Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Cloning and chromosomal mapping of a human immunodeficiency virus 1 "TATA" element modulatory factor.
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TMF was originally identified as a 123 kDa cellular protein that binds the HIV-1 LTR TATA element in gel-retardation assays and inhibits TBP-mediated transcriptional activation in vitro.
"TMF binds to the human immunodeficiency virus 1 TATA element in gel-retardation assays and inhibits activation of the viral long terminal repeat by the TATA-binding protein in in vitro transcription assays."
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The original characterisation was a viral-promoter / in vitro context; no endogenous cellular target genes were demonstrated.
"TMF is a transcription factor that likely regulates the expression of both viral and cellular genes."
Isolation and characterization of ARA160 as the first androgen receptor N-terminal-associated coactivator in human prostate cells.
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AR N-terminal peptide directly binds TMF1/ARA160 in far-Western and co-IP assays in vitro.
"The far-Western blotting and co-immunoprecipitation assays demonstrate that the AR can interact directly with ARA160/TMF."
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A transient transfection AR-reporter assay in PC-3 cells suggests TMF1/ARA160 enhances AR transactivation.
"Transient transfection assays demonstrated that ARA160 might function as a coactivator for AR-mediated transactivation in human prostate cancer PC-3 cells."
A putative nuclear receptor coactivator (TMF/ARA160) associates with hbrm/hSNF2 alpha and BRG-1/hSNF2 beta and localizes in the Golgi apparatus.
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TMF1 isoforms differentially localize between Golgi and nucleus; the Golgi pool is dominant.
"Immunofluorescence and Western blot studies revealed that the TMF isoforms differentially localize in the Golgi apparatus and the nucleus."
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The C-terminal region of TMF1 binds the conserved N-terminal regions of the SWI/SNF ATPases hbrm/hSNF2alpha and BRG-1/hSNF2beta in vitro and in vivo.
"hbrm/hSNF2 alpha and BRG-1/hSNF2 beta, the ATPase subunits of the human SNF/SWI complexes, specifically associate in vitro and in vivo with TATA element modulatory factor (TMF)/ARA160."
TMF/ARA160 is a BC-box-containing protein that mediates the degradation of Stat3.
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TMF/ARA160 is described as a Golgi-resident protein.
"TMF/ARA160 is a Golgi resident protein whose cellular functions have not been conclusively revealed."
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TMF/ARA160 contains a BC-box motif that binds Elongin C and directs Stat3 ubiquitination/proteasomal degradation in serum-starved C2C12 cells.
"Amino-acid sequence analysis identified a BC-box element in TMF/ARA160 that mediated the binding of this protein to elongin C. Ectopic expression of TMF/ARA160 in serum-starved C2C12 cells drove the ubiquitination and proteasomal degradation of Stat3."
Functional involvement of TMF/ARA160 in Rab6-dependent retrograde membrane traffic.
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TMF1 surrounds Rab6-positive Golgi structures and is concentrated at cisternal-tip budding structures.
"TMF signal surrounded Rab6-positive Golgi structures and immunoelectron microscopy revealed that TMF is concentrated at the budding structures localized at the tips of cisternae."
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TMF1 knockdown phenocopies Rab6 knockdown for retrograde transport of Shiga toxin from early/recycling endosomes to the trans-Golgi network.
"The knockdown of either TMF or Rab6 by RNA interference blocked retrograde transport of endocytosed Shiga toxin from early/recycling endosomes to the trans-Golgi network, causing missorting of the toxin to late endosomes/lysosomes."
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TMF1 is required for Golgi retention of GalNAc-T2 (but not GalT), and is implicated in Rab6-dependent retrograde transport from Golgi to ER.
"These observations suggest critical roles for TMF in two Rab6-dependent retrograde transport processes - one from endosomes to the Golgi and the other from the Golgi to the ER."
A comprehensive resource of interacting protein regions for refining human transcription factor networks.
