Affinage

STK38

Serine/threonine-protein kinase 38 · UniProt Q15208

Length
465 aa
Mass
54.2 kDa
Annotated
2026-06-10
34 papers in source corpus 23 papers cited in narrative 23 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

STK38 (NDR1) is a serine/threonine kinase that functions as a context-dependent signaling hub, acting through both catalytic and kinase-independent mechanisms across the Hippo, autophagy, MAPK, and DNA-damage response programs (PMID:17906693, PMID:26387716, PMID:42128666). As a negative regulator of MAPK signaling, STK38 binds MEKK1/2 and suppresses MEKK2 autophosphorylation, and it constitutively associates with the E3 ligase Smurf1 to promote K48-linked ubiquitination and degradation of MEKK2, thereby restraining TLR9/ERK-driven inflammatory cytokine output (PMID:17906693, PMID:25981615). STK38 is a core regulator of autophagy: it binds Beclin1, supports Exo84-RalB-Beclin1 complex assembly, and promotes autophagosome formation and Vps34/PI3P activity (PMID:26387716). Within the Hippo pathway it exerts dual, opposing control of YAP1 — phosphorylating and deactivating YAP1 in quiescent cells (an activity reversed when STK38 is degraded by autophagy during tissue regeneration), while also competitively binding MOB1 to disrupt the LATS-MOB1 complex and inhibit LATS in a kinase-independent, evolutionarily conserved manner (PMID:42128666, PMID:41911447). STK38 additionally phosphorylates XPO1 at Ser1055 to activate XPO1-dependent nuclear export, controlling its own nucleocytoplasmic shuttling as well as that of Beclin1 and YAP1 (PMID:31544310). Beyond catalysis, STK38 acts as a reader of monoufmylated histone H4 (Lys31) that recruits SUV39H1 to DNA double-strand breaks to promote ATM activation (PMID:32537488). Further substrates and partners place STK38 in ferroptosis resistance (GPX4 Ser45), lysosomal membrane repair (DOK1), and oncogenic Ras programs (PMID:41145774, PMID:37987447, PMID:27283898).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2007 High

    Established STK38 as a negative regulator of MAPK signaling by defining its direct, non-phosphorylating action on MEKK1/2.

    Evidence Co-IP, in vitro kinase assays, shRNA, and domain mapping showing STK38 binds MEKK1/2 catalytic domains and suppresses MEKK2 autophosphorylation

    PMID:17906693

    Open questions at the time
    • Mechanism by which binding suppresses autophosphorylation not resolved
    • Physiological contexts of this regulation untested in this study
  2. 2012 Medium

    Linked STK38 kinase activity to control of MYC stability and to NF-κB activation, revealing pro-survival and pro-inflammatory roles.

    Evidence Kinase-dead mutants, knockdown, protein stability assays, and NF-κB reporter/Co-IP with TRAF2 in B-cell and TNFα systems

    PMID:22674419 PMID:23178486

    Open questions at the time
    • Direct substrate phosphorylation underlying MYC stabilization not biochemically resolved
    • NF-κB findings rest on reporter/Co-IP from a single lab
  3. 2015 High

    Defined two distinct STK38 functions: facilitating Smurf1-mediated MEKK2 degradation to limit innate immune signaling, and promoting autophagosome formation via Beclin1/exocyst.

    Evidence Reciprocal Co-IP, ubiquitination assays, STK38 knockout mice and sepsis model; yeast two-hybrid plus LC3B/PI3P assays and Drosophila genetics

    PMID:25981615 PMID:26387716

    Open questions at the time
    • Whether STK38 kinase activity is required for Smurf1/MEKK2 degradation not fully defined
    • Direct STK38 substrate in the autophagy machinery not identified
  4. 2016 Medium

    Placed STK38 upstream of PINK1/Parkin mitophagy to support oncogenic Ras transformation.

    Evidence shRNA, genetic epistasis with PINK1/Parkin/USP30, soft agar and xenograft assays in Ras-transformed cells

    PMID:27283898

    Open questions at the time
    • Molecular connection between STK38 and PINK1/Parkin not biochemically defined
    • Single lab
  5. 2017 High

    Identified STK38 as a degradation target (SOCS2-Cullin5) and as a kinase acting on Rbm24, expanding its regulatory inputs and substrate repertoire.

