{ "bcoid": "GLY_000133", "title": "Human Refseq Protein Function", "description": "The Human RefSeq Protein Function dataset contains biological function annotaion of human [taxid:9606] ...", "filename": "human_protein_function_refseq.csv", "filetype": "csv", "categories": { "status": "Reviewed" }, "minitable": { "content": [ [ "Q13618-1...", "RefSeq..." ], [ "Q13618-1...", "RefSeq..." ] ], "headers": [ "uniprotkb_ca...", "database_nam..." ], "colwidth": [ "40%", "20%" ] }, "sampledata": { "type": "table", "data": [ [ { "type": "string", "label": "uniprotkb_canonical_ac" }, { "type": "string", "label": "database_name" }, { "type": "string", "label": "database_id" }, { "type": "string", "label": "evidence" }, { "type": "string", "label": "annotation" } ], [ "Q13618-1", "RefSeq", "NP_003581.1", "29550478", "Cullin 3 regulates ADAM17-mediated ectodomain shedding of AREG." ], [ "Q13618-1", "RefSeq", "NP_003581.1", "29249570", "The CRL3 complexes evolved to fulfill a pivotal role in mammalian cell differentiation. Review article" ], [ "Q13618-1", "RefSeq", "NP_003581.1", "29306329", "Our study emphasizes the discovery of a gene signature regulated by the KEAP1-NRF2-CUL3 axis which is strongly associated with tumorigenesis and drug resistance in head and neck squamous cell cancer . Publication Status: Online-Only" ], [ "Q13618-1", "RefSeq", "NP_003581.1", "22266938", "Fundamental role for KLHL3 and CUL3 in blood pressure, K(+) and pH homeostasis Publication Status: Online-Only" ], [ "Q96LR9-1", "RefSeq", "NP_001123887.1", "20628086", "Observational study of gene-disease association, gene-environment interaction, and pharmacogenomic / toxicogenomic. (HuGE Navigator)" ], [ "Q96LR9-1", "RefSeq", "NP_001123887.1", "19913121", "Observational study of gene-disease association. (HuGE Navigator)" ], [ "P07900-1", "RefSeq", "NP_005339.3", "30153855", "Chemotherapy agents can induce HSP90AA1 expression in osteosarcoma cells. And HSP90AA1, acting as an important regulator of autophagy, is a critical factor in the development of osteosarcoma chemoresistance both in vitro and in vivo. HSP90AA1 provides a novel therapeutic target for improving osteosarcoma treatment. Publication Status: Online-Only" ], [ "P07900-1", "RefSeq", "NP_005339.3", "29888262", "We confirm that miR-628-3p promotes apoptosis and inhibits migration in A549 cells by negatively regulating HSP90. Our results may reveal a novel strategy for lung cancer treatment Publication Status: Online-Only" ], [ "P07900-1", "RefSeq", "NP_005339.3", "29662162", "The study shows that a conserved tryptophan in the middle domain senses the interaction of Hsp90 with a stringent client protein and transfers this information via a cation-pi interaction with a neighboring lysine. Publication Status: Online-Only" ], [ "P07900-1", "RefSeq", "NP_005339.3", "29662061", "RPAP3 provides a flexible scaffold for coupling HSP90 to the human R2TP co-chaperone complex. Erratum:[Nat Commun. 2018 Jul 31;9(1):3063. PMID: 30065299] Publication Status: Online-Only" ], [ "P07900-1", "RefSeq", "NP_005339.3", "29491085", "High Hsp70 and Hsp90 expression was associated with worse overall survival and disease-free survival [review and meta-analysis] Review article" ], [ "Q8NBS9-1", "RefSeq", "NP_110437.2", "29749460", "Hypoxia induces the expression of TXNDC5 via upregulating HIF-1alpha in colorectal cancer cells." ], [ "Q8NBS9-1", "RefSeq", "NP_110437.2", "28604976", "TXNDC5 is also closely associated with rheumatoid arthritis, diabetes, hepatic steatosis and vitiligo. [review] Review article" ], [ "Q8NBS9-1", "RefSeq", "NP_110437.2", "26810069", "High TXNDC5 expression is associated with renal cell carcinoma." ], [ "Q8NBS9-1", "RefSeq", "NP_110437.2", "25500540", "We defined an important role of TXNDC5 in CRPC and further investigations are needed to screen TXNDC5 antagonists as a novel therapeutic approaches to treat PCa patients with Castration-resistant prostate cancer." ], [ "Q8NBS9-1", "RefSeq", "NP_110437.2", "24594673", "Suggest that the tumorigenic