Affinage

ECSIT

Evolutionarily conserved signaling intermediate in Toll pathway, mitochondrial · UniProt Q9BQ95

Length
431 aa
Mass
49.1 kDa
Annotated
2026-06-09
38 papers in source corpus 21 papers cited in narrative 21 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ECSIT is a multifunctional adaptor protein that couples innate immune signaling to mitochondrial function, operating both as a scaffold in Toll/IL-1 receptor pathways and as an essential factor for respiratory complex I assembly (PMID:10465784, PMID:17344420). In TLR/IL-1 signaling it bridges TRAF6 to MEKK-1 to drive NF-κB activation (PMID:10465784), assembles a TAK1–ECSIT–TRAF6 trimeric complex through distinct interaction domains required for cytokine production (PMID:25371197), and scaffolds RIG-I and MDA5 onto MAVS to induce type I interferon during antiviral responses (PMID:25228397). ECSIT ubiquitination at lysine 372 is required for its interaction with NF-κB p65/p50 and their nuclear function following TLR4 stimulation (PMID:25355951), and the integrity of the TRAF6–ECSIT complex — controlled by competitive binders including Prdx6, CRBN, p62/SQSTM1, and the pathogen factors HBx and HBHA — governs ECSIT ubiquitination, mitochondrial ROS production, and bactericidal/autophagic activity (PMID:28393051, PMID:31620128, PMID:31281713, PMID:41209015). Independently, ECSIT localizes to mitochondria via an N-terminal targeting signal where it partners with the assembly chaperone NDUFAF1 and is indispensable for complex I assembly and oxidative phosphorylation (PMID:17344420, PMID:29514094); loss of ECSIT collapses complex I, shifts metabolism toward glycolysis, raises constitutive mitochondrial ROS, and impairs mitophagy, with ECSIT associating with PINK1 and undergoing Parkin-dependent ubiquitination (PMID:29514094). This mitochondrial role underlies tissue-specific physiology: human ECSIT lability or point mutations cause cardiac complex I deficiency and hypertrophy (PMID:34032637, PMID:37395010), a cardiomyocyte ECSIT-X4 isoform sustains bioenergetics through mitochondrial STAT3 (PMID:39746855), and ECSIT supports RANKL-driven osteoclast metabolism (PMID:37152948). ECSIT also acts at the chromatin/metabolite interface, cooperating with Smad1/Smad4 as a BMP co-factor essential for mesoderm formation (PMID:14633973) and, in CD8+ T cells, driving fumarate synthesis that suppresses KDM5-dependent demethylation of the TCF-1 promoter to support memory differentiation (PMID:38326554).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1999 High

    Established ECSIT's founding role as a signaling adaptor, answering how TRAF6 connects to downstream MAP3K activity in Toll/IL-1 signaling.

    Evidence Yeast two-hybrid, Co-IP, and dominant-negative NF-κB reporter assays identifying ECSIT as a TRAF6–MEKK-1 bridge

    PMID:10465784

    Open questions at the time
    • Did not resolve whether MEKK-1 processing is direct or requires additional factors
    • No structural basis for the bridging interaction
  2. 2003 High

    Revealed an unexpected developmental function, showing ECSIT acts as a BMP/Smad transcriptional co-factor required for embryonic mesoderm formation.

    Evidence Ecsit-null mice (embryonic lethal E7.5), Smad1/Smad4 Co-IP, ChIP at BMP target promoters, shRNA and reporter assays

    PMID:14633973

    Open questions at the time
    • Mechanistic link between ECSIT's TLR-adaptor and Smad co-factor roles unresolved
    • Direct DNA-binding vs. recruitment by Smads not distinguished
  3. 2007 High

    Identified a distinct mitochondrial function, answering where ECSIT localizes and revealing it is essential for respiratory complex I assembly.

