Affinage

TNIP2

TNFAIP3-interacting protein 2 · UniProt Q8NFZ5

Length
429 aa
Mass
48.7 kDa
Annotated
2026-06-10
37 papers in source corpus 19 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/7 claims corpus-supported (86%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TNIP2/ABIN-2 is a multifunctional ubiquitin-binding adaptor that operates at the intersection of NF-κB and ERK MAP kinase signaling downstream of innate immune and inflammatory receptors (PMID:11390377, PMID:15169888, PMID:16633345). It is a stable component of a ternary complex with the kinase TPL-2 and NF-κB1 p105 in macrophages, where it is required for TPL-2 protein stability; loss of TNIP2 collapses steady-state TPL-2 levels and consequently blunts ERK activation downstream of TLR4, TNFR1, and CD40, while receptor-induced TPL-2 activation correlates with its release from TNIP2 (PMID:15169888, PMID:16633345, PMID:19754427). As a structural subunit it also reshapes the catalytic properties of TPL-2, altering substrate selection and inhibitor sensitivity relative to the isolated kinase domain (PMID:29229763). Independently of this scaffolding role, TNIP2 restrains NF-κB activation upstream of the IKK complex by binding A20 and by binding IKKγ (NEMO) to block RIP recruitment (PMID:11390377, PMID:14653779), and it engages linear (M1-linked) polyubiquitin through its AHD1-UBAN module, whose crystal structure with linear tri-ubiquitin reveals a 2:1 ubiquitin-bridged dimer-of-dimers architecture (PMID:27916521). Genetic dissection separates these activities: a ubiquitin-binding mutant retains TPL-2 stabilization but loses its ability to suppress DSS colitis via a COX2/PGE2 pathway, while an A20-binding mutant exacerbates allergic airway inflammation, both occurring independently of TPL-2 catalytic activity (PMID:30355787, PMID:30337469). TNIP2 protein abundance is controlled by ubiquitin-dependent turnover, with USP35 stabilizing it through deubiquitination (PMID:26348204). Beyond immune signaling, TNIP2 binds the activated Tie2 receptor to promote PI3K-dependent endothelial survival (PMID:12609966, PMID:12933576) and post-transcriptionally destabilizes BACE1 mRNA through its 3'UTR (PMID:37085111).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 2001 High

    Established TNIP2/ABIN-2 as an A20-binding inhibitor of NF-κB acting upstream of the IKK complex, defining its initial role as a brake on inflammatory signaling.

    Evidence Co-expression/interaction assays and NF-κB reporter epistasis with overexpressed pathway components

    PMID:11390377

    Open questions at the time
    • Mechanism by which A20 binding restrains IKK was not resolved
    • Endogenous-level validation absent
  2. 2003 Medium

    Identified a non-immune function: TNIP2 binds activated Tie2 (not Tie1) and mediates angiopoietin-1-driven endothelial survival via PI3K, showing the adaptor couples to receptor tyrosine kinase signaling.

    Evidence Yeast two-hybrid, co-IP in CHO cells, deletion mapping, apoptosis assays with pharmacological PI3K inhibition in endothelial cells

    PMID:12609966 PMID:12933576

    Open questions at the time
    • TNIP2 is not phosphorylated by Tie2, so the signaling output mechanism is unresolved
    • Downstream effectors linking TNIP2 to PI3K not defined
    • In vivo endothelial relevance untested
  3. 2004 High

    Resolved a molecular mechanism for NF-κB inhibition and revealed the scaffolding role: TNIP2 binds IKKγ to block RIP recruitment, and forms a TPL-2/p105 ternary complex required for TPL-2 protein stability.

    Evidence Co-IP and deletion mapping in overexpression systems; affinity purification, RNAi, and pulse-chase half-life assays in bone marrow-derived macrophages

    PMID:14653779 PMID:15169888

    Open questions at the time
    • How TNIP2 binding protects TPL-2 from degradation was not defined
    • Relationship between IKKγ-binding and TPL-2-stabilizing functions unclear
  4. 2006 High

    Genetic knockout established that TNIP2 positively regulates ERK signaling by stabilizing TPL-2 across multiple receptors, dissociating its ERK role from NF-κB regulation in vivo.

