A proteome-scale map of the human interactome network.
A reference map of the human binary protein interactome.
Multimodal cell maps as a foundation for structural and functional genomics.
Dephosphorylation of the transcriptional cofactor NACA by the PP1A phosphatase enhances cJUN transcriptional activity and osteoblast differentiation.
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NACA affinity purification and mass spectrometry identified BTF3L4 as an interactor recruited to dephosphorylated NACA.
"NACA dephosphorylation was associated with specific recruitment of novel NACA interactants, such as basic transcription factor 3 (BTF3) and its homolog BTF3L4."
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
Panorama of ancient metazoan macromolecular complexes.
DSBSO-Based XL-MS Analysis of Breast Cancer PDX Tissues to Delineate Protein Interaction Network in Clinical Samples.
Quantitative proteomics analysis of chondrogenic differentiation of C3H10T1/2 mesenchymal stem cells by iTRAQ labeling coupled with on-line two-dimensional LC/MS/MS.
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Mouse Btf3l4 was experimentally implicated in BMP-2-induced chondrogenic differentiation of C3H10T1/2 mesenchymal stem cells.
"the biological roles of BTF3l4 and fibulin-5, two novel chondrogenesis-related proteins identified in the present study, were verified in the context of chondrogenic differentiation."
Basic Transcription Factor 3 Like 4 Enhances Malignant Phenotypes through Modulating Tumor Cell Function and Immune Microenvironment in Glioma.
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BTF3L4 down-regulation reduced proliferation, migration, and invasion in a human glioma cell line.
"the down-regulation of BTF3L4 protein in the glioma cell line had a detrimental effect on cell migration, invasion, and proliferation."
MIR194-2HG, a miRNA host gene activated by HNF4A, inhibits gastric cancer by regulating microRNA biogenesis.
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BTF3L4 is a miR-194 and miR-192 target whose knockdown counteracted the proliferation and invasion phenotype caused by MIR194-2HG depletion in gastric-cancer cells.
"knockdown of BTF3L4 significantly recovered the promotion effect of MIR194-2HG knockdown on GC cell proliferation and invasion"
BTF3L4 Overexpression Mediates APAP-induced Liver Injury in Mouse and Cellular Models.
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BTF3L4 perturbation altered apoptosis, inflammatory responses, oxidative stress, and mitochondrial morphology in mouse acetaminophen-injury models.
"Increased BTF3L4 expression increases the degree of apoptosis, reactive oxygen species generation, and oxidative stress, which induces cell death and liver injury."
UniProtKB record for human BTF3L4 (Q96K17)
Manual deep research synthesis for human BTF3L4
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The evidence supports BTF3L4 as an alternative NACA beta-chain partner while leaving direct ribosome-associated and cotranslational activities unresolved.
"BTF3L4 is an alternative beta-chain partner of NACA in a human nascent polypeptide-associated complex."
Manual BTF3L4 curation notes
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Records the evidence boundaries, annotation decisions, automated-research failures, and experimental priorities for this review.
"Core function: alternative NAC-beta partner of NACA in a nascent polypeptide-associated complex."