Affinage

ECSIT

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

Length
431 aa
Mass
49.1 kDa
Annotated
2026-04-28
38 papers in source corpus 22 papers cited in narrative 22 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ECSIT is a multifunctional adaptor/scaffold protein that operates in cytosolic, mitochondrial, and nuclear compartments to integrate innate immune signaling, mitochondrial bioenergetics, and developmental transcription. In the cytosol, ECSIT bridges TRAF6 to MEKK-1 and TAK1, forming a signaling complex essential for TLR/IL-1-induced NF-κB activation, and undergoes K372 ubiquitination required for nuclear interaction with p65/p50 NF-κB subunits (PMID:10465784, PMID:25371197, PMID:25355951); it also scaffolds RIG-I/MDA5 to MAVS for antiviral type I interferon induction (PMID:25228397). In mitochondria, ECSIT interacts with NDUFAF1 to direct respiratory complex I assembly, associates with PINK1 to regulate Parkin-dependent mitophagy, controls fumarate-dependent epigenetic programming of CD8+ T cell memory via TCF-1 promoter methylation, and interacts with STAT3 to sustain oxidative phosphorylation in cardiomyocytes (PMID:17344420, PMID:29514094, PMID:38326554, PMID:39746855). In the nucleus, ECSIT functions as a BMP-inducible cofactor that associates with Smad1/Smad4 to activate BMP target gene transcription essential for mesoderm formation during embryogenesis (PMID:14633973).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1999 High

    Identifying ECSIT as the missing link between TRAF6 and MEKK-1 established how TLR/IL-1 receptor signals reach the NF-κB cascade through a dedicated adaptor protein.

    Evidence Co-IP and dominant-negative overexpression with NF-κB reporter assays in mammalian cells

    PMID:10465784

    Open questions at the time
    • No structural basis for the TRAF6-ECSIT-MEKK-1 interaction
    • In vivo requirement for NF-κB signaling not tested
  2. 2003 High

    Demonstrating that ECSIT knockout mice fail to form mesoderm and that ECSIT associates with Smad1/Smad4 on BMP target promoters revealed a second, transcription-regulatory function independent of its innate immune role.

    Evidence ECSIT-null mouse, co-IP, and ChIP at BMP target gene promoters

    PMID:14633973

    Open questions at the time
    • How ECSIT switches between cytosolic signaling and nuclear cofactor roles is unknown
    • Whether ECSIT's BMP function persists in adult tissues beyond embryogenesis is untested
  3. 2007 High

    Discovery that ECSIT localizes to mitochondria via an N-terminal signal and partners with NDUFAF1 for complex I assembly redefined ECSIT as a mitochondrial biogenesis factor, not solely a signaling adaptor.

    Evidence Affinity purification, reciprocal RNAi, subcellular fractionation, and blue native PAGE

    PMID:17344420

    Open questions at the time
    • Precise step in complex I assembly pathway where ECSIT acts was not defined
    • Relationship between ECSIT's signaling and mitochondrial functions not clarified
  4. 2014 High

    Mapping the endogenous TAK1-ECSIT-TRAF6 complex and showing that K372 ubiquitination of ECSIT is required for NF-κB nuclear interaction resolved how ECSIT's post-translational modification couples upstream signaling to transcription factor activation.

    Evidence Endogenous co-IP, domain-deletion mutagenesis, K372A site-directed mutagenesis, nuclear fractionation, and knockdown-rescue in multiple studies

    PMID:25355951 PMID:25371197

    Open questions at the time
    • E3 ligase responsible for K372 ubiquitination not definitively identified in these studies
    • Whether K372 ubiquitination also affects mitochondrial ECSIT functions is unknown
  5. 2014 Medium

    Showing that ECSIT scaffolds RIG-I/MDA5 to MAVS extended ECSIT's innate immune role from TLR signaling to antiviral RLR-mediated type I interferon induction.