    Evidence ABIN-2-deficient mice with Erk/MAP kinase and NF-κB assays in primary macrophages and B cells; transgenic liver overexpression in a hepatectomy model

    PMID:16480954 PMID:16633345

    Open questions at the time
    • NF-κB regulatory role seen in overexpression not reflected in knockout phenotype
    • Reconciliation of NF-κB-inhibitory versus ERK-stabilizing functions incomplete
  5. 2009 Medium

    Showed that receptor-triggered dissociation of TPL-2 from TNIP2 is a discrete activation step independent of IRAK1 and IKKβ, refining how the complex is activated.

    Evidence Co-IP of transfected proteins in IRAK1-null HEK-293 cells with pharmacological inhibitors and kinase assays

    PMID:19754427

    Open questions at the time
    • Identity of the PP2-sensitive kinase driving dissociation unknown
    • Endogenous validation of dissociation kinetics lacking
  6. 2011 Medium

    Revealed an IKKα-specific positive function: TNIP2 promotes IKKα autophosphorylation and transcription of select NF-κB target genes in a manner dependent on serine 146.

    Evidence Affinity purification, co-IP, proteasome inhibitor and kinase assays, S146 mutagenesis, NF-κB reporters

    PMID:21784860

    Open questions at the time
    • Single lab; how S146 controls IKKα activation unclear
    • Physiological gene targets in vivo not defined
  7. 2015 Medium

    Identified USP35 as a deubiquitinase that stabilizes TNIP2 protein, placing TNIP2 abundance under ubiquitin-dependent control to tune NF-κB output.

    Evidence Co-IP, deubiquitination assay, overexpression/knockdown with NF-κB reporters and xenograft

    PMID:26348204

    Open questions at the time
    • The E3 ligase that ubiquitinates TNIP2 not identified
    • Ubiquitin linkage type and sites on TNIP2 unresolved
  8. 2016 High

    Determined the structural basis of linear ubiquitin recognition by the TNIP2 AHD1-UBAN module and mapped a broader interaction network including ESCRT-I and select mRNAs.

    Evidence X-ray crystallography of AHD1-UBAN with linear tri-ubiquitin plus ITC and mutagenesis; Halo AP-MS, point-mutant mapping, and RNA-Seq of associated mRNAs

    PMID:27609421 PMID:27916521

    Open questions at the time
    • Functional consequence of ESCRT-I (TSG101) and KHDRBS1 associations not established
    • Significance of mRNA association for the transcription-related targets unclear
  9. 2017 High

    Showed the p105-TNIP2-TPL-2 complex incorporates RelAp43 and is targeted by rabies virus M protein, which displaces TNIP2 to reprogram NF-κB-dependent antiviral and inflammatory gene expression.

    Evidence TAP-MS, protein-fragment complementation, BRET, and recombinant rabies viruses in mice

    PMID:29084252

    Open questions at the time
    • Direct binding interface between M protein and TNIP2 not mapped
    • Generality beyond rabies infection unknown
  10. 2018 High

    Genetic knock-in mutants cleanly separated TNIP2 adaptor and ubiquitin-binding functions from TPL-2 kinase activity, attributing colitis and allergic airway phenotypes to TNIP2-specific, kinase-independent activities.

    Evidence ABIN2[D310N] and A20-binding knock-in mice, kinase-dead TPL-2 mice, DSS colitis and HDM airway models, COX2/PGE2 measurement; peptide-library substrate profiling of the native complex

    PMID:29229763 PMID:30337469 PMID:30355787

    Open questions at the time
    • Cell-type-specific contributions of ubiquitin-binding to PGE2 production partly undefined
    • How ubiquitin-binding drives COX2 expression mechanistically unclear
  11. 2023 Medium

    Extended TNIP2 function to post-transcriptional control, showing it destabilizes BACE1 mRNA via 3'UTR binding to reduce amyloidogenic processing.

    Evidence Overexpression in APP-expressing cells, Western blots for BACE1/ADAM10/C99/Aβ, 3'UTR luciferase reporter and mRNA stability assays

    PMID:37085111

    Open questions at the time
    • Direct RNA-binding by TNIP2 versus an intermediary not distinguished
    • Endogenous and in vivo relevance to amyloid pathology untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the distinct TNIP2 functions — TPL-2 stabilization, IKKγ/A20-mediated NF-κB inhibition, linear-ubiquitin sensing, RTK survival signaling, and mRNA destabilization — are coordinated within a single cell, and what regulates partitioning of TNIP2 among these activities, remains unresolved.
  • No unified model linking adaptor, ubiquitin-binding, and RNA-regulatory roles
  • Stoichiometry and competition among partners in vivo unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0098772 molecular function regulator activity 3 GO:0003723 RNA binding 2
Localization
GO:0005829 cytosol 2 GO:0005634 nucleus 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-168256 Immune System 3 R-HSA-5357801 Programmed Cell Death 1
Partners
CHUKIKBKGMAP3K8NFKB1RIPK1TEKTNFAIP3USP35
Complex memberships
TPL-2/NF-κB1 p105/ABIN-2 ternary complex