properties of ERp46 in RCC cells are not related to an inhibitory modulation of AdipoR1 Publication Status: Online-Only" ], [ "Q8NBS9-1", "RefSeq", "NP_110437.2", "17895523", "Upregulation of TXNDC5 are involved in the early development of colorectal cancer" ], [ "Q8NBS9-1", "RefSeq", "NP_110437.2", "12963716", "Member of the protein disulphide isomerase family and highly expressed in endothelial cells. Protects endothelial cells from apoptosis under hypoxia." ], [ "Q9C0K0-1", "RefSeq", "NP_612808.1", "29039465", "These results suggest that the upregulation of miR-650 contributes to the development of acute renal allograft rejection by suppression of BCL11B, which leads to apoptosis and inflammatory responses. Thus, miR-650 and BCL11B may represent potential therapeutic targets for the prevention of acute renal allograft rejection." ], [ "Q9C0K0-1", "RefSeq", "NP_612808.1", "28232744", "Studies show BCL11B is a key regulator of the initial stages of human T-cell differentiation and delineate the BCL11B transcriptional program, enabling the dissection of the underpinnings of normal T-cell differentiation and providing a resource for understanding dysregulations in T-ALL" ], [ "Q9C0K0-1", "RefSeq", "NP_612808.1", "28794504", "Decreased transcript and increased promoter methylation levels of BCL11B gene were identified in ankylosing spondylitis patients." ], [ "Q9C0K0-1", "RefSeq", "NP_612808.1", "28669733", "Human T-cell leukemia virus type 1 (HTLV-1) Tax directly binds to BCL11B. Tax enhances BCL11B degradation through proteasome pathway. Loss of BCL11B enhances cell growth in HTLV-1-infected cells." ], [ "Q9C0K0-1", "RefSeq", "NP_612808.1", "28288848", "BCL11B showed increased but varied expression in advanced tumor stage. Analysis of four patients receiving SAHA treatment suggested a positive correlation between BCL11B expression and favorable response to SAHA treatment. In conclusion, BCL11B may serve as a therapeutic target and a useful marker for improving HDACi efficacy in advanced CTCL." ], [ "P17858-1", "RefSeq", "NP_002617.3", "28646105", "Liver PFK1 isoform assembles into filaments in a tetramer- and substrate-dependent manner,organizing isoform specific glucose metabolism in cells." ], [ "P17858-1", "RefSeq", "NP_002617.3", "22923583", "Findings showed glycosylation inhibited PFK1 activity and redirected glucose flux through the pentose phosphate pathway, thereby conferring a selective growth advantage on cancer cells" ], [ "Q8N1L9-1", "RefSeq", "NP_612465.3", "28739720", "Our findings expanded the understanding of the role of BATF2 in tumors, and also suggested a potential of using BATF2 as a therapeutic target to hinder bevacizumab induced epithelial-mesenchymal transition in glioblastoma." ], [ "Q8N1L9-1", "RefSeq", "NP_612465.3", "27785591", "BATF2 gene was modulated after treatment with zebularine and was a poor prognostic marker, since its low levels were correlated with relapse and a poor prognosis for medulloblastoma patients. Erratum:[Invest New Drugs. 2017 Feb;35(1):124. PMID: 27900530]" ], [ "Q8N1L9-1", "RefSeq", "NP_612465.3", "27926863", "Gain- and loss-of-function studies uncovered a role for Batf2 in myeloid differentiation in both murine and human systems. We thus demonstrate that chronic infection can deplete HSPCs and identify BATF2 as a mediator of infection-induced HSPC terminal differentiation" ], [ "Q8N1L9-1", "RefSeq", "NP_612465.3", "26808579", "Results demonstrate that SARI is a novel target gene of glucocorticoid receptor, and the upregulation of SARI plays an important role in dexamethasone's killing effect on B lymphoma cells." ], [ "Q8N1L9-1", "RefSeq", "NP_612465.3", "26977016", "BATF2 may exert selective pressure on the recombination machinery via a repetitive motif-based mechanism for the maintenance of heterochromatin stability." ], [ "Q8N1L9-1", "RefSeq", "NP_612465.3", "20473897", "Decreased expression of BATF2 is associated with hepatocellular carcinoma." ], [ "Q15758-1", "RefSeq", "NP_005619.1", "30272366", "Results