    Evidence Affinity purification with NDUFAF1, subcellular fractionation, bidirectional RNAi, blue native PAGE

    PMID:17344420

    Open questions at the time
    • How a single protein partitions between signaling and mitochondrial pools not defined
    • Biochemical role within the assembly intermediate not specified
  4. 2014 High

    Dissected the architecture and ubiquitination requirements of ECSIT in TLR signaling, establishing the trimeric TAK1–ECSIT–TRAF6 complex and a K372 ubiquitination switch for NF-κB engagement.

    Evidence Endogenous Co-IP, domain-deletion and K372A mutant rescue in knockdown cells, EMSA, cytokine readouts

    PMID:25355951 PMID:25371197

    Open questions at the time
    • Identity of the K372 E3 ligase not established
    • Whether ubiquitination is mono- or poly- and its chain type undefined
  5. 2014 Medium

    Extended ECSIT's immune scaffolding to antiviral sensing and identified viral and host regulators, showing it bridges RIG-I/MDA5 to MAVS and is targeted by HBx and TRIM59.

    Evidence Co-IP, siRNA/overexpression IRF3 and IFNB1 assays; GST pulldown and reporter assays for HBx and TRIM59

    PMID:22588174 PMID:25228397 PMID:25449573

    Open questions at the time
    • RIG-I/MDA5-MAVS bridging shown by Co-IP without reciprocal structural validation
    • Host vs. viral regulation hierarchy unresolved
  6. 2018 High

    Linked ECSIT's mitochondrial role to immune effector output and mitophagy, showing complex I loss reprograms metabolism, elevates ROS, and disrupts PINK1/Parkin-dependent mitophagy.

    Evidence Macrophage conditional knockout, complex I assays, Seahorse, PINK1 Co-IP, Parkin-dependent ubiquitination assay; ENKTL ECSIT-V140A knock-in mouse and S100A8/A9 binding

    PMID:29291352 PMID:29514094

    Open questions at the time
    • How ECSIT integrates into mitophagy beyond PINK1 association not defined
    • Mechanism of V140A gain-of-function affinity change not structurally explained
  7. 2019 Medium

    Defined the TRAF6–ECSIT complex as a regulatory node, showing competitive binders (CRBN, p62) and the requirement of ECSIT ubiquitination for mitochondrial ROS and bactericidal activity.

    Evidence Co-IP/domain mapping, p62-KO cells and mice, CRBN knockdown, mROS and bacterial survival assays

    PMID:28393051 PMID:31281713 PMID:31620128

    Open questions at the time
    • Whether competitive disruptors act at the same TRAF-C interface for all is not unified
    • Quantitative contribution of each regulator in vivo unclear
  8. 2021 High

    Demonstrated species- and tissue-specific physiological consequences of ECSIT abundance, with human ECSIT lability causing complex I deficiency and cardiac hypertrophy.

    Evidence Humanized hECSIT knock-in mice, complex I assembly/activity assays, Seahorse, mitochondrial morphology imaging, cardiac phenotyping

    PMID:34032637

    Open questions at the time
    • Molecular basis of human ECSIT instability not defined
    • Cardiomyocyte-intrinsic vs. systemic contributions only partly separated
  9. 2023 High

    Generalized ECSIT's metabolic-gatekeeper role across osteoclasts, cardiac tissue, and intestine, including a translation-control mechanism affecting YAP.

    Evidence RANKL osteoclast Co-IP and Seahorse; ENU ECSIT-N209I cardiac mutant; intestinal conditional KO with proteomics, metabolomics, and ribosome profiling

    PMID:37152948 PMID:37395010 PMID:37409430

    Open questions at the time
    • Mechanism linking complex I loss to eIF4F demethylation and YAP translation incompletely defined
    • Tissue specificity of complex I requirement mechanistically unexplained
  10. 2024 High

    Connected ECSIT-dependent mitochondrial metabolism to epigenetic control of cell fate, showing ECSIT-driven fumarate suppresses KDM5 demethylation of the TCF-1 promoter for memory CD8+ T cell formation.