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 ABIN-2 (TNIP2) binds to the C-terminal zinc finger domain of A20 and inhibits NF-κB activation induced by TNF and IL-1, as well as by overexpression of RIP or TRAF2, but not by overexpression of IKKβ or direct IKK activators such as Tax, indicating that ABIN-2 acts upstream of the IKK complex. Co-expression/interaction assays, NF-κB reporter gene assays, overexpression of pathway components The Journal of biological chemistry High 11390377
2003 ABIN-2 interacts with the intracellular domain of the endothelial receptor tyrosine kinase Tie2, but not Tie1. The interaction requires Tie2 autophosphorylation, is stimulated by angiopoietin-1, and maps to residues 171–272 of ABIN-2. ABIN-2 is not tyrosine-phosphorylated by Tie2. Expression of ABIN-2 deletion mutants suppressed angiopoietin-1-mediated inhibition of NF-κB-dependent reporter activity in endothelial cells. Yeast two-hybrid screening, co-expression in CHO cells (co-immunoprecipitation), deletion mapping, NF-κB reporter assays in endothelial cells Circulation research High 12609966
2003 ABIN-2 inhibits endothelial cell apoptosis and rescues cells from death following growth factor deprivation. This anti-apoptotic function requires the carboxy-terminus of ABIN-2 and is dependent on PI3-kinase activity. Expression of truncated ABIN-2 blocked angiopoietin-1/Tie2-mediated endothelial survival. Overexpression of ABIN-2 and deletion mutants in endothelial cells, apoptosis assays, pharmacological PI3K inhibition (wortmannin, LY294002) Blood Medium 12933576
2003 ABIN-2 can enter the nucleus and functions as a transcriptional coactivator in yeast; only the C-terminal fragment activates transcription in mammalian cells. The N-terminal 195 amino acids retain full-length ABIN-2 in the cytoplasm of mammalian cells. ABIN-2 interacts with BAF60a, a component of the chromatin-remodeling complex, in a yeast two-hybrid assay. GAL4-fusion reporter assays in yeast, subcellular localization in mammalian cells, yeast two-hybrid (BAF60a interaction) FEBS letters Low 12753905
2004 ABIN-2 inhibits NF-κB activation by binding to IKKγ (NEMO) and blocking the association of IKKγ with RIP. A stretch of 50 amino acids in ABIN-2 is essential for IKKγ binding; an ABIN-2 mutant lacking these 50 amino acids neither binds IKKγ nor inhibits NF-κB. A homologous region in RIP is also required for RIP-IKKγ interaction. Co-immunoprecipitation, deletion mapping in overexpression system, NF-κB reporter assays, apoptosis assays The Biochemical journal Medium 14653779
2004 ABIN-2 forms a ternary complex with TPL-2 and NF-κB1 p105 in macrophages. ABIN-2 is required for TPL-2 protein stability: RNAi-mediated depletion of ABIN-2 dramatically reduces steady-state TPL-2 protein levels without affecting TPL-2 mRNA or p105 levels, and ABIN-2 increases the half-life of co-transfected TPL-2. TPL-2 that can activate MEK after LPS stimulation is not associated with ABIN-2, and LPS-induced activation of TPL-2 correlates with its release from ABIN-2. Affinity purification, co-immunoprecipitation, RNAi knockdown, pulse-chase half-life assay, endogenous complex characterization in bone marrow-derived macrophages Molecular and cellular biology High 15169888