    Evidence Co-IP, overexpression, shRNA knockdown, IRF3 activation and IFNB1 expression assays

    PMID:25228397

    Open questions at the time
    • No in vitro reconstitution of the RIG-I/MDA5-ECSIT-MAVS complex
    • Requirement not validated with genetic knockout
  6. 2018 High

    Conditional ECSIT knockout in macrophages showed that ECSIT is essential for complex I holoenzyme integrity, mROS-dependent bactericidal activity, and PINK1/Parkin-dependent mitophagy, unifying its mitochondrial assembly and innate immune functions.

    Evidence Myeloid-specific conditional knockout mouse, Seahorse metabolic flux, blue native PAGE, co-IP with PINK1, ubiquitination assays

    PMID:29514094

    Open questions at the time
    • Whether ECSIT is a direct substrate of Parkin or ubiquitinated indirectly was not fully resolved
    • Mechanism linking complex I loss to mitophagy defects not delineated
  7. 2018 High

    The V140A gain-of-function mutation in NK/T cell lymphoma, which enhances ECSIT interaction with S100A8/S100A9 and hyperactivates NF-κB and NADPH oxidase, provided the first disease-linked ECSIT variant demonstrating pathological consequences of dysregulated ECSIT signaling.

    Evidence Exome sequencing, knock-in mouse, co-IP, NADPH oxidase and NF-κB assays, xenograft model

    PMID:29291352

    Open questions at the time
    • Whether V140A affects mitochondrial complex I assembly is untested
    • Frequency and penetrance of ECSIT mutations across lymphoma subtypes not established
  8. 2017 Medium

    Identification of negative regulators—Prdx6, p62, and CRBN—that competitively disrupt the TRAF6-ECSIT complex defined a regulatory layer controlling ECSIT-dependent mROS production and NF-κB activation.

    Evidence Competitive co-IP, knockout MEFs, CRISPR knockout, ubiquitination assays, mROS and NF-κB functional readouts across multiple studies

    PMID:28393051 PMID:31281713 PMID:31620128

    Open questions at the time
    • Relative physiological importance of Prdx6, p62, and CRBN in tuning ECSIT activity is unknown
    • No in vivo validation for Prdx6 or CRBN regulatory roles
  9. 2021 High

    Humanized ECSIT knock-in mice revealed that human ECSIT protein is far more labile than murine ECSIT, causing reduced complex I activity, impaired mitophagy, and cardiac hypertrophy with aging—establishing tissue-specific vulnerability to ECSIT dosage.

    Evidence Humanized knock-in mouse, cardiomyocyte-specific CKO, Seahorse, complex I assays, mitophagy assays

    PMID:34032637

    Open questions at the time
    • Molecular basis for differential human vs. murine ECSIT protein stability is unresolved
    • Whether therapeutic stabilization of human ECSIT can rescue cardiac phenotype is untested
  10. 2023 High

    The N209I point mutation demonstrated that ECSIT requirements for complex I assembly are tissue-specific, with heart being most vulnerable, explaining cardiac hypertrophy as a primary manifestation of ECSIT deficiency.

    Evidence ENU mutagenesis mouse, blue native PAGE, Seahorse, CI activity assays across multiple tissues

    PMID:37395010

    Open questions at the time
    • Why heart mitochondria are selectively dependent on ECSIT for CI assembly is mechanistically unexplained
    • No structural information on how N209I disrupts ECSIT function
  11. 2023 Medium

    Intestinal ECSIT loss causing metabolic reprogramming, eIF4F-YAP pathway activation, and stem cell transformation revealed an unexpected tumor-suppressive function through metabolic control of translational programs.

    Evidence Intestinal epithelium-specific ECSIT KO mouse, metabolomics, methylation analysis, polysome profiling, organoids

    PMID:37409430

    Open questions at the time
    • Whether the tumorigenic effect is solely through complex I loss or involves signaling functions is unclear
    • No clinical validation in human colorectal cancer
  12. 2024 High

    Demonstrating that ECSIT controls fumarate synthesis to maintain H3K4me3 at the TCF-1 promoter via KDM5 regulation established a metabolite-to-epigenome axis through which mitochondrial ECSIT directs CD8+ T cell memory fate decisions.