    Evidence T cell-specific conditional KO, fumarate metabolomics, ChIP/methylation, KDM5 inhibition, adoptive transfer

    PMID:38326554

    Open questions at the time
    • How ECSIT enzymatically/structurally controls fumarate flux not detailed
    • Generality of the fumarate-KDM5 axis to other cell types unknown
  11. 2025 Medium

    Identified an isoform-specific and STAT3-dependent cardioprotective mechanism, plus a pathogen-driven autophagy-suppression mechanism, refining ECSIT's context-dependent outputs.

    Evidence Ecsit-X4 AAV9 therapy and cardiomyocyte KO with STAT3 Co-IP and pS727 blot; M. tuberculosis HBHA binding, ECSIT KD, autophagy markers and bacterial survival

    PMID:39746855 PMID:41209015

    Open questions at the time
    • Functional distinction between ECSIT-X4 and canonical isoform not fully mapped
    • HBHA-ECSIT interface and selectivity over TRAF6 binding undefined
  12. 2026 Medium

    Showed mitochondrial ECSIT can recruit a deubiquitinase to control mitochondrial protein stability and oxidative stress, extending its mitochondrial scaffolding role to metabolic disease.

    Evidence Mitochondria-targeted ECSIT transgenic mice, OTUD3 Co-IP, SIRT3 deubiquitination assay, mtDNA oxidation and MASH models

    PMID:41640247

    Open questions at the time
    • Whether ECSIT directly recruits OTUD3 or acts indirectly not resolved
    • Relationship to complex I assembly function unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How ECSIT's distinct molecular activities — TRAF6/NF-κB scaffolding, complex I assembly, Smad co-factor function, and metabolite-driven epigenetic regulation — are partitioned and coordinated within a single protein remains unresolved.
  • No structural model unifying the signaling and mitochondrial functions
  • Mechanism switching ECSIT between cytosolic and mitochondrial pools unknown
  • E3 ligase and deubiquitinase network controlling ECSIT modification incompletely defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 3 GO:0005198 structural molecule activity 2 GO:0140110 transcription regulator activity 1
Localization
GO:0005739 mitochondrion 4 GO:0005634 nucleus 2 GO:0005829 cytosol 2
Pathway
R-HSA-168256 Immune System 4 R-HSA-1430728 Metabolism 3 R-HSA-162582 Signal Transduction 3 R-HSA-1852241 Organelle biogenesis and maintenance 3 R-HSA-1266738 Developmental Biology 1
Partners
MEKK-1NDUFAF1PINK1SMAD1SMAD4STAT3TAK1TRAF6
Complex memberships
TAK1-ECSIT-TRAF6 complexmitochondrial complex I assembly intermediate (with NDUFAF1)