2006 ABIN-2-deficient mice show reduced activation of Erk MAP kinase downstream of TPL-2-coupled receptors (TLR4 in macrophages, TNFR1 in macrophages, CD40 in B cells), establishing that ABIN-2 positively regulates ERK signaling by stabilizing TPL-2. ABIN-2 deficiency does not affect agonist-induced NF-κB regulation. Genetic knockout mice, Erk/MAP kinase activity assays in primary antigen-presenting cells, NF-κB activity assays, Western blot for TPL-2 protein levels Nature immunology High 16633345
2009 IL-1 triggers dissociation of TPL-2 from ABIN-2 independently of IRAK1, IKKβ, and the PP2-sensitive kinase, identifying dissociation from ABIN-2 as a distinct signaling event upstream of TPL-2 activation. IL-1 also activates TPL-2 via an IRAK1- and IKKβ-independent but PP2-sensitive mechanism distinct from the p105 phosphorylation pathway. Co-immunoprecipitation of transfected Tpl2 and ABIN-2 in IRAK1-null HEK-293 cells, pharmacological inhibitors (PS1145, PP2), kinase activity assays The Biochemical journal Medium 19754427
2011 IKKα and IKKβ both interact with ABIN-2 and impair its constitutive proteasomal degradation. ABIN-2 specifically enhances IKKα- but not IKKβ-mediated NF-κB activation by inducing IKKα autophosphorylation and kinase activity. ABIN-2 serine 146 is critical for IKKα-driven transcriptional upregulation of specific NF-κB target genes. Affinity purification of IKKα-associated proteins, co-immunoprecipitation, proteasome inhibitor assays, kinase activity assays, site-directed mutagenesis (S146), NF-κB reporter assays The Journal of biological chemistry Medium 21784860
2015 USP35 deubiquitinase stabilizes ABIN-2 protein by promoting its deubiquitination, thereby inhibiting TNFα-induced NF-κB activation. Overexpression of ABIN-2 rescues the NF-κB activation caused by USP35 loss. Co-immunoprecipitation, deubiquitination assay, overexpression and knockdown, NF-κB reporter assays, in vivo xenograft Oncotarget Medium 26348204
2016 Crystal structure of the AHD1-UBAN fragment of ABIN-2 in complex with linear tri-ubiquitin reveals a 2:1 (ABIN-2:tri-ubiquitin) stoichiometry. The interaction occurs primarily through a primary ubiquitin-binding site, with a secondary site engaged under high local concentration. Three ubiquitin units form a right-handed helical trimer bridging two ABIN-2 dimers. Residues around the M1-linkage are crucial for recognition; mutagenesis confirmed functional significance. X-ray crystallography, mutagenesis, pull-down assays, isothermal titration calorimetry (ITC) Structure High 27916521
2016 AP-MS mapping shows TNIP2 is an NF-κB network hub. NF-κB interacts with the N-terminal region of TNIP2. A central region of TNIP2 interacts with ESCRT-I complex via TSG101; a single point mutation in TNIP2 disrupts this interaction. TNIP2 associates with a specific limited set of mRNAs enriched for transcription-related functions (including Sin3A complex, Mediator complex, JUN, HOXC6, GATA2 mRNAs), and RNA-dependent protein interactions include KHDRBS1. MudPIT/Halo Affinity Purification Mass Spectrometry (AP-MS), deletion and point mutant mapping, RNA-Seq of TNIP2-associated RNAs, RNA depletion experiments Molecular & cellular proteomics Medium 27609421
2017 RelAp43 associates with the p105-ABIN-2-TPL-2 ternary complex; RelAp43-p105 interaction stabilizes the formation of a complex with ABIN-2 and TPL-2. Rabies virus M protein interacts with ABIN-2 (and TPL-2 and RelAp43) and promotes the release of ABIN-2 from this complex, thereby favoring RelAp43-p50 NF-κB dimer production and controlling IFNβ, TNF, and CXCL2 expression. Tandem affinity purification coupled with mass spectrometry (TAP-MS), protein-fragment complementation assay, bioluminescent resonance energy transfer (BRET), recombinant rabies viruses in mice PLoS pathogens High 29084252