    Evidence T cell-specific ECSIT KO, metabolomics, ChIP/methylation analysis, viral infection and tumor models in vivo

    PMID:38326554

    Open questions at the time
    • Whether ECSIT directly catalyzes fumarate production or acts indirectly through complex I is not resolved
    • Applicability to human T cell immunotherapy not tested
  13. 2025 Medium

    Discovery that a 42-kDa ECSIT isoform (ECSIT-X4) interacts with mitochondrial STAT3 to promote its Ser727 phosphorylation and bioenergetic function identified a cardioprotective ECSIT-STAT3 axis and a therapeutic isoform for heart failure.

    Evidence AAV9 gene therapy, cardiomyocyte-specific KO, co-IP with STAT3, Seahorse, TAC pressure-overload model

    PMID:39746855

    Open questions at the time
    • Kinase mediating STAT3 Ser727 phosphorylation downstream of ECSIT-X4 is unidentified
    • Whether ECSIT-X4 has distinct functions from full-length ECSIT beyond the heart is unknown
  14. 2025 Medium

    Mycobacterium tuberculosis HBHA directly binding ECSIT to disrupt TRAF6 interaction and suppress autophagy revealed ECSIT as a pathogen-targeted node for immune evasion.

    Evidence Direct binding assay, co-IP, ECSIT knockdown, autophagy markers, intracellular bacterial survival in RAW264.7 macrophages

    PMID:41209015

    Open questions at the time
    • Not validated in primary human macrophages or in vivo infection models
    • Whether other mycobacterial factors also target ECSIT is unknown
  15. 2026 Medium

    Mitochondrial ECSIT overexpression recruiting OTUD3 to stabilize SIRT3 and showing that ECSIT sustains β-catenin/Wnt signaling in Lgr5+ intestinal stem cells expanded ECSIT's role to metabolic liver disease and intestinal homeostasis.

    Evidence Mito-targeted ECSIT transgenic mice with MASH models; intestinal epithelium-specific KO with scRNA-seq and β-catenin rescue

    PMID:41611204 PMID:41640247

    Open questions at the time
    • Mechanism by which ECSIT recruits OTUD3 to mitochondria is not defined
    • Whether Wnt/β-catenin stabilization by ECSIT is direct or secondary to metabolic changes is unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How ECSIT partitions between cytosolic, mitochondrial, and nuclear pools, what determines isoform-specific targeting, and how its dual signaling and bioenergetic functions are coordinated in different cell types remain major open questions.
  • No structural model of ECSIT or any of its complexes exists
  • Mechanism governing ECSIT partitioning among subcellular compartments is unknown
  • Whether ECSIT's BMP/Smad, NF-κB, and complex I functions are mutually exclusive or concurrent in single cells is untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 3 GO:0140110 transcription regulator activity 1
Localization
GO:0005739 mitochondrion 5 GO:0005829 cytosol 3 GO:0005634 nucleus 2
Pathway
R-HSA-168256 Immune System 8 R-HSA-1430728 Metabolism 5 R-HSA-162582 Signal Transduction 3 R-HSA-9612973 Autophagy 2 R-HSA-1266738 Developmental Biology 1 R-HSA-5357801 Programmed Cell Death 1
Partners
MAVSNDUFAF1PINK1SMAD1SMAD4STAT3TAK1TRAF6
Complex memberships
ECSIT-NDUFAF1 complex I assembly intermediateTAK1-ECSIT-TRAF6 complex