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 ECSIT acts as an adaptor protein bridging TRAF6 to MEKK-1 in the Toll/IL-1 signaling pathway; wild-type ECSIT accelerates MEKK-1 processing while a dominant-negative fragment blocks MEKK-1 processing and NF-κB activation. Yeast two-hybrid, co-immunoprecipitation, dominant-negative overexpression, NF-κB reporter assays Genes & development High 10465784
2003 ECSIT is required for BMP signaling during mouse embryogenesis; it associates constitutively with Smad4 and associates with Smad1 in a BMP-inducible manner, and together with Smad1/Smad4 binds promoters of specific BMP target genes. Ecsit null mice show impaired mesoderm formation and embryonic lethality at E7.5. Targeted gene knockout (null mutation), co-immunoprecipitation, chromatin immunoprecipitation, shRNA knockdown, reporter assays Genes & development High 14633973
2007 ECSIT localizes to mitochondria via an N-terminal targeting signal, where it interacts with the assembly chaperone NDUFAF1 in 500–850 kDa complexes; RNAi knockdown of either ECSIT or NDUFAF1 severely impairs mitochondrial complex I assembly and function. Affinity purification, subcellular fractionation, RNAi knockdown, blue native PAGE, mitochondrial function assays Genes & development High 17344420
2012 TRIM59 interacts with ECSIT (co-immunoprecipitation) and acts as a negative regulator of NF-κB and IRF-3/7-mediated signaling; overexpression of TRIM59 represses NF-κB, IFN-β promoter, and ISRE transcriptional activities, while TRIM59 knockdown enhances them. TRIM59 also inhibits phosphorylation and dimerization of IRF3 and IRF7. Co-immunoprecipitation, luciferase reporter assays, siRNA knockdown, Western blot (phosphorylation) Biochemical and biophysical research communications Medium 22588174
2014 Upon LPS stimulation, ECSIT forms a trimeric complex with TAK1 and TRAF6; ECSIT interacts with each protein and regulates TAK1 activity to activate NF-κB. ECSIT mutants lacking the TAK1- or TRAF6-interacting domain cannot restore NF-κB activity or cytokine production in ECSIT-knockdown cells. Co-immunoprecipitation of endogenous proteins, ECSIT-knockdown (THP-1), domain-deletion mutant rescue, NF-κB reporter assay, cytokine ELISA The Journal of biological chemistry High 25371197
2014 ECSIT ubiquitination at lysine 372 is required for its interaction with p65/p50 NF-κB proteins and their nuclear co-localization following TLR4 stimulation; the K372A mutant fails to interact with NF-κB subunits and cannot restore NF-κB DNA-binding activity or cytokine production in ECSIT-knockdown cells. Co-immunoprecipitation, site-directed mutagenesis (K372A), subcellular fractionation, NF-κB EMSA/reporter assays, cytokine measurement, ECSIT-knockdown rescue Molecular biology of the cell High 25355951
2014 ECSIT serves as an essential scaffolding protein that bridges RIG-I and MDA5 to VISA (MAVS) on mitochondria, mediating virus-triggered type I IFN induction; ECSIT overexpression potentiates IRF3 activation and IFNB1 expression, while ECSIT knockdown impairs these antiviral responses. Co-immunoprecipitation, siRNA knockdown, overexpression, IRF3 activation assay, IFNB1 reporter/expression assay Journal of innate immunity Medium 25228397