    Evidence MS, Co-IP, ubiquitination assays, SOCS2-/- colitis model; Co-IP/MS and inhibitor/activator effects on Rbm24 and sarcomere assembly

    PMID:28216640 PMID:28322254

    Open questions at the time
    • Rbm24 phospho-sites not mapped
    • How SOCS2-driven turnover integrates with STK38 signaling outputs unclear
  6. 2018 Medium

    Showed Kir2.1 antagonizes the STK38/Smurf1/MEKK2 axis to drive cancer EMT, reinforcing the established degradation mechanism in a disease context.

    Evidence Co-IP, ubiquitination assay, knockdown, invasion/migration and metastasis models in gastric cancer

    PMID:29549164

    Open questions at the time
    • Direct effect of Kir2.1 on STK38 catalytic state not defined
    • Single lab
  7. 2019 High

    Revealed STK38 as an activator of XPO1-dependent nuclear export and defined a reciprocal regulatory loop where MEKK2 phosphorylates STK38 to protect it from calpain cleavage; also identified kinase-independent inhibition of BAG3-mediated CASA.

    Evidence Proximity labeling, phospho-site mutagenesis, fractionation and imaging (XPO1 S1055); in vitro calpain/MEKK2 reconstitution (Ser91); Co-IP and autophagy flux (BAG3)

    PMID:31326538 PMID:31544310 PMID:31690749

    Open questions at the time
    • Full set of XPO1 cargoes regulated by STK38 not enumerated
    • Physiological triggers of MEKK2-STK38 phospho-protection beyond hyperthermia unclear
  8. 2020 High

    Established a kinase-independent chromatin function for STK38 as a reader of ufmylated histone H4 that drives ATM activation at DNA double-strand breaks.

    Evidence Co-IP, ChIP, UFM1-binding-motif and kinase-dead mutants, H3K9me3/Tip60 activity assays

    PMID:32537488

    Open questions at the time
    • Single lab
    • How STK38 recruitment to breaks is temporally coordinated with repair not defined
  9. 2021 Medium

    Extended STK38's kinase-independent scaffold roles to metabolism via PPARγ stabilization and adipogenesis.

    Evidence Pulldown/MS, Co-IP, reporter and cycloheximide-chase half-life assays, kinase-dead mutant

    PMID:34670478

    Open questions at the time
    • Mechanism of PPARγ stabilization not resolved
    • Single lab
  10. 2023 Medium

    Expanded the substrate/partner network to DOK1 (lysosomal repair and senescence), NLRP12/GSK3β (Wnt suppression), and TBK1/AMPK (hepatic inflammation and lipogenesis).

    Evidence Phosphorylation and recruitment imaging with C. elegans genetics (DOK1); Co-IP and Nlrp12 knockout mice; Co-IP and in vivo HFD liver model (TBK1/AMPK)

    PMID:37028764 PMID:37581937 PMID:37987447

    Open questions at the time
    • Precise catalytic role of STK38 on GSK3β not resolved
    • TBK1 axis rests on abstract-level kinase detail
    • Each axis from a single lab
  11. 2025 Medium

    Defined STK38 as a GPX4 Ser45 kinase conferring ferroptosis resistance and as a MerTK-complex kinase supporting Ras-driven migration.

    Evidence Co-IP, in vitro phosphorylation, CMA and lipid peroxidation assays (GPX4/SCRN1); MS, kinase-dead mutant, Rac1/Cdc42 and migration assays (MerTK)

    PMID:41145774 PMID:41226428

    Open questions at the time
    • How SCRN1 selectively enhances STK38-GPX4 interaction unclear
    • Direct MerTK phosphorylation by STK38 not established
    • Single lab each
  12. 2026 High

    Resolved STK38's dual relationship with the Hippo/YAP1 axis — kinase-independent disruption of LATS-MOB1 versus direct YAP1-deactivating phosphorylation degraded during regeneration — and added Hedgehog/KIF7 and RFC4/BECN1 autophagy roles.