2018 The ubiquitin-binding function of ABIN-2 (residue D310) is not required for TPL-2 stability or its activation by TLR agonists or IL-1β, but is required to suppress DSS-induced colitis. ABIN-2 ubiquitin-binding promotes COX2 expression and PGE2 secretion in intestinal myofibroblasts via a Tpl2 kinase-independent pathway. The hypersensitivity of Tpl2 KO mice to DSS-colitis is attributed to loss of ABIN-2, not loss of TPL-2 catalytic activity. Knock-in mouse (ABIN2[D310N]), DSS colitis model, bone marrow transplantation, MEF and intestinal myofibroblast assays, pharmacological Tpl2 inhibition, COX2/PGE2 measurement Journal of immunology High 30355787
2018 ABIN-2 (TNIP2) is a negative regulator of allergic airway inflammation. Tnip2 knock-in mutation reducing ABIN-2 binding to A20 augments HDM-induced airway inflammation without affecting TPL-2 expression or signaling. TPL-2 kinase dead mice have unaltered responses to HDM, indicating that the allergic phenotype of Map3k8−/− mice is due to loss of TPL-2 adaptor function (i.e., reduced ABIN-2 levels) rather than loss of TPL-2 kinase activity. Knock-in mice (kinase-dead TPL-2, Tnip2 A20-binding mutant), house dust mite (HDM) allergic airway inflammation model, TPL-2 signaling assays The Journal of experimental medicine High 30337469
2018 The optimal substrate specificity of the TPL-2/NF-κB1 p105/ABIN-2 complex was determined using a positional scanning peptide library. The complex shows significantly altered sensitivity to existing ATP-competitive TPL-2 inhibitors compared to the isolated TPL-2 kinase domain, indicating that ABIN-2 (and p105) alter the catalytic properties of TPL-2. Positional scanning peptide library, high-throughput mass spectrometry kinase assay with the tripartite complex The Biochemical journal Medium 29229763
2006 ABIN-2 is rapidly and transiently induced after partial hepatectomy. Transgenic overexpression of ABIN-2 in liver inhibits NF-κB nuclear translocation post-hepatectomy, impairs G1/S transition, and delays hepatocyte cell cycle progression. Overexpression also suppresses endogenous ABIN-2 mRNA induction, suggesting a negative feedback mechanism. Transgenic mouse overexpression, partial hepatectomy model, NF-κB nuclear translocation assay, BrdU incorporation/cell cycle analysis, RT-PCR Biochemical and biophysical research communications Medium 16480954
2021 Overexpression of GRβ (glucocorticoid receptor beta) promotes TNIP2 mRNA levels in human monocytes. Depletion of TNIP2 partially attenuates GRβ-mediated enhancement of TNF-α expression, indicating that TNIP2 is required for GRβ-promoted TNF-α production. GRβ overexpression in human monocytes, siRNA knockdown of TNIP2, RT-PCR for mRNA levels Brain, behavior, and immunity Low 33932528
2023 TNIP2 overexpression decreases BACE1 protein levels, reduces Aβ peptides (Aβ40 and Aβ42) and C99 in APP-expressing cells, without affecting α-secretase (ADAM10) levels. TNIP2 promotes degradation of BACE1 mRNA by binding to its 3'UTR, as confirmed by luciferase reporter assay with reduced activity upon TNIP2 binding. Overexpression in SH-SY5Y-APP and HEK-APP cells, Western blot for BACE1/ADAM10/C99/Aβ, luciferase 3'UTR reporter assay, mRNA stability assay Neuroscience letters Medium 37085111