2014 Hepatitis B virus X protein (HBx) physically interacts with ECSIT (GST pulldown and co-IP); the interacting region of HBx maps to amino acids 51–80; the HBx–ECSIT interaction augments IL-1β-induced NF-κB activation by increasing IKK and IκBα phosphorylation and promoting p65/p50 nuclear translocation. GST pulldown, co-immunoprecipitation, CytoTrap two-hybrid, deletion analysis, NF-κB reporter assay, Western blot (phosphorylation) Virus research Medium 25449573
2017 Peroxiredoxin-6 (Prdx6) competitively interacts with ECSIT at the TRAF-C domain of TRAF6, disrupting the TRAF6–ECSIT complex; this inhibits ECSIT ubiquitination, reduces mitochondrial ROS production, and suppresses TLR4-induced NF-κB activation and bactericidal activity. Co-immunoprecipitation, Prdx6 knockdown, competitive binding assay, mitochondrial ROS measurement, NF-κB reporter, cytokine assay, bacterial survival assay Frontiers in cellular and infection microbiology Medium 28393051
2018 Conditional knockout of ECSIT in macrophages completely disrupts complex I activity and the CI holoenzyme, causes a metabolic shift to glycolysis, increases constitutive mitochondrial ROS, and impairs mitophagy. ECSIT associates with the mitophagy regulator PINK1 and undergoes Parkin-dependent ubiquitination; ECSIT deletion increases mitochondrial Parkin without restoring mitophagy. Conditional knockout mouse (Cre-lox), complex I activity assay, blue native PAGE, metabolic flux (Seahorse), mROS measurement, co-immunoprecipitation (PINK1), ubiquitination assay Cell reports High 29514094
2018 The ECSIT V140A mutation increases ECSIT affinity for the S100A8/S100A9 heterodimer, potentiating NF-κB activation and NADPH oxidase activity. ECSIT-T419C knock-in mice showed higher peritoneal NADPH oxidase activity than wild-type in response to LPS. ECSIT-V140A-expressing ENKTL cells produced TNF-α and IFN-γ that induced macrophage activation and cytokine secretion. Exome sequencing, knock-in mouse model, co-immunoprecipitation, NADPH oxidase activity assay, NF-κB reporter, cytokine measurement, xenograft model Nature medicine High 29291352
2019 CRBN (cereblon) translocates to mitochondria upon TLR4 stimulation and disrupts the ECSIT–TRAF6 complex, thereby inhibiting TRAF6-induced ubiquitination of ECSIT and suppressing mitochondrial ROS production and bactericidal activity. Co-immunoprecipitation, CRBN knockdown/knockout, mitochondrial fractionation, mROS measurement, bacterial survival assay Frontiers in immunology Medium 31620128
2019 p62 (SQSTM1) interacts with the internal domain of ECSIT, inhibits TRAF6–ECSIT association, and attenuates ECSIT ubiquitination, thereby suppressing TLR4-mediated NF-κB activation; p62-knockout MEF cells and mice show markedly enhanced TLR4 signaling and inflammatory responses. Co-immunoprecipitation, domain mapping, p62 knockout MEF cells, p62 knockout mice, NF-κB reporter, cytokine measurement, ubiquitination assay Immune network Medium 31281713
2021 Human ECSIT (hECSIT) is highly labile compared to murine Ecsit; low hECSIT levels lead to reduced complex I assembly and activity, impaired oxidative phosphorylation, reduced ATP production, altered mitochondrial dynamics (reduced fusion, increased fission), and severe cardiac hypertrophy in humanized knock-in mice. ECSIT also has a cardiomyocyte-intrinsic role in mitochondrial function. Humanized knock-in mouse (mEcsit replaced by hECSIT), complex I activity/assembly assay, Seahorse metabolic flux, mitochondrial morphology imaging, cardiac function assays JCI insight High 34032637