    Evidence Competitive binding and Drosophila genetics (MOB1/LATS); in vivo stomach paligenosis model and NF2 Co-IP (YAP1); Co-IP/ciliary imaging (KIF7); phospho-mutant and xenograft (RFC4/BECN1 T444)

    PMID:41540036 PMID:41872171 PMID:41911447 PMID:42128666

    Open questions at the time
    • How the opposing kinase-dependent (YAP1-inhibiting) and kinase-independent (LATS-inhibiting) activities are balanced in a given cell is unresolved
    • Trigger determining autophagic degradation of STK38 during paligenosis not fully defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How a single kinase reconciles its many opposing, catalytic and non-catalytic activities into context-specific outcomes remains the central open question.
  • No unifying framework for choosing between kinase-dependent and scaffold modes
  • Structural basis for distinct partner engagement unmapped
  • Tissue-specific substrate repertoire incomplete

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 4 GO:0016740 transferase activity 3 GO:0060090 molecular adaptor activity 3 GO:0042393 histone binding 1
Localization
GO:0005634 nucleus 2 GO:0000228 nuclear chromosome 1 GO:0005829 cytosol 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-9612973 Autophagy 3 R-HSA-168256 Immune System 2 R-HSA-73894 DNA Repair 1 R-HSA-9609507 Protein localization 1
Partners
BECN1MEKK2MOB1NF2SMURF1SUV39H1XPO1YAP1
Complex memberships
Exo84-RalB-Beclin1 complexMerTK complex