Source papers

Stage 0 corpus · 37 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2003 The antiinflammatory endothelial tyrosine kinase Tie2 interacts with a novel nuclear factor-kappaB inhibitor ABIN-2. Circulation research 130 12609966
2001 Identification of a novel A20-binding inhibitor of nuclear factor-kappa B activation termed ABIN-2. The Journal of biological chemistry 85 11390377
2004 ABIN-2 forms a ternary complex with TPL-2 and NF-kappa B1 p105 and is essential for TPL-2 protein stability. Molecular and cellular biology 82 15169888
2006 ABIN-2 is required for optimal activation of Erk MAP kinase in innate immune responses. Nature immunology 74 16633345
2003 ABIN-2 protects endothelial cells from death and has a role in the antiapoptotic effect of angiopoietin-1. Blood 59 12933576
2004 Identification of a novel mechanism of NF-kappaB inactivation by progesterone through progesterone receptors in Hec50co poorly differentiated endometrial cancer cells: induction of A20 and ABIN-2. Gynecologic oncology 52 15297189
2017 MiR-663a/MiR-423-5p are involved in the pathogenesis of lupus nephritis via modulating the activation of NF-κB by targeting TNIP2. American journal of translational research 40 28861170
2020 microRNA-15a-5p participates in sepsis by regulating the inflammatory response of macrophages and targeting TNIP2. Experimental and therapeutic medicine 34 32256793
2015 USP35 activated by miR let-7a inhibits cell proliferation and NF-κB activation through stabilization of ABIN-2. Oncotarget 34 26348204
2016 MiR-1180 promoted the proliferation of hepatocellular carcinoma cells by repressing TNIP2 expression. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 30 27044843
2004 The inhibitor ABIN-2 disrupts the interaction of receptor-interacting protein with the kinase subunit IKKgamma to block activation of the transcription factor NF-kappaB and potentiate apoptosis. The Biochemical journal 30 14653779
2017 Regulation of NF-κB by the p105-ABIN2-TPL2 complex and RelAp43 during rabies virus infection. PLoS pathogens 29 29084252
2016 TNIP2 is a Hub Protein in the NF-κB Network with Both Protein and RNA Mediated Interactions. Molecular & cellular proteomics : MCP 28 27609421
2011 A20-binding inhibitor of nuclear factor-kappaB (NF-kappaB)-2 (ABIN-2) is an activator of inhibitor of NF-kappaB (IkappaB) kinase alpha (IKKalpha)-mediated NF-kappaB transcriptional activity. The Journal of biological chemistry 27 21784860
2015 Characterization and structure prediction of partial length protein sequences of pcoA, pcoR and chrB genes from heavy metal resistant bacteria from the Klip River, South Africa. International journal of molecular sciences 23 25837632
2021 TNIP2 mediates GRβ-promoted inflammation and is associated with severity of major depressive disorder. Brain, behavior, and immunity 22 33932528
2019 ABIN-2, of the TPL-2 Signaling Complex, Modulates Mammalian Inflammation. Trends in immunology 20 31401161
2018 A20-binding inhibitor of NF-κB (ABIN) 2 negatively regulates allergic airway inflammation. The Journal of experimental medicine 19 30337469
2016 Structural Insights into Linear Tri-ubiquitin Recognition by A20-Binding Inhibitor of NF-κB, ABIN-2. Structure (London, England : 1993) 18 27916521
2009 IRAK1-independent pathways required for the interleukin-1-stimulated activation of the Tpl2 catalytic subunit and its dissociation from ABIN2. The Biochemical journal 17 19754427
2013 Ebola virus VP35 induces high-level production of recombinant TPL-2-ABIN-2-NF-κB1 p105 complex in co-transfected HEK-293 cells. The Biochemical journal 16 23557442
2019 The clinical responses of TNIP2-ALK fusion variants to crizotinib in ALK-rearranged lung adenocarcinoma. Lung cancer (Amsterdam, Netherlands) 15 31521978
2017 Protective Role of TNIP2 in Myocardial Injury Induced by Acute Pancreatitis and Its Mechanism. Medical science monitor : international medical journal of experimental and clinical research 15 29176547
2023 Aberrant Histone Modification of TNFAIP3, TLR4, TNIP2, miR-146a, and miR-155 in Major Depressive Disorder. Molecular neurobiology 14 37148522
2021 Novel TNIP2 and TRAF2 Variants Are Implicated in the Pathogenesis of Pulmonary Arterial Hypertension. Frontiers in medicine 14 33996849
2022 Hyperoxia Induced Bronchopulmonary Dysplasia-Like Inflammation via miR34a-TNIP2-IL-1β Pathway. Frontiers in pediatrics 10 35433535
2003 The A20-binding protein ABIN-2 exerts unexpected function in mediating transcriptional coactivation. FEBS letters 9 12753905
2018 ABIN2 Function Is Required To Suppress DSS-Induced Colitis by a Tpl2-Independent Mechanism. Journal of immunology (Baltimore, Md. : 1950) 8 30355787
2006 Overexpression of ABIN-2, a negative regulator of NF-kappaB, delays liver regeneration in the ABIN-2 transgenic mice. Biochemical and biophysical research communications 8 16480954
2023 TNIP2 inhibits amyloidogenesis by regulating the 3'UTR of BACE1: An in vitro study. Neuroscience letters 6 37085111
2019 Expression and role of TNIP2 in multiple organ dysfunction syndrome following severe trauma. Molecular medicine reports 6 30720079
2023 Protective effect of TNIP2 on the inflammatory response of microglia after spinal cord injury in rats. Neuropeptides 5 37329819
2024 Propofol Ameliorates Spinal Cord Injury Process by Mediating miR-672-3p/TNIP2 Axis. Biochemical genetics 3 38379038
2022 Long noncoding RNA NAV2-AS5 relieves chondrocyte inflammation by targeting miR-8082/TNIP2 in osteoarthritis. Cell cycle (Georgetown, Tex.) 3 36503346
2026 Atractylenolide II alleviates LPS-induced acute lung injury in A549 cells via the TNIP2/NF-κB pathway. Journal of cardiothoracic surgery 0 41992343
2025 Icariside II Alleviates Chondrocyte Inflammatory Injury by Inhibiting the TNIP2/NF-κB Pathway. Cell biochemistry and biophysics 0 39775470
2018 Assaying kinase activity of the TPL-2/NF-κB1 p105/ABIN-2 complex using an optimal peptide substrate. The Biochemical journal 0 29229763

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