2023 RANKL promotes ECSIT–TRAF6 interaction and increases mitochondrial ECSIT levels in osteoclast progenitors; ECSIT silencing decreases complex I activity, oxygen consumption, NAD+/NADH ratio, ATP production, and increases mitochondrial ROS, abrogating RANKL-driven stimulation of oxidative phosphorylation and osteoclastogenesis. 17β-estradiol (E2) abrogates these RANKL-induced effects on ECSIT. Co-immunoprecipitation, subcellular fractionation, shRNA knockdown, Seahorse XF metabolic analysis, complex I activity assay, ROS measurement, mitochondrial membrane potential assay Frontiers in endocrinology High 37152948
2023 ECSIT-N209I ENU-induced mutation causes tissue-specific complex I assembly defects specifically in cardiac tissue, leading to hypertrophic cardiomyopathy without affecting complex I in other tissues, demonstrating tissue-specific requirements for ECSIT in complex I assembly. ENU mutagenesis screen, Seahorse extracellular flux, biochemical complex I assays, blue native PAGE, cardiac phenotyping Cardiovascular research Medium 37395010
2023 Intestinal cell-specific ablation of ECSIT causes metabolic reprogramming toward amino acid-based metabolism, demethylation and upregulation of eIF4F pathway genes, and consequently enhanced YAP protein translation (not transcription), disrupting intestinal differentiation and promoting tumorigenesis. Intestinal epithelium-specific conditional knockout, proteomics, metabolomics, ribosome profiling/translation assays, Western blot, reporter assays Advanced science Medium 37409430
2024 ECSIT mediates fumarate synthesis in CD8+ T cells; T cell-specific ECSIT ablation abolishes fumarate production and abrogates TCF-1 expression via KDM5-mediated demethylation of the TCF-1 promoter, impairing memory CD8+ T cell differentiation in a cell-intrinsic manner. T cell-specific conditional knockout, metabolomics (fumarate measurement), ChIP/methylation analysis, KDM5 inhibition, adoptive transfer experiments Nature cell biology High 38326554
2025 A novel 42-kDa ECSIT isoform encoded by transcript variant Ecsit-X4 localizes to mitochondria of adult cardiomyocytes; it interacts with STAT3 and increases mitochondrial STAT3 levels and serine 727 phosphorylation, thereby promoting mitochondrial bioenergetics and protecting against pressure overload-induced cardiac hypertrophy. AAV9-mediated gene therapy, cardiomyocyte-specific Ecsit conditional knockout, co-immunoprecipitation (STAT3 interaction), Western blot (phospho-STAT3-S727), mitochondrial fractionation, Seahorse metabolic analysis, TAC surgical model Advanced science Medium 39746855
2025 Mycobacterium tuberculosis virulence factor HBHA directly binds ECSIT, disrupts the ECSIT–TRAF6 complex, and inhibits ECSIT ubiquitination in macrophages, thereby suppressing autophagy (LC3-II conversion and Beclin-1 expression unchanged in ECSIT-knockdown cells upon HBHA treatment) and promoting intracellular mycobacterial survival. Co-immunoprecipitation, ECSIT knockdown (RAW264.7), ubiquitination assay, LC3-II/Beclin-1 Western blot, intracellular bacterial survival assay Frontiers in immunology Medium 41209015
2026 Mitochondria-targeted ECSIT overexpression promotes localization of deubiquitinase OTUD3 to mitochondria; OTUD3 then stabilizes SIRT3 via deubiquitination, inhibiting mtDNA oxidation and alleviating diet-induced MASH phenotypes. Mitochondria-targeted transgenic mice (ECSITMTG), co-immunoprecipitation, deubiquitination assay, mitochondrial fractionation, mtDNA oxidation measurement, dietary MASH models Advanced science Medium 41640247