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2007 STK38 physically interacts with MEKK1 and MEKK2 via their carboxy-terminal catalytic domains and negatively regulates MEKK1/2 activation by suppressing MEKK2 autophosphorylation and converting MEKK2 from its phosphorylated to non-phosphorylated form, without preventing MEKK1/2 binding to its substrate SEK1 and without phosphorylating MEKK1/2 itself. Co-immunoprecipitation, in vitro kinase assays, shRNA knockdown, domain mapping Oncogene High 17906693
2015 STK38 constitutively associates with the E3 ubiquitin ligase Smurf1 and facilitates Smurf1-mediated K48-linked ubiquitination and proteasomal degradation of MEKK2, thereby negatively regulating TLR9/CpG-induced ERK1/2 activation and downstream TNF-α and IL-6 production in macrophages. STK38-deficient mice show increased lethality upon E. coli infection and sepsis. Co-immunoprecipitation, ubiquitination assay, STK38 knockout mice, cytokine measurement, shRNA knockdown Nature communications High 25981615
2015 STK38 is a novel binding partner of Beclin1 (identified by yeast-two-hybrid), promotes autophagosome formation, supports the interaction of exocyst component Exo84 with Beclin1 and RalB, and is activated in a MOB1- and exocyst-dependent manner upon autophagy induction. STK38 depletion impairs LC3B-II conversion, ATG14L/ATG12/WIPI-1 puncta formation, and Vps34 activity (PI3P production). Yeast two-hybrid, Co-immunoprecipitation, RNAi knockdown in human cells and Drosophila, PI3P formation assay, LC3B lipidation assay Current biology : CB High 26387716
2012 STK38 regulates MYC protein stability and turnover in a kinase activity-dependent manner in human B-cell lymphoma cells; STK38 kinase inactivation abrogates apoptosis following B-cell receptor activation, and STK38 knockdown decreases MYC protein levels and increases apoptosis. Kinase-dead mutant overexpression, siRNA knockdown, protein stability assay, in vivo xenograft, regulatory network analysis Oncogene Medium 23178486
2012 STK38 (NDR1) potentiates TNFα-induced NF-κB activation in a kinase activity-dependent manner and interacts with multiple NF-κB signaling components; kinase-dead mutant fails to interact with TRAF2 and fails to enhance NF-κB activation induced by TRAF2 (but not RIP1). Co-immunoprecipitation, overexpression of kinase-dead mutants, siRNA knockdown, NF-κB reporter assay Cell biochemistry and function Medium 22674419
2017 SOCS2 (Cullin5 E3 ligase) interacts with STK38 (NDR1) and promotes its K48-linked ubiquitination and proteasomal degradation; SOCS2 overexpression antagonizes STK38-induced NF-κB activity upon TNFα stimulation, and NDR1 depletion rescues the effect of SOCS2 deficiency on NF-κB transactivation. Mass spectrometry proteomics, co-immunoprecipitation, ubiquitination assay, siRNA knockdown, SOCS2-/- mouse model of colitis Scientific reports High 28216640
2017 STK38 phosphorylates Rbm24 to regulate its protein stability in cardiomyocytes; co-immunoprecipitation with mass spectrometry identified STK38 as an endogenous binding partner of Rbm24, and STK38 knockdown or kinase inhibition reduced Rbm24 protein levels and impaired sarcomere assembly. Co-immunoprecipitation/mass spectrometry, STK38 knockdown, kinase inhibitor/activator treatment, sarcomere staining Scientific reports Medium 28322254
2018 Kir2.1 interacts with STK38 and inhibits Smurf1-mediated ubiquitination and degradation of MEKK2, thereby activating MEK1/2-ERK1/2-Snail pathway to drive EMT and invasion in gastric cancer cells, independent of ion permeation. Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, invasion/migration assay, mouse metastasis model Cancer research Medium 29549164
2019 STK38 phosphorylates XPO1 on serine 1055 (in XPO1's C-terminal auto-inhibitory domain), activating XPO1-dependent nuclear export; STK38 itself shuttles between the nucleus and cytoplasm and its nuclear exit requires both XPO1 and STK38 kinase activity. This mechanism also regulates nuclear export of Beclin1 and YAP1. Proximity-labeling assay, phospho-site mutagenesis, live-cell imaging, nuclear/cytoplasmic fractionation, co-immunoprecipitation, kinase-dead mutant EMBO reports High 31544310
2019 MEKK2 phosphorylates STK38 at Ser91, protecting STK38 from calpain-mediated cleavage at its proximal N-terminal region; calpain I directly cleaves STK38 in vitro, and deletion of the N-terminal region or phosphorylation-defective Ser91 mutant alters STK38 stability under hyperthermia. In vitro calpain cleavage assay, in vitro MEKK2 kinase assay, phosphorylation-defective mutants, calpain inhibitor (calpeptin) treatment, heat/calcium ionophore stress Scientific reports High 31690749
2019 STK38 inhibits BAG3-mediated chaperone-assisted selective autophagy (CASA) by binding BAG3 and disrupting its functional interplay with HSPB8 and SYNPO2, independently of STK38 kinase activity. Co-immunoprecipitation, kinase-dead mutant overexpression, RNAi knockdown, autophagy flux assay Biochimica et biophysica acta. Molecular cell research Medium 31326538
2016 STK38 supports oncogenic Ras-driven transformation by promoting detachment-induced autophagy and mitophagy; STK38 knockdown impairs anoikis resistance and anchorage-independent growth, and knockdown of PINK1 or Parkin similarly impairs these, while knockdown of USP30 rescues anchorage-independent growth in STK38-depleted Ras-transformed cells, placing STK38 upstream of PINK1/Parkin-mediated mitophagy. shRNA knockdown, genetic epistasis (PINK1/Parkin/USP30), soft agar assay, xenograft model, mitochondrial ROS measurement Oncotarget Medium 27283898