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High-throughput mRNA-display screen reports a TMF1-NR3C1 (glucocorticoid receptor) interaction; no functional follow-up.
"present the first large-scale IR data set obtained using mRNA display for 50 human transcription factors (TFs)."
Testosterone deficiency accompanied by testicular and epididymal abnormalities in TMF(-/-) mice.
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TMF/ARA160 is a Golgi-associated protein essential for spermiogenesis; its loss in mouse causes Leydig-cell proliferation, testosterone deficiency and epididymal apoptosis - a phenotype consistent with disrupted Golgi-derived acrosome biogenesis and secretion rather than loss of an AR coregulator.
"TMF/ARA160 is a Golgi-associated protein, which is essential for spermiogenesis. In this study, we show that lack of TMF/ARA160 leads to defects in both the testis and the epididymis."
Molecular insights into vesicle tethering at the Golgi by the conserved oligomeric Golgi (COG) complex and the golgin TATA element modulatory factor (TMF).
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TMF1 is a Golgi-tethering coiled-coil ("golgin") that binds the COG complex at both ends and to Golgi membranes via its central coiled-coil after COPI uncoating.
"We find that the COG complex interacts with two different Rabs in addition to each end of the golgin "TATA element modulatory factor" (TMF). This allows COG to potentially bridge the distance between the distal end of the golgin and the target membrane thereby promoting tighter docking. Concurrently we show that the central portion of TMF can bind to Golgi membranes that are liberated of their COPI cover."
Reprogrammed and transmissible intestinal microbiota confer diminished susceptibility to induced colitis in TMF-/- mice.
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TMF/ARA160 is referred to as a multifunctional Golgi-associated protein; TMF-/- colon shows altered MUC2 mucin oligomerisation, consistent with disrupted Golgi-dependent glycosylation/secretion.
"Tata Element Modulatory Factor (TMF/ARA160) is a multifunctional Golgi-associated protein, which accumulates in colonic enterocytes and goblet cells."
The golgin coiled-coil proteins capture different types of transport carriers via distinct N-terminal motifs.
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TMF1, when relocated to mitochondria, captures intra-Golgi transport vesicles - direct demonstration of vesicle-tethering activity.
"When relocated to mitochondria, TMF captures intra-Golgi transport vesicles, but these contain some proteins from later in the stack than those captured by GMAP-210 and golgin-84."
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A short N-terminal motif (M-S-W-L/F, conserved across metazoa and shared with golgin-84 and GMAP-210) and a central/C-terminal coiled-coil region both contribute vesicle-capture activity.
"The first 36 residues of the protein are necessary for the capture activity of the N-terminal half, and sufficient to confer capture activity when attached to two different heterologous coiled-coil proteins."
A reference map of the human binary protein interactome.
In vivo characterization of Drosophila golgins reveals redundancy and plasticity of vesicle capture at the Golgi apparatus.
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In Drosophila, ectopic TMF captures intra-Golgi transport vesicles and the loss-of-function mutant recapitulates the male-fertility phenotype seen in mouse Tmf1 knockouts, supporting a conserved role in Golgi vesicle traffic.
"We show that ectopic forms can capture intra-Golgi transport vesicles, but strikingly, the cargo present in the vesicles captured by each golgin varies between tissues. Loss-of-function mutants show that the golgins are individually dispensable, although the loss of TMF recapitulates the male fertility defects observed in mice."
RAB6:GTP binds the GARP and COG complexes, t-SNAREs and endosome-derived vesicles
ARL1 recruits TGN Golgin homodimers
Fusion of early-endosome derived vesicles at the TGN
TMF1 research notes (this review)
Falcon deep research report for TMF1
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Falcon supports the Golgi-associated golgin/Rab6-effector role as the most reproducible TMF1 function, while treating transcriptional, proteostasis, and nuclear RTK roles as conditional or context-dependent.
"The Golgi/tethering axis is supported by multiple cell biological methods (Golgi localization, Rab6-binding, trafficking defects, Golgi morphology quantification)."