demonstrated that ASCT2 and pmTOR protein levels were significantly higher in epithelial ovarian cancer (EOC) tissues and predicting a poor prognosis. The expression levels of ASCT2 and pmTOR in EOC were positively correlated indicating a synergistic effect on the growth and development of early EOC." ], [ "Q15758-1", "RefSeq", "NP_005619.1", "30029480", "These data collectively establish that in an in vitro context, human epithelial and mesenchymal hepatocellular carcinoma cell lines adapt to ASCT2 or LAT1 knockout. Publication Status: Online-Only" ], [ "Q15758-1", "RefSeq", "NP_005619.1", "29495336", "The experimental data allowed identifying C467 residue as crucial for substrate binding and for transport activity modulation of hASCT2. Publication Status: Online-Only" ], [ "Q15758-1", "RefSeq", "NP_005619.1", "30071532", "SLC1A5 expression is increased in tumor samples from esophageal cancer patients, and downregulation of SLC1A5 inhibited cell cycle progression and esophageal cancer growth." ], [ "Q9UM22-1", "RefSeq", "NP_060019.2", "27805251", "EPDR1 exhibits a pattern of isoform abundance dependent on KRAS G13D and G12D mutations." ], [ "Q9UM22-1", "RefSeq", "NP_060019.2", "27245865", "Study results suggest functional involvement of EPDR1 in the etiology of Dupuytren's Disease." ], [ "Q9UM22-1", "RefSeq", "NP_060019.2", "24089297", "Results of this study suggest that EPDR1 gene can be added to a growing list of genes associated with Dupuytren's disease development." ], [ "Q9UM22-1", "RefSeq", "NP_060019.2", "16954209", "Shows that the mouse ortholog is a lysosomal protein." ], [ "Q63HQ0-1", "RefSeq", "NP_061039.3", "21525240", "Conclude that a specific fraction of the AP2-derived endocytic pathway is dedicated to secretory purposes under the control of AP1 and Gadkin" ], [ "Q63HQ0-1", "RefSeq", "NP_061039.3", "20332099", "Observational study of gene-disease association. (HuGE Navigator) Erratum:[Hum Mol Genet. 2010 Oct 15;19(20):4121. Hesselbrock, Victor [added]; Tischfield, Jay A [added]]" ], [ "Q63HQ0-1", "RefSeq", "NP_061039.3", "19965873", "Studies unravel the molecular basis for Gadkin-mediated AP-1 recruitment to TGN/endosomal membranes and identify a novel subtype of the AP-1-binding motif." ], [ "Q63HQ0-1", "RefSeq", "NP_061039.3", "19706427", "Gadkin (gamma-BAR), a peripheral membrane protein localized to the trans-Golgi network and to endosomal vesicles, directly associates with the clathrin adaptor AP-1 and the motor protein kinesin KIF5, potentially regulating endosomal vesicle dynamics." ], [ "Q6P4Q7-1", "RefSeq", "NP_064569.3", "29421602", "Here, we report the 2 first families with Jalili Syndrome in Brazil. Molecular analysis of the first family identified a previously described homozygous mutation (p.Leu324Pro) in exon 1 of CNNM4 gene. In the second family, affected patients demonstrated a compound heterozygous mutation in CNNM4, the p.Leu324Pro and the novel nonsense mutation p.Tyr581*." ], [ "Q6P4Q7-1", "RefSeq", "NP_064569.3", "29322253", "Results identified linkage at chromosome 2p14-2q14 and found a homozygous mutation in the CNNM4 gene (p.R605X) causing Jalili syndrome. The truncated CNNM4 protein starting at R605 significantly increased the rate of apoptosis, and significantly increased the interaction between CNNM4 and IQCB1. This mutation may cause Jalili syndrome by a nonsense-mediated decay mechanism, affecting the function of IQCB1 and apoptosis." ], [ "Q6P4Q7-1", "RefSeq", "NP_064569.3", "29421294", "Jalili Syndrome is a rare cone-rod dystrophy (CORD) and amelogenesis imperfecta (AI), We have further characterized its ocular phenotype, including describing SD-OCT, FAF, and electrophysiological features; and report several novel disease-causing sequence variants." ], [ "Q6P4Q7-1", "RefSeq", "NP_064569.3", "28586144", "Mutational analysis showed in all three brothers a novel likely pathogenic homozygous missense substitution in exon 1 (c.1076T>C, p.