tools such as gene chips have been widely developed.This accomplishment has provided us with deeper insights into the molecular events underlying skin aging. 137Gene expression profiling has led to identification of pathways affected by aging, and this information has led to the development of new strategies to enable better skin repair and antiaging benefits. 138ene expression patterns were examined in sun-protected (buttocks) and sun-exposed skin (extensor forearm) from 10 young (age 19 to 20 years) and 10 older women (age 63 to 67 years) to examine gene expression profiles associated with chronologic skin aging and photoaging.Chronologic and photoaging were both associated with downregulation of the biologic process of lipid synthesis.In particular, genes involved in cholesterol and fatty acid synthesis were downregulated, as were genes associated with epidermal differentiation, including keratin filaments and cornified envelope components.An upregulation of the biologic processes of inflammatory response and wound healing, the molecular functions of cytokine activity and protease activity and the cellular component theme of extracellular matrix was also observed in both skin aging types.Elastin gene expression was upregulated with aging only in the photodamaged arm and remained unchanged in the sunprotected buttock.This finding corresponds to the histopathologic findings that show typical elastotic changes, the \"solar elastosis,\" in photoaged skin. 139urther studies conducted to investigate changes in gene expression during skin aging have been performed on naturally aged human foreskin obtained from children and elderly men.Some of the mechanisms proposed to be involved in the induction of aging comprise disturbed lipid metabolism, altered insulin and STAT3 signalling, upregulation of apoptotic genes partly due to the deregulation of FOXO1, downregulation of members of the jun and fos family, differential expression of cytoskeletal proteins (eg, keratin 2A, 6A, and 16A), extracellular matrix components (eg, PI3, S100A2, A7, A9, SPRR2B), and proteins involved in cell-cycle control (eg, CDKs, GOS2). 140Similar results have been presented by a study related to aging of skeletal muscle. 141n a previous study, we proposed that one of the factors significantly involved in the initiation of aging might be the physiologic decline of hormones occurring with age.Human SZ95 sebocytes in vitro treated with hormone levels that can be found in 60 year-old women produce less lipids than sebocytes treated with a hormone mixture representing that found in the serum of 20 year-old women. 6A differential gene expression between SZ95 sebocytes under the 20 and 60 year-old hormone mixture detected differentially expressed genes that are involved in biologic processes such as DNA repair and stability, mitochondrial function, oxidative stress, cell cycle and apoptosis, ubiquitin-induced proteolysis, and transcriptional regulation. 139,140A comparison of these results with data obtained from the aged kidney 142 identified key genes that may be of great importance for global aging.The most significantly altered signalling pathway was that of TGF-β.A disturbed function of this cascade has been also c-Fos, which heterodimerize to form the activator protein 1 (AP-1) complex.AP-1 is a key regulator of skin aging, because it induces the expression of the MMP family and inhibits type I procollagen gene expression through interference with TGF-β signalling pathway.It has been postulated that MAP kinases may be activated by excess production of reactive oxygen species (ROS) that occurs with advanced age and may be superimposed by extrinsic factors such as ultraviolet irradiation.Excess ROS production also leads to accumulation of cellular damage, which includes oxidation of DNA resulting in mutations, oxidation of proteins leading to reduced function, and oxidation of membrane lipids resulting in reduced transport efficiency and altered transmembrane signalling.IL, interleukin; NF-κB, nuclear factor-κB; TGF-β, transforming growth factor-β; TSP-1, thrombospondin-1; TSP-2, thrombospondin-2; VEGF, vascular endothelial growth factor.associated with tumorigenesis, such as in pancreatic, prostate, intestine, breast, and uterine cancer." + } + ], + "555a1533-2905-4d91-a3b6-2fca3679ab02": [ + { + "document_id": "555a1533-2905-4d91-a3b6-2fca3679ab02", + "text": "\n\nAnalysis of prior research (Online Resource 5) shows that the revealed genes can be explicitly involved in other key biological processes in an organism whose role is known to be changing with aging.Specifically, ten genes (BAZ2B, HMGB4, NOC2L, RAI1, SIK1, SMARCA2, SPZ1, TBP, TRIP13, and ZKSCAN1) regulate transcription which is believed to be disrupted when an organism is getting older (Roy et al. 2002).The DBH, TPO, and LSS genes are involved in synthesis of catecholamine, thyroid, and vitamin D hormones, respectively.The GPER binds estrogen and HCRTR2 binds orexin-A and orexin-B neuropeptid hormones.Hormonal deregulation with aging is considered to be one