2020 STK38 serves as a reader for monoufmylated histone H4 at Lys31 via a UFM1-binding motif; in a kinase-independent manner, STK38 recruits SUV39H1 to DNA double-strand breaks, leading to H3K9 trimethylation and Tip60 activation, which promotes ATM activation. Co-immunoprecipitation, chromatin immunoprecipitation, kinase-dead mutant, UFM1-binding motif mutation, H3K9me3 and Tip60 activity assays Science advances High 32537488
2021 STK38 interacts with PPARγ (identified by Flag-PPARγ pulldown/MS), enhances PPARγ transactivation activity and protein stability (extending half-life from ~1.08 to 1.95 h), and promotes adipogenesis in a PPARγ-dependent manner, without requiring STK38 kinase activity. Flag-tag pulldown/mass spectrometry, co-immunoprecipitation, reporter assay, protein half-life assay (cycloheximide chase), STK38 overexpression/knockdown, kinase-dead mutant Adipocyte Medium 34670478
2023 STK38 phosphorylates the scaffold protein DOK1, which is required for lysosomal recruitment of the AAA+ ATPase VPS4 to terminate microlysophagy (ESCRT disassembly); STK38 depletion impairs VPS4 recruitment and accelerates DNA damage-induced cellular senescence in human cells. Phosphorylation assay, RNAi knockdown, lysosomal recruitment imaging, senescence assay, genetic analysis in C. elegans EMBO reports Medium 37987447
2023 NLRP12 interacts with STK38 (identified by proteomics), and the NLRP12/STK38 axis inhibits phosphorylation of GSK3β, leading to β-catenin degradation and suppression of Wnt/β-catenin signaling in intestinal epithelial cells; NLRP12-deficient mice show elevated p-GSK3β and β-catenin in colorectal tumors. Proteomic interaction studies, co-immunoprecipitation, Nlrp12 conditional knockout mice, intestinal organoids, phosphorylation assay The Journal of clinical investigation Medium 37581937
2023 STK38 binds TBK1 and induces TBK1 phosphorylation to promote NF-κB nuclear translocation and proinflammatory cytokine release; STK38 also reduces AMPK-ACC signaling to enhance de novo lipogenesis, causing hepatic lipid accumulation in HFD-fed mice. Co-immunoprecipitation, siRNA/ectopic expression in mouse liver, NF-κB nuclear translocation assay, AMPK-ACC phosphorylation assay, in vivo mouse model The Journal of biological chemistry Medium 37028764
2025 STK38 phosphorylates GPX4 at Ser45; SCRN1 enhances the STK38-GPX4 interaction to promote this phosphorylation, which impairs HSC70 recognition and chaperone-mediated autophagy-dependent GPX4 degradation, thereby conferring ferroptosis resistance in hepatocellular carcinoma. Co-immunoprecipitation, in vitro phosphorylation assay, chaperone-mediated autophagy assay, lipid peroxidation measurement, ferroptosis assay Nature cancer Medium 41145774
2026 STK38 and STK38L inhibit LATS kinase by competitively binding MOB1 and disrupting the LATS-MOB1 complex, independent of their kinase activity; this mechanism is evolutionarily conserved (Drosophila ortholog Tricornered similarly impairs Warts-Mats complex formation), resulting in YAP activation and tissue overgrowth. Co-immunoprecipitation, competitive binding assays, kinase-dead mutants, Drosophila genetic model (wing size phenotype), ovarian cancer xenograft Genes & development High 42128666
2026 STK38 is a non-canonical YAP1 kinase that phosphorylates and deactivates YAP1 in uninjured chief cells; during paligenosis, STK38 is degraded by autophagy, leading to YAP1 dephosphorylation and activation, which is necessary and sufficient for conversion of chief cells into metaplastic proliferating progenitors. STK38 interacts with NF2/Merlin, like canonical Hippo kinases. In vivo mouse stomach model, STK38 knockdown/overexpression, YAP1 phosphorylation assay, co-immunoprecipitation with NF2, autophagy inhibition experiments Proceedings of the National Academy of Sciences of the United States of America High 41911447
2026 STK38 interacts with KIF7 and GSK3β to promote Hedgehog signaling by facilitating KIF7 ciliary localization and reprogramming GSK3β substrate selectivity (leading to GLI1 stabilization and β-catenin suppression); GLI1 in turn directly enhances STK38 transcription, establishing a positive feedback loop. Co-immunoprecipitation, ciliary localization imaging, GSK3β substrate assay, GLI1 ChIP, siRNA knockdown, organoid model Cell death & disease Medium 41540036
2026 RFC4 stabilizes STK38 and the RFC4-STK38 complex facilitates BECN1 (Beclin1) recruitment to promote autophagy and temozolomide resistance in glioblastoma; phosphorylation of STK38 at T444 stabilizes this complex, and a phospho-deficient T444 mutant impairs autophagy. Multi-omics analysis, co-immunoprecipitation, phospho-deficient mutant, autophagy flux assay, in vivo xenograft, autophagy inhibitor rescue Nature communications Medium 41872171
2025 STK38 kinase activity is required for MerTK tyrosine phosphorylation and activation of Rac1 and Cdc42 downstream of oncogenic Ras; STK38 was identified as a MerTK complex binding partner by mass spectrometry, and its kinase-dead form failed to support Ras-induced cell migration. MerTK complex purification/mass spectrometry, Co-immunoprecipitation, kinase-dead mutant, siRNA knockdown, Rac1/Cdc42 activation assay, cell migration assay International journal of molecular sciences Medium 41226428