(Leu359Pro)) of CNNM4. Both parents were carriers for the variant." ], [ "Q6P4Q7-1", "RefSeq", "NP_064569.3", "28246031", "Used Sanger sequencing to analyze a large consanguineous family with three siblings affected with Jalili syndrome, suspected clinically after dental and ophthalmological examination. These patients are carrying a novel homozygous mutation in the splice site acceptor of intron 3 (c.1682-1G > C) in the CNNM4 gene" ], [ "Q02548-1", "RefSeq", "NP_057953.1", "30257940", "The functional role of PAX5-ELN as a potent oncoprotein in B-cell acute lymphoblastic leukemia development." ], [ "Q02548-1", "RefSeq", "NP_057953.1", "30194145", "Study demonstrated that Pax-5 regulates numerous miRNAs including miR-215 which is aberrantly under-expressed in breast cancer tumors. Pax-5 was found to inhibit aggressive features of breast cancer cells in a miR-215- dependent manner." ], [ "Q02548-1", "RefSeq", "NP_057953.1", "28978690", "This study demonstrates a role for the AHR in regulating human B cell development, and it suggests that transcriptional alterations of PAX5 by the AHR are involved in the underlying mechanism" ], [ "Q02548-1", "RefSeq", "NP_057953.1", "28886309", "The correlation between Pax5 deletion and patients survival in Iranian children with precursor B-cell acute lymphocytic leukemia hs been reported. Publication Status: Online-Only" ], [ "Q02548-1", "RefSeq", "NP_057953.1", "29099287", "PAX5 gene methylation can predict poor survival outcomes and cisplatin sensitivity in esophageal squamous cell carcinomaand could be a useful diagnostic tool for cancer therapy selection" ], [ "Q6UXS9-1", "RefSeq", "NP_001177945.2", "28731145", "Piezo1 plays an important role in the apoptosis of human osteoarthritis-derived chondrocytes through a caspase-12-dependent pathway." ], [ "Q6UXS9-1", "RefSeq", "NP_001177945.2", "28380444", "Study indicated the potential effect of Casp12 was on the activation of NF-kappaB by the degradation of IkappaBalpha in NPC cells." ], [ "Q6UXS9-1", "RefSeq", "NP_001177945.2", "27130368", "Endoplasmic reticulum stress may be associated with apoptosis of LECs, resulting in cataract formation in diabetic patients." ], [ "Q6UXS9-1", "RefSeq", "NP_001177945.2", "16917906", "Observational study of genotype prevalence. (HuGE Navigator)" ], [ "Q6UXS9-1", "RefSeq", "NP_001177945.2", "15129283", "Csp12-L attenuates the inflammatory and innate immune response to endotoxins and in doing so may constitute a risk factor for developing sepsis" ], [ "Q6UXS9-1", "RefSeq", "NP_001177945.2", "12054529", "Caspase 12 has acquired deleterious mutations" ], [ "P00167-1", "RefSeq", "NP_683725.1", "28684414", "Data suggest CYP17A1, with electron donor NADPH-P450 reductase, is inherently distributive enzyme but that some processivity is present; some 17alpha-hydroxy pregnenolone formed does not dissociate from CYP17A1 before conversion to dehydroepiandrosterone; CYB5A does not enhance reaction by decreasing k(off) of ligands of CYP17A1. (CYP17A1 = cytochrome P450, family 17, subfamily A, polypeptide 1; CYB5A = cytochrome b5)" ], [ "P00167-1", "RefSeq", "NP_683725.1", "28671819", "Data suggest that cytochrome b5 (CYB5) and cytochrome b5 reductase 3 (CYB5R3) can reduce human cytoglobin (CYGB) and zebrafish cytoglobins at rates up to 250-fold higher than those reported for the known physiological substrates, hemoglobin and myoglobin; the three proteins (CYB5+CYB5R3+CYGB) appear to constitute a metabolon involved in generation of nitric oxide." ], [ "P00167-1", "RefSeq", "NP_683725.1", "28000554", "A homodimer model can resolve the conundrum as to how cytochrome P450 oxidoreductase and cytochrome b5 compete for the same binding site on cytochrome P450c17. (Review) Review article" ], [ "P00167-1", "RefSeq", "NP_683725.1", "27297105", "Thus, although Mn-b5 binds to CYP17A1, it is unable to enhance the lyase reaction, strongly suggesting that cyt b5 has a redox effector role in enhancement of the CYP17A1 mediated lyase reaction necessary for androgen synthesis." ], [ "P00167-1", "RefSeq", "NP_683725.1", "26918755", "This study constructed a model of