of the major components of senescent processes in an organism (Barzilai and Gabriely 2010).Five genes (ATG2A, NEDD4L, PSMB1, UBXN4, and USP6) are involved in degradation of proteins through ubiquitin-proteasome and the lysosomal/autophagic system.Dysfunction of this system leads to accumulation of damaged proteins in an organism that is associated with aging (Koga et al. 2011).Protein degradation through ubiquitin-mediated proteolysis plays an important role in cell-cycle regulation (Reed 2003).The PSMB1, SIK1, TRIP13, and TTN genes in the revealed set coordinate cell cycle.Cell cycle is linked with the aging-related processes in humans through a gradual increase in cell division errors in all tissues in an organism (Ly et al. 2000).Five genes (EEF1A2, DBH, ITGB2, TUBB2C, and WRN) take part in regulation of apoptosis which plays an important role in the aging process and tumorigenesis (Salvioli et al. 2008).Seven genes (ABCA7, AZGP1, CD36, DEGS2, LSS, PI4KA, and SOAT2) are involved in lipid metabolism which plays one of the key roles in human longevity and healthy aging (Barzilai et al. 2003)." + } + ], + "5e6ad994-9cad-4b8b-903d-2d5c350e25dc": [ + { + "document_id": "5e6ad994-9cad-4b8b-903d-2d5c350e25dc", + "text": "\n\nGenes that are age-regulated in all tissues would reveal genes involved in core mechanisms that underlie cellular ageing.Zahn et al. [63] discovered genetic pathways that show common age regulation in human kidney, brain and muscle.They used microarrays to analyse expression in 81 skeletal muscle samples from patients aged 16 -86 years and found 250 age-regulated muscle genes [63].Similar to the ageing expression profile for the kidney, the overall expression behaviour of this set of age-regulated muscle genes correlated with the physiological as well as chronological age of the muscle sample.Next, they compared their muscle-ageing results to previously published data on kidney and brain ageing of similarly large sample size [56,60].Although most of the age-related changes were tissue specific, they found evidence for common age regulation of six genetic pathways in all three tissues.Specifically, there is an overall increase in expression of the extracellular matrix genes, the ribosomal genes, the cell growth genes and the complement activation genes in all three tissues.Increased overall expression of the extracellular matrix and complement activation gene sets with advancing age may contribute to widespread fibrosis and inflammation in the elderly.There is an overall decrease in expression of the chloride transport genes and the electron transport genes in all three tissues.Decreased overall expression of electron transport chain genes with age might support the mitochondrial free-radical theory of ageing [67], as free-radical generation by mitochondria would preferentially damage the electron transport chain protein complexes.Decreased expression of the electron transport genes (encoded in the nucleus) might be caused by feedback regulation from damage to the electron transport chain protein complexes [63].However, it is also possible that increased oxidative damage occurs as a consequence of the decreased expression of the electron transport chain genes.In addition, an increasing number of studies in model organisms have critically challenged the mitochondrial free-radical theory of ageing [68]." + } + ], + "6ac32a33-e2af-40bb-aad6-9971c46023d4": [ + { + "document_id": "6ac32a33-e2af-40bb-aad6-9971c46023d4", + "text": "Discussion\n\nAging studies from model organisms such as yeast, worms, and flies have repeatedly shown that changes in the expression of certain genes have an effect upon longevity.Although similar aging processes are likely to operate across multiple species [30], it has been much more difficult to identify longevity candidate genes in human studies [30].A key question in human aging is to what extent a signature of aging may be detectable across tissues.Until now there has been a lack of large transcriptional profiles from the same human individuals in multiple tissues.The MuTHER study provides insight into the human aging process by interrogating the largest multiple human tissue gene expression resource to identify genes in which expression was affected by chronological age.The analysis of the skin and adipose tissues samples identified several hundred genes responsive to changes in chronological age.However, the 43 shared genes in skin and adipose tissue showed a single common identifiable pathway related to the stress response.From over 1,800 transcripts that have altered expression with age in skin and adipose tissues, 14 also had age-related differential expression in brain.The limited overlap in these two experiments may partly reflect the smaller sample size of the brain expression dataset, the differences in age range between the studies (16 to 83 years for brain samples; 39 to 85 years for MUTHER samples), or the inclusion of males in the brain samples.But it may also imply, as other studies have suggested, that the effects of age on