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 ECSIT is a cytosolic adaptor protein that bridges TRAF6 to MEKK-1 in the Toll/IL-1 signaling pathway, and acts as a regulator of MEKK-1 processing; wild-type ECSIT accelerates MEKK-1 processing while a dominant-negative fragment blocks MEKK-1 processing and NF-κB activation. Co-immunoprecipitation, dominant-negative overexpression, NF-κB reporter assays Genes & development High 10465784
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 ECSIT severely impairs mitochondrial complex I assembly and function. Affinity purification, reciprocal RNAi knockdowns, subcellular fractionation, blue native PAGE Genes & development High 17344420
2003 ECSIT is essential for BMP signaling during mouse embryogenesis; it constitutively associates with Smad4 and associates with Smad1 in a BMP-inducible manner, and together with Smad1/Smad4 binds to the promoters of specific BMP target genes. Targeted null mutation (knockout mouse), co-immunoprecipitation, chromatin immunoprecipitation, shRNA knockdown Genes & development High 14633973
2014 Upon LPS stimulation, ECSIT forms a high-molecular-weight endogenous complex with TAK1 and TRAF6; ECSIT interacts with each protein and regulates TAK1 activity to activate NF-κB, and ECSIT mutants lacking specific interaction domains for TAK1 or TRAF6 cannot restore NF-κB activation. Co-immunoprecipitation of endogenous proteins, shRNA knockdown, domain-deletion mutagenesis, NF-κB reporter assays, cytokine measurement The Journal of biological chemistry High 25371197
2014 ECSIT ubiquitination at lysine 372 (K372) is required for its interaction with p65/p50 NF-κB proteins and their nuclear colocalization; K372A mutant ECSIT 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), nuclear fractionation, NF-κB DNA-binding assay, shRNA knockdown rescue Molecular biology of the cell High 25355951
2018 ECSIT deletion in macrophages causes complete disruption of complex I activity, loss of the CI holoenzyme and multiple subassemblies, shifts metabolism to glycolysis, and causes defective mitophagy; ECSIT associates with the mitophagy regulator PINK1 and undergoes Parkin-dependent ubiquitination. Conditional knockout mouse, Seahorse metabolic flux, blue native PAGE for complex assembly, co-immunoprecipitation with PINK1, ubiquitination assay Cell reports High 29514094
2012 TRIM59 interacts with ECSIT as an adaptor protein in the TLR signaling pathway and negatively regulates NF-κB and IRF-3/7-mediated signaling; TRIM59 overexpression inhibits phosphorylation and dimerization of IRF3 and IRF7. Co-immunoprecipitation, luciferase reporter assay, shRNA knockdown, phosphorylation/dimerization analysis Biochemical and biophysical research communications Medium 22588174
2014 ECSIT acts as an essential scaffolding protein bridging RIG-I and MDA5 to VISA (MAVS) on mitochondria, mediating virus-triggered type I IFN induction; overexpression potentiated IRF3 activation and IFNB1 expression, while knockdown impaired antiviral responses. Co-immunoprecipitation, overexpression, shRNA knockdown, IRF3 activation assay, IFNB1 expression analysis Journal of innate immunity Medium 25228397
2017 Peroxiredoxin-6 (Prdx6) competitively interacts with ECSIT for TRAF6 binding via TRAF6's C-terminal TRAF-C domain, thereby disrupting the TRAF6-ECSIT complex and suppressing TLR4-induced mROS production and NF-κB activation. Co-immunoprecipitation, competitive binding assay, shRNA knockdown, mitochondrial ROS measurement, NF-κB reporter assay Frontiers in cellular and infection microbiology Medium 28393051
2018 The ECSIT V140A mutation increases ECSIT's affinity for the S100A8/S100A9 heterodimer, leading to potentiated NF-κB activation and increased NADPH oxidase activity, triggering hyperinflammation in extranodal NK/T cell lymphoma. Exome sequencing, knock-in mouse model, co-immunoprecipitation, NADPH oxidase activity assay, NF-κB reporter assay, xenograft mouse model Nature medicine High 29291352
2019 Cereblon (CRBN) disrupts the ECSIT-TRAF6 complex by interacting with ECSIT, thereby inhibiting TRAF6-induced ubiquitination of ECSIT and suppressing mROS production and bactericidal activity following TLR4 stimulation. Co-immunoprecipitation, ubiquitination assay, shRNA/CRISPR knockdown/knockout, mitochondrial ROS measurement, bacterial survival assay Frontiers in immunology Medium 31620128
2019 p62 interacts with the internal domain of ECSIT, competitively inhibiting TRAF6-ECSIT complex formation and attenuating ECSIT ubiquitination, thereby negatively regulating TLR4-mediated NF-κB activation. Co-immunoprecipitation, p62 knockout MEF cells, ubiquitination assay, NF-κB activation assay, in vivo LPS challenge Immune network Medium 31281713