the membrane-bound full-length human P450 1A2-cyt b5 complex. The model was assembled from several parts using a multiscale modeling approach covering all-atom and coarse-grained molecular dynamics (MD)." ], [ "Q9NVM4-1", "RefSeq", "NP_001276947.1", "28874563", "These kinetic studies suggest a biochemical explanation for the interplay between PRMT5- and PRMT7-mediated methylation of the same substrate at different residues and also suggest a general model for regulation of PRMTs." ], [ "Q9NVM4-1", "RefSeq", "NP_001276947.1", "28587924", "The authors showed that ASS1 mutations linked to type I citrullinemia disrupt the ASS1-PRMT7 interaction, which might explain the molecular pathogenesis of the disease." ], [ "Q9NVM4-1", "RefSeq", "NP_001276947.1", "27718516", "Loss of PRMT7 causes decreases in arginine methylation throughout the proteome.Loss of the arginine methyltranserase PRMT7 causes syndromic intellectual disability with microcephaly and brachydactyly." ], [ "Q9NVM4-1", "RefSeq", "NP_001276947.1", "17709427", "That in human cells, PRMT5 and PRMT7 are required for Sm protein sDMA modification, and that Sm protein symmetric dimethylarginine modification is required for snRNP biogenesis in human cells." ], [ "Q9NVM4-1", "RefSeq", "NP_001276947.1", "15494416", "PRMT7 (like PRMT5) is a Type II methyltransferase capable of producing symmetric dimethylarginine modifications in proteins." ], [ "Q9NVM4-1", "RefSeq", "NP_001276947.1", "15044439", "Both domains are required for functionality" ], [ "P49238-1", "RefSeq", "NP_001164642.1", "30066854", "Study demonstrated that CX3CL1/CX3CR1 was overexpressed in prostate cancer tissues with spinal metastasis compared with primary tumors. Overexpression of CX3CR1 increased cell proliferation, migration and invasion. Also, study observed that EGFR/Src/FAK pathway was activated by CX3CL1/CX3CR1." ], [ "P49238-1", "RefSeq", "NP_001164642.1", "29485193", "CX3CR1 major allele carriers V249 and T280 are significantly associated with an increased total arterial blood volume of the whole brain, especially around the bilateral precuneus, left posterior cingulate cortex, and left posterior parietal cortex." ], [ "P49238-1", "RefSeq", "NP_001164642.1", "29565837", "Investigated the association of CX3CR1 839C/T, CX3CR1 745G/A, polymorphisms with Age-Related Macular Degeneration (AMD) risk. These associated with an increased AMD risk (CX3CR1 839C/T, additive model: aOR=2.682, 95% CI=1.119-5.709, P=0.022, recessive model: aOR=2.729, 95% CI=1.141-6.048, P=0.010; CX3CR1 745G/A, additive model: aOR=2.614, 95% CI=1.231-6.012, P=0.020, recessive model: aOR=2.340, 95% CI=1.227-5.993, P=0.011 Publication Status: Online-Only" ], [ "P49238-1", "RefSeq", "NP_001164642.1", "29274778", "Our findings demonstrate that motility, invasion, and contact-independent growth of PDAC cells all increase following CX3CL1 exposure, and that antagonism of CX3CR1 by the inhibitor JMS-17-2 reduces each of these phenotypes and correlates with a downregulation of AKT phosphorylation." ], [ "P49238-1", "RefSeq", "NP_001164642.1", "29326275", "In Crohn's disease patients, a missense mutation in the gene encoding CX3CR1 was identified and found to be associated with impaired antifungal responses" ], [ "Q8NER1-1", "RefSeq", "NP_061197.4", "29562624", "A strong capacity to positively regulate skin sensitization mechanisms related to the TRPV1 receptors. Publication Status: Online-Only" ], [ "Q8NER1-1", "RefSeq", "NP_061197.4", "29378958", "Disruption of the association of Sig-1R with TRPV1 by synthetic or natural antagonists leads to degradation of TRPV1 protein and to decreased levels of the ion channel protein as well as to a decrease in TRPV1-associated pain." ], [ "Q8NER1-1", "RefSeq", "NP_061197.4", "29578437", "Correlation between heat pain threshold and TRPV1 receptor protein level over various phases of the ovarian-menstrual cycle has been reported." ], [ "Q8NER1-1", "RefSeq", "NP_061197.4", "29203659", "TRPV1 interacts physically with MOR-1 and modulates MOR-1 activity