gene transcription are tissue specific [6,31,32].This hypothesis was supported by the comparison with known related aging genes from the GenAge database, which identified an overlap for a small number of aging-related genes with our data.The GenAge database was the result of a meta-analysis using age-related expression profiles from human brain, kidney, and skeletal muscle, and several expression profiles from mouse and rat; no adipose tissue or skin samples were included (Additional file, Table 1 in [7]).The limited overlap between these datasets supports the idea that molecular signatures of aging reflect predominantly a tissue-specific transcriptional response.The lack of age-related genes in transformed LCLs, suggest that the transformation to immortalize a cell line may mask or even remove the age-related signatures in gene expression.The transformation of primary B lymphocytes into LCLs requires infection by the Epstein-Barr virus which has the effect of disrupting the p53 signaling pathway in order to induce growth and survival [33].Joehanes et al. [15] identified only five genes with age-associated expression in LCLs, including p53 itself (TP53).Although the authors attribute the lack of age-affected genes to their small sample size (n=50) and narrow age range, our analysis with a much larger sample size found even fewer age-related changes, suggesting a lack of detectable aging signature in LCLs.The analysis in the subset of fresh lymphocytes suggested an age influence in fresh lymphocytes may potentially be detectable with a larger sample size." + } + ], + "71cc1ce5-d23c-42cf-97b8-bb6110ed8d72": [ + { + "document_id": "71cc1ce5-d23c-42cf-97b8-bb6110ed8d72", + "text": "\n\nGenes Whose Expression Decreased with Age.Of the 26 genes that decreased expression with age in control mice, 23% are involved in DNA replication and the cell cycle (Table 2).Most of these have a negative effect on cell growth and division.Among these, the product of phosphatase and tensin homolog (Pten) gene is a tumor suppressor that induces cell-cycle arrest through inhibition of the phosphoinositide 3-kinase pathway (28).B cell translocation gene 2 (Btg2) is a tumor suppressor that increases expression in response to DNA damage (29).The murine gene product of the amino-terminal enhancer of split (Aes) is a potent corepressor of gene expression and cellular proliferation (30).Calcium-binding protein A11 (S100a10) binds to and regulates the activity of annexin II, which is involved in the transduction of calcium-related mitogenic signals (31).Insulin-like growth factor (IGF) binding protein 1 (Igfbp1) plays an important role in the negative regulation of the IGF-1 system, a stimulator of mitogenesis (32)." + } + ], + "8a8bea99-d3b9-4109-88e4-ad459dcd7173": [ + { + "document_id": "8a8bea99-d3b9-4109-88e4-ad459dcd7173", + "text": "daf-16 dependent genes\n\nAmong the 52 genes that we have tested, 29 genes act almost completely in a daf-16 dependent manner, to regulate lifespan (Table 2).One of the genes identified was daf-2 (Y55D5A_391.b).This serves as a proof of principle that our screen is effective in identification of aging genes." + } + ], + "9fed8fd1-fce5-4fc1-9911-05d312f88521": [ + { + "document_id": "9fed8fd1-fce5-4fc1-9911-05d312f88521", + "text": "\n\nSeveral of the genes we identify have previously been shown to influence lifespan in experiments on model organisms.For example, knockouts of the orthologs of APOE, LDLR, CDKN2B, and RBM38 in mice shortens their lifespan [24][25][26][27] , while knockout of IGF1R has the opposite effect 28 .Similarly, overexpression of the FOXO3 orthologue in Drosophila melanogaster 29 and the SNCA orthologue in Caenorhabditis elegans 30 have shown to extend their respective lifespans.Many of our genes are also enriched for pathways previously related to ageing in eukaryotic model organisms, including genomic stability, cellular senescence, and nutrient sensing 31 .For example, FOXO3 and IGF1R are well-known players modulating survival in response to dietary restriction 32 , but we also highlight genes involved in the response to DNA damage and apoptosis, such as CDKN2B, USP28, E2F2, and BCL3.In addition to hallmarks discovered in model organisms, our results suggest that haem metabolism may play a role in human ageing.This pathway includes genes involved in processing haem and differentiation of erythroblasts 33 .Although the enrichment is largely driven by genes linked to the LDLR locus, genes linked to other loci of interest (such as FOXO3, CDKN2B, LINC02513) are involved in similar biological pathways: myeloid differentiation, erythrocyte homeostasis, and chemical homeostasis." + } + ], + "adf2d31e-e83d-47df-97af-3764e42aa80e": [ + { + "document_id": "adf2d31e-e83d-47df-97af-3764e42aa80e", + "text": "\n\nHundreds of genes in several pathways act as regulators of ageing (1,32).However, analysis of DrugAge and other HAGR databases has revealed that the overlap between the targets of lifespan-extending drugs and known ageing related genes is modest (31).This