2021 Human ECSIT is highly labile compared to murine ECSIT; low-level human ECSIT expression leads to reduced complex I assembly and activity, impaired oxidative phosphorylation, reduced ATP production, and severe cardiac hypertrophy with impaired mitophagy in aging humanized mice. Humanized knock-in mouse, Seahorse metabolic flux, complex I activity assay, mitochondrial fractionation, mitophagy assay, cardiomyocyte-specific conditional knockout JCI insight High 34032637
2023 An ENU-induced N209I mutation in ECSIT causes tissue-specific defects in complex I assembly, with profound effects in heart tissue (loss of CI expression and assembly, hypertrophic cardiomyopathy) but not in other tissues, revealing tissue-specific requirements for ECSIT in complex I assembly. ENU mutagenesis mouse model, Seahorse extracellular flux, blue native PAGE, biochemical CI activity assay, histology Cardiovascular research High 37395010
2023 ECSIT promotes RANKL-induced mitochondrial stimulation in osteoclasts via TRAF6 interaction and mitochondrial localization; RANKL promotes ECSIT-TRAF6 interaction and ECSIT mitochondrial translocation, while estradiol abrogates these effects; ECSIT silencing abolishes estrogen's anti-osteoclastogenic effects. Co-immunoprecipitation, subcellular fractionation, shRNA knockdown, Seahorse metabolic flux, complex I activity assay, ROS measurement, osteoclast differentiation assay Frontiers in endocrinology Medium 37152948
2023 ECSIT loss in intestinal epithelium leads to metabolic reprogramming toward amino acid-based metabolism, demethylation and upregulation of eIF4F pathway genes, enhanced YAP protein translation, and transformation of intestinal cells to stem-like cells promoting tumorigenesis. Intestinal cell-specific ECSIT knockout mouse, metabolomics, methylation analysis, polysome profiling, Western blot, intestinal organoids Advanced science Medium 37409430
2024 ECSIT mediates memory CD8+ T cell differentiation by controlling fumarate synthesis; ECSIT ablation in T cells causes loss of fumarate, leading to KDM5-mediated demethylation of the TCF-1 promoter and abrogation of TCF-1 expression, impairing memory CD8+ T cell development. T cell-specific ECSIT knockout, metabolomics (fumarate measurement), ChIP/methylation analysis, viral infection model, tumor models Nature cell biology High 38326554
2025 A 42-kDa ECSIT isoform (ECSIT-X4) localizes to mitochondria of adult cardiomyocytes and interacts with STAT3, increasing 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 knockout mouse, co-immunoprecipitation with STAT3, mitochondrial fractionation, Seahorse metabolic flux, TAC surgical model Advanced science Medium 39746855
2014 Hepatitis B virus X protein (HBx) augments IL-1β-induced NF-κB activation by directly interacting with ECSIT (via HBx aa 51-80); co-expression of HBx and ECSIT increases IKK and IκB phosphorylation, and ECSIT knockdown abolishes this augmentation. GST pulldown, co-immunoprecipitation, CytoTrap two-hybrid, deletion mutagenesis, siRNA knockdown, NF-κB reporter assay Virus research Medium 25449573
2026 Mitochondria-targeted ECSIT overexpression promotes localization of the deubiquitinase OTUD3 to mitochondria; OTUD3 then stabilizes SIRT3 via deubiquitination, inhibiting mitochondrial DNA oxidation and alleviating metabolic disorders in MASH. Mitochondria-targeted ECSIT transgenic mice, co-immunoprecipitation, deubiquitination assay, HFHC/MCD diet MASH models, mitochondrial fractionation Advanced science Medium 41640247
2025 Mycobacterium tuberculosis HBHA virulence factor binds directly to ECSIT, disrupting the ECSIT-TRAF6 complex and inhibiting ECSIT ubiquitination in BCG-infected macrophages, thereby suppressing autophagy and promoting intracellular mycobacterial persistence; ECSIT deficiency abolishes HBHA-mediated autophagy suppression. Direct binding assay, co-immunoprecipitation, ECSIT knockdown (RAW264.7), LC3-II/Beclin-1 autophagy assay, intracellular bacterial survival assay Frontiers in immunology Medium 41209015
2026 ECSIT stabilizes the β-catenin complex and sustains Wnt signaling, regulating Lgr5+ intestinal stem cell proliferation and differentiation; intestinal epithelium-specific ECSIT knockout reduces β-catenin nuclear translocation and Lgr5 stem cell numbers, worsening chemotherapy-induced intestinal mucositis. Intestinal epithelium-specific ECSIT knockout mouse, Lgr5-specific inducible knockout, single-cell RNA-seq, β-catenin nuclear fractionation, ECSIT complementation rescue Life sciences Medium 41611204