Source papers

Stage 0 corpus · 38 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1999 ECSIT is an evolutionarily conserved intermediate in the Toll/IL-1 signal transduction pathway. Genes & development 259 10465784
2007 Cytosolic signaling protein Ecsit also localizes to mitochondria where it interacts with chaperone NDUFAF1 and functions in complex I assembly. Genes & development 160 17344420
2014 TAK1-ECSIT-TRAF6 complex plays a key role in the TLR4 signal to activate NF-κB. The Journal of biological chemistry 87 25371197
2012 TRIM59 interacts with ECSIT and negatively regulates NF-κB and IRF-3/7-mediated signal pathways. Biochemical and biophysical research communications 82 22588174
2003 Ecsit is required for Bmp signaling and mesoderm formation during mouse embryogenesis. Genes & development 78 14633973
2018 An Essential Role for ECSIT in Mitochondrial Complex I Assembly and Mitophagy in Macrophages. Cell reports 72 29514094
2018 Recurrent ECSIT mutation encoding V140A triggers hyperinflammation and promotes hemophagocytic syndrome in extranodal NK/T cell lymphoma. Nature medicine 58 29291352
2017 Peroxiredoxin-6 Negatively Regulates Bactericidal Activity and NF-κB Activity by Interrupting TRAF6-ECSIT Complex. Frontiers in cellular and infection microbiology 40 28393051
2012 Towards Alzheimer's root cause: ECSIT as an integrating hub between oxidative stress, inflammation and mitochondrial dysfunction. Hypothetical role of the adapter protein ECSIT in familial and sporadic Alzheimer's disease pathogenesis. BioEssays : news and reviews in molecular, cellular and developmental biology 35 22513506
2014 Ubiquitination of ECSIT is crucial for the activation of p65/p50 NF-κBs in Toll-like receptor 4 signaling. Molecular biology of the cell 31 25355951
2014 ECSIT bridges RIG-I-like receptors to VISA in signaling events of innate antiviral responses. Journal of innate immunity 27 25228397
2019 CRBN Is a Negative Regulator of Bactericidal Activity and Autophagy Activation Through Inhibiting the Ubiquitination of ECSIT and BECN1. Frontiers in immunology 24 31620128
2017 ECSIT links TLR and BMP signaling in FOP connective tissue progenitor cells. Bone 24 29288875
2003 Diagnostic pathway of syncope and analysis of the impact of guidelines in a district general hospital. The ECSIT study (epidemiology and costs of syncope in Trento). Italian heart journal : official journal of the Italian Federation of Cardiology 23 12762272
2014 Role of evolutionarily conserved signaling intermediate in Toll pathways (ECSIT) in the antibacterial immunity of Marsupenaeus japonicus. Developmental and comparative immunology 18 24796866
2019 p62 Negatively Regulates TLR4 Signaling via Functional Regulation of the TRAF6-ECSIT Complex. Immune network 17 31281713
2007 The nexus of iron and inflammation in hepcidin regulation: SMADs, STATs, and ECSIT. Hepatology (Baltimore, Md.) 17 17187402
2021 ECSIT is a critical limiting factor for cardiac function. JCI insight 15 34032637
2024 ECSIT facilitates memory CD8+ T cell development by mediating fumarate synthesis during viral infection and tumorigenesis. Nature cell biology 14 38326554
2023 ECSIT is essential for RANKL-induced stimulation of mitochondria in osteoclasts and a target for the anti-osteoclastogenic effects of estrogens. Frontiers in endocrinology 14 37152948
2022 The ECSIT Mediated Toll3-Dorsal-ALFs Pathway Inhibits Bacterial Amplification in Kuruma Shrimp. Frontiers in immunology 14 35173723
2014 Hepatitis B virus X protein increases the IL-1β-induced NF-κB activation via interaction with evolutionarily conserved signaling intermediate in Toll pathways (ECSIT). Virus research 14 25449573
2023 ECSIT Is a Critical Factor for Controlling Intestinal Homeostasis and Tumorigenesis through Regulating the Translation of YAP Protein. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 11 37409430
2015 Identification and function of an evolutionarily conserved signaling intermediate in Toll pathways (ECSIT) from Crassostrea hongkongensis. Developmental and comparative immunology 11 26204814
2024 ECSIT: Biological function and involvement in diseases. International immunopharmacology 9 39488037
2023 Tissue-specific differences in the assembly of mitochondrial Complex I are revealed by a novel ENU mutation in ECSIT. Cardiovascular research 8 37395010
2020 Identification, characterization, and functional analysis of Toll and ECSIT in Exopalaemon carinicauda. Developmental and comparative immunology 8 33238179
2022 Molecular characterization of the evolutionary conserved signaling intermediate in Toll pathways (ECSIT) of soiny mullet (Liza haematocheila). Fish & shellfish immunology 7 36087818
2025 ECSIT-X4 is Required for Preventing Pressure Overload-Induced Cardiac Hypertrophy via Regulating Mitochondrial STAT3. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 6 39746855
2024 Emerging roles of ECSIT in immunity and tumorigenesis. Trends in cell biology 5 39384444
2016 Characterization, molecular cloning, and expression analysis of Ecsit in the spinyhead croaker, Collichthys lucidus. Genetics and molecular research : GMR 5 26909903
2022 Pleiotropic roles of evolutionarily conserved signaling intermediate in toll pathway (ECSIT) in pathophysiology. Journal of cellular physiology 4 35853181
2022 ECSIT inhibits cell death to increase tumor progression and metastasis via p53 in human breast cancer. Translational cancer research 3 35571656
2023 Large-scale lysine crotonylation analysis reveals the role of TRAF6-Ecsit complex in endoplasmic reticulum stress in mud crab (Scylla paramamosain). Developmental and comparative immunology 2 37531975
2025 HBHA-ECSIT interaction disrupts macrophage autophagy to promote Mycobacterium tuberculosis persistence. Frontiers in immunology 1 41209015
2017 [Amphioxus ortholog of ECSIT, an evolutionarily conserved adaptor in the Toll and BMP signaling pathways]. Molekuliarnaia biologiia 1 28251965
2026 A protective role of ECSIT in chemotherapy-induced intestinal mucositis by maintaining Lgr5+ intestinal stem cells and gut homeostasis. Life sciences 0 41611204
2026 Targeted Mitochondrial ECSIT Overexpression Attenuates MASH by Increasing OTUD3 Expression. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 0 41640247

Missed literature

Know a paper Affinage missed for ECSIT? Flag it for the maintainers and the community.

No submissions yet.