indicates that most ageing-related pathways have yet to be targeted pharmacologically; DrugAge may aid in guiding further assays.This was recently demonstrated in one study where machine learning was used to predict whether a compound would increase lifespan in worms using data from Dru-gAge.The best model had 80% prediction accuracy and the top hit compounds could broadly be divided into compounds affecting mitochondria, inflammation, cancer, and gonadotropin-releasing hormone (33)." + } + ], + "b1ffece8-f805-4d99-8e3b-402df309f1ed": [ + { + "document_id": "b1ffece8-f805-4d99-8e3b-402df309f1ed", + "text": "\n\nTop 25genes co-expressed with aging related genes" + }, + { + "document_id": "b1ffece8-f805-4d99-8e3b-402df309f1ed", + "text": "Aging-related gene prediction and putative transcriptional mechanisms\n\nGeneFriends was used to identify genes related to aging.A seed list of genes known to be consistently overexpressed with age in mammals was used [18].In total, 1119 genes were co-expressed with the aging seed list at p <10 -6 ; Table 1 shows the top 25 genes.Many of these genes have been associated with age-related diseases.Several other genes that have been shown to play a role in aging such as lysosomal-associated membrane protein-2 Lamp2 [19] (p = 5.68 -30 ), Fas [20] (p = 2.70 -31 ) and growth hormone receptor Ghr [21] (p = 1.34 -19 ) also showed a significant co-expression.Anxa2, Anxa3 and Anxa4 also show a low p-value (p < 10 -25 ) as well as several S100 calcium binding proteins which have been shown to interact with annexins [22]." + } + ], + "dc322053-2672-4c26-b739-5b58c50476ed": [ + { + "document_id": "dc322053-2672-4c26-b739-5b58c50476ed", + "text": "\n\nGenetic studies have shown that aging can be slowed in mutants that are defective in a wide range of cellular processes (such as mitochondrial function, chromatin regulation, insulin signaling, transcriptional regulation, and genome stability).This indicates that aging is a complex process driven by diverse molecular pathways and biochemical events.As such, a powerful approach to study aging is to use systems biology, which allows a multitude of factors affecting aging to be analyzed in parallel.For example, DNA microarrays and gene expression chips have been used to perform a genome-wide analysis of changes in gene expres-sion in old age.Extensive studies in Caenorhabditis elegans and Drosophila melanogaster have identified hundreds of ageregulated genes (Hill et al. 2000;Zou et al. 2000;Lund et al. 2002;Pletcher et al. 2002;Murphy et al. 2003).Several studies have described age-regulated genes in the muscle and brain of mice (Lee et al. 1999(Lee et al. , 2000) ) and the retina and muscle of humans (Yoshida et al. 2002;Welle et al. 2003Welle et al. , 2004).These age-regulated genes may serve as markers of aging, enabling one to assess physiological age independently of chronological age.Analysis of the functions of these age-regulated genes has identified specific biochemical mechanisms that change toward the end of life." + } + ], + "e562a7f1-f43a-4ca4-bf18-4196276b6170": [ + { + "document_id": "e562a7f1-f43a-4ca4-bf18-4196276b6170", + "text": "\n\nAge-Regulated Genes Involved in Reproductive Capacity.Decline in reproductive capacity is an age-related phenotype, and the reproductive system seems to play an important role in longevity (22).For example, signals from germ cells can affect lifespan in C. elegans (23).In our study, we observed decreased RNA levels for several genes involved in reproduction (Fig. 3).These include two genes that encode members of the Acp family.The Acp from male flies stimulates female egg-laying and facilitates storage of sperm in the female genital tract (24).In addition, two ESTs showing age-regulated decrease of transcript levels represent different genes with homology to Arabidopsis MALE STERIL- In Northern analysis, the ratios were calculated by dividing mRNA levels at 25-, 40-, and 50-day time points by those at 3-day time points after normalization with mRNA levels of the control gene rp49.Ratios in microarray analysis are provided from each of the duplicate experiments for comparison.ITY 2 (MS2; ref. 25), a gene involved in gametogenesis.Furthermore, an EST with homology to peanut, a member of the septin family (26), is down-regulated in older flies.This downregulation may reflect a decrease in spermatogenesis." + } + ] + }, + "data_source": [], + "document_id": "A1B97AFC3BB6C31EBB65B7E046A0A55E", + "engine": "gpt-4", + "first_load": false, + "focus": "api", + "keywords": [ + "daf-16", + "aging", + "genes", + "lifespan", + "daf-2", + "transcription", + "protein°radation", + "apoptosis", + "lipid&metabolism", + "cell&cycle" + ], + "metadata": [], + "question": "which genes are involved in the aging process", + "subquestions": null, + "task_id": "A1B97AFC3BB6C31EBB65B7E046A0A55E", + "usage": { + "chatgpt": 10445, + "gpt-4": 6328, + "gpt-4-turbo-preview": 5402 + }, + "user_id": 2 + }, + "document_id": "A1B97AFC3BB6C31EBB65B7E046A0A55E", + "task_id": "A1B97AFC3BB6C31EBB65B7E046A0A55E" +} |