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 257 10465784
2007 Cytosolic signaling protein Ecsit also localizes to mitochondria where it interacts with chaperone NDUFAF1 and functions in complex I assembly. Genes & development 158 17344420
2014 TAK1-ECSIT-TRAF6 complex plays a key role in the TLR4 signal to activate NF-κB. The Journal of biological chemistry 86 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 71 29514094
2018 Recurrent ECSIT mutation encoding V140A triggers hyperinflammation and promotes hemophagocytic syndrome in extranodal NK/T cell lymphoma. Nature medicine 57 29291352
2017 Peroxiredoxin-6 Negatively Regulates Bactericidal Activity and NF-κB Activity by Interrupting TRAF6-ECSIT Complex. Frontiers in cellular and infection microbiology 39 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 30 25355951
2014 ECSIT bridges RIG-I-like receptors to VISA in signaling events of innate antiviral responses. Journal of innate immunity 27 25228397
2017 ECSIT links TLR and BMP signaling in FOP connective tissue progenitor cells. Bone 23 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
2019 CRBN Is a Negative Regulator of Bactericidal Activity and Autophagy Activation Through Inhibiting the Ubiquitination of ECSIT and BECN1. Frontiers in immunology 22 31620128
2014 Role of evolutionarily conserved signaling intermediate in Toll pathways (ECSIT) in the antibacterial immunity of Marsupenaeus japonicus. Developmental and comparative immunology 18 24796866
2007 The nexus of iron and inflammation in hepcidin regulation: SMADs, STATs, and ECSIT. Hepatology (Baltimore, Md.) 17 17187402
2019 p62 Negatively Regulates TLR4 Signaling via Functional Regulation of the TRAF6-ECSIT Complex. Immune network 16 31281713
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
2021 ECSIT is a critical limiting factor for cardiac function. JCI insight 14 34032637
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
2024 ECSIT facilitates memory CD8+ T cell development by mediating fumarate synthesis during viral infection and tumorigenesis. Nature cell biology 13 38326554
2022 The ECSIT Mediated Toll3-Dorsal-ALFs Pathway Inhibits Bacterial Amplification in Kuruma Shrimp. Frontiers in immunology 13 35173723
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 8 39488037
2020 Identification, characterization, and functional analysis of Toll and ECSIT in Exopalaemon carinicauda. Developmental and comparative immunology 8 33238179
2023 Tissue-specific differences in the assembly of mitochondrial Complex I are revealed by a novel ENU mutation in ECSIT. Cardiovascular research 7 37395010
2022 Molecular characterization of the evolutionary conserved signaling intermediate in Toll pathways (ECSIT) of soiny mullet (Liza haematocheila). Fish & shellfish immunology 6 36087818
2025 ECSIT-X4 is Required for Preventing Pressure Overload-Induced Cardiac Hypertrophy via Regulating Mitochondrial STAT3. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 5 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
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
2025 HBHA-ECSIT interaction disrupts macrophage autophagy to promote Mycobacterium tuberculosis persistence. Frontiers in immunology 0 41209015