in HEK293 cells." ], [ "Q9BT67-1", "RefSeq", "NP_085048.1", "29333944", "We identified Nedd4-family interacting protein 1 as a direct target of miR-155, and the expression of Nedd4-family interacting protein 1 was inhibited by miR-155. Furthermore, ectopic expression of Nedd4-family interacting protein 1 restored the effects of miR-155 on cell proliferation and invasion of uveal melanoma cells" ], [ "Q9BT67-1", "RefSeq", "NP_085048.1", "27173227", "The expression of Ndfipl reduced expression of a-synuclein. In conclusion, Ndfipl plays a significant role in protecting SH-SY5Y cells in in vitro Parkinson's disease models. Publication Status: Online-Only" ], [ "Q9BT67-1", "RefSeq", "NP_085048.1", "26363003", "Data show that membrane protein Ndfip1 recruits E3 ubiquitin (Ub) ligase Nedd4-2 to the Golgi to target ether-a-go-go-related gene (hERG) channel for degradation while membrane protein Ndfip2 also mediates Nedd4-2 interaction with hERG in the Golgi." ], [ "Q9BT67-1", "RefSeq", "NP_085048.1", "26319551", "Silencing of Ndfip1 inhibited cytokine-induced apoptosis of pancreatic islets and promoted glucose-stimulated insulin secretion. These effects were associated with an increase in the cellular content of JunB, a potent inhibitor of ER stress and apoptosis." ], [ "Q9BT67-1", "RefSeq", "NP_085048.1", "25631046", "Ndfip1 is required during stress for ubiquitinating and trafficking BRAT1 into the nucleus." ] ] }, "readme": "Name\n - Human Refseq Protein Function\n\nVersion\n - 1.0.13\n\nCreated on\n - 2019-03-16T15:35:15.248632\n\nModified on\n - 2019-04-24T10:47:03.644563\n\nCreated by\n - Jeet Vora [jeetvora@gwu.edu], Rahi Navelkar [rsn13@gwu.edu], Robel Kahsay [rykahsay@gwu.edu]\n\nAuthors\n - \n\nChecksum\n - \n\nUsability Domain\n - The Human RefSeq Protein Function dataset contains biological function annotaion of human [taxid:9606] genes from GeneRIF section in the NCBI RefSeq database\n - The data is downloaded from NCBI RefSeq and is processed into a dataset by GlyGen. If you use this dataset please provide proper attribution to NCBI RefSeq and GlyGen\n\nDescription Domain\n Keywords\n - protein function\n - NCBI RefSeq\n\n Pipeline Steps\n - Step-1: The script extract-from-gp.py extracts protein function information from NCBI RefSeq gpff format files and maps it to the UniProtKB canonical accessions for a final dataset output in a csv format\n\nExecution Domain\n Scripts - https://github.com/glygener/glygen-backend-integration/blob/master/pipeline/extractor/extract-from-gp.py\n\n\n Software Prerequisites\n Name: Python\n Version: 2.7.5\n URI: https://www.python.org/download/releases/2.7.5/\n\nI/O Domain\n Input Subdomain\n Name: refseq_protein_all_9606.gpff\n URI: https://data.glygen.org/ln2data/releases/data/v-1.0.13/source/refseq_protein_all_9606.gpff\n Name: human_protein_idmapping.csv\n URI: https://data.glygen.org/ln2data/releases/data/v-1.0.13/reviewed/human_protein_idmapping.csv\n Output Subdomain\n Name: human_protein_function_refseq.csv\n URI: https://data.glygen.org/ln2data/releases/data/v-1.0.13/reviewed/human_protein_function_refseq.csv\n Name: human_protein_function_refseq.stat.csv\n URI: https://data.glygen.org/ln2data/releases/data/v-1.0.13/reviewed/human_protein_function_refseq.stat.csv\n\nFields\n Name: \"database_id\"\n Description: \"Identifier in the database\"\n Unique Values: \"8331\"\n Name: \"uniprotkb_canonical_ac\"\n Description: \"Accession assigned to the protein isoform chosen to be the canonical sequence to which all positional annotation refers in UniProtKB database\"\n Unique Values: \"8331\"\n Name: \"database_name\"\n Description: \"The name of the source database\"\n Unique Values: \"1\"\n Name: \"annotation\"\n Description: \"Function annotation from UniProtKB|RefSeq database\"\n Unique Values: \"30552\"\n Name: \"evidence\"\n Description: \"NCBI PubMed Id (PMID) as evidence for the entry/annotation\"\n Unique Values: \"30413\"", "downloadurl": "/ln2data/releases/data/v-1.0.13/reviewed/human_protein_function_refseq.csv" }