Source papers

Stage 0 corpus · 34 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2018 Kir2.1 Interaction with Stk38 Promotes Invasion and Metastasis of Human Gastric Cancer by Enhancing MEKK2-MEK1/2-ERK1/2 Signaling. Cancer research 56 29549164
2015 Stk38 protein kinase preferentially inhibits TLR9-activated inflammatory responses by promoting MEKK2 ubiquitination in macrophages. Nature communications 52 25981615
2020 STK38 promotes ATM activation by acting as a reader of histone H4 ufmylation. Science advances 51 32537488
2015 The Pro-apoptotic STK38 Kinase Is a New Beclin1 Partner Positively Regulating Autophagy. Current biology : CB 51 26387716
2012 STK38 is a critical upstream regulator of MYC's oncogenic activity in human B-cell lymphoma. Oncogene 48 23178486
2019 STK38 kinase acts as XPO1 gatekeeper regulating the nuclear export of autophagy proteins and other cargoes. EMBO reports 45 31544310
2017 The ubiquitin ligase Cullin5SOCS2 regulates NDR1/STK38 stability and NF-κB transactivation. Scientific reports 35 28216640
2023 Microautophagy regulated by STK38 and GABARAPs is essential to repair lysosomes and prevent aging. EMBO reports 30 37987447
2007 Negative regulation of MEKK1/2 signaling by serine-threonine kinase 38 (STK38). Oncogene 28 17906693
2023 NLRP12 downregulates the Wnt/β-catenin pathway via interaction with STK38 to suppress colorectal cancer. The Journal of clinical investigation 27 37581937
2017 Stk38 Modulates Rbm24 Protein Stability to Regulate Sarcomere Assembly in Cardiomyocytes. Scientific reports 27 28322254
2019 The Hippo network kinase STK38 contributes to protein homeostasis by inhibiting BAG3-mediated autophagy. Biochimica et biophysica acta. Molecular cell research 25 31326538
2016 Mitochondrial clearance by the STK38 kinase supports oncogenic Ras-induced cell transformation. Oncotarget 21 27283898
2020 The STK38-XPO1 axis, a new actor in physiology and cancer. Cellular and molecular life sciences : CMLS 19 33145612
2012 NDR1/STK38 potentiates NF-κB activation by its kinase activity. Cell biochemistry and function 19 22674419
2016 STK38 at the crossroad between autophagy and apoptosis. Autophagy 17 26890257
2019 Prevention of calpain-dependent degradation of STK38 by MEKK2-mediated phosphorylation. Scientific reports 12 31690749
2023 The Role of Mammalian STK38 in DNA Damage Response and Targeting for Radio-Sensitization. Cancers 9 37046714
2019 Grass carp STK38 regulates IFN I expression by decreasing the phosphorylation level of GSK3β. Developmental and comparative immunology 9 31175887
2023 Diet-induced induction of hepatic serine/threonine kinase STK38 triggers proinflammation and hepatic lipid accumulation. The Journal of biological chemistry 7 37028764
2025 SCRN1 confers hepatocellular carcinoma resistance to ferroptosis by stabilizing GPX4 via STK38-mediated phosphorylation. Nature cancer 3 41145774
2020 The hippo kinase STK38 ensures functionality of XPO1. Cell cycle (Georgetown, Tex.) 3 33017560
2025 Dynamic bidirectional regulation between Stk38 and rabies virus M protein coordinates apoptosis progression during neurotropic infection. International journal of biological macromolecules 2 40398756
2022 ZSWIM1 Promotes the Proliferation and Metastasis of Lung Adenocarcinoma Cells through the STK38/MEKK2/ERK1/2 Axis. Journal of proteome research 2 36511424
2021 STK38 is a PPARγ-interacting protein promoting adipogenesis. Adipocyte 2 34670478
2025 STK38 Kinase Promotes Cell Migration Induced by Oncogenic Ras via MerTK Activation. International journal of molecular sciences 1 41226428
2018 Correction: Mitochondrial clearance by the STK38 kinase supports oncogenic Ras-induced cell transformation. Oncotarget 1 29854321
2026 STK38-mediated feedback loop regulation of the hedgehog pathway governing tumor heterogeneity in renal papillary carcinoma. Cell death & disease 0 41540036
2026 CTCF/STK38 axis drives tumor progression via the Wnt/β-catenin and Hippo pathways. Acta biochimica et biophysica Sinica 0 41821474
2026 RFC4 drives temozolomide resistance in glioblastoma by activating STK38-BECN1-dependent autophagy. Nature communications 0 41872171
2026 Regulation of STK38 by autophagy governs YAP1 activity during paligenosis. Proceedings of the National Academy of Sciences of the United States of America 0 41911447
2026 SDPR-STK38 axis controls the proliferation-differentiation balance in alveolar type II cells. Animal models and experimental medicine 0 42089599
2026 STK38/L promote tissue growth and cancer by inhibiting the Hippo pathway. Genes & development 0 42128666
2017 Corrigendum: Stk38 Modulates Rbm24 Protein Stability to Regulate Sarcomere Assembly in Cardiomyocytes. Scientific reports 0 28753211

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