Affinage

ULK2

Serine/threonine-protein kinase ULK2 · UniProt Q8IYT8

Length
1036 aa
Mass
112.7 kDa
Annotated
2026-04-28
44 papers in source corpus 20 papers cited in narrative 19 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ULK2 is a serine/threonine kinase that functions both as a core initiator of canonical autophagy—redundantly with ULK1 downstream of mTORC1 in response to amino acid deprivation—and as an effector of multiple autophagy-independent signaling pathways including axon guidance, focal adhesion turnover, stress granule disassembly, and innate immune activation (PMID:21460635, PMID:29099309, PMID:38163960, PMID:30979586, PMID:34560002). ULK2 autophosphorylates in its proline/serine-rich domain and operates within an ATG13–FIP200–AMPK complex; PKA-mediated phosphorylation at Ser1027 drives its Kapβ2-dependent nuclear import and attenuates autophagic activity, while PKCλ/ι phosphorylation targets ULK2 for endosomal microautophagic degradation (PMID:10557072, PMID:26052940, PMID:34560002, PMID:16). ULK2 directly phosphorylates substrates including VCP/p97 (enhancing stress granule clearance), paxillin (inhibiting focal adhesion assembly and cell migration), TBK1 (activating STING-mediated interferon signaling), CARMA2sh (suppressing NF-κB), and c-Jun (suppressing glycolysis), and is uniquely required in skeletal muscle for selective autophagy of ubiquitinated protein aggregates (PMID:30979586, PMID:38163960, PMID:34560002, PMID:28230860, PMID:41719166, PMID:31361156). In neurons, ULK2 deficiency causes p62 accumulation that sequesters GABARAP-family proteins and reduces GABAA receptor surface expression, producing excitatory–inhibitory imbalance (PMID:29893844).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1999 High

    Establishing that ULK2 possesses intrinsic serine/threonine kinase activity with autophosphorylation in its PS domain, and that kinase/PS domain functions are evolutionarily conserved with C. elegans UNC-51, provided the foundational biochemical identity of ULK2 as an active kinase.

    Evidence In vitro autophosphorylation assays with truncation mutants and ULK2/UNC-51 chimeric rescue in C. elegans

    PMID:10557072

    Open questions at the time
    • No mammalian in vivo substrates identified
    • Kinase regulation mechanisms unknown
    • Physiological role in mammalian cells untested
  2. 2011 High

    Demonstrating that ULK1 and ULK2 are functionally redundant for amino-acid-deprivation-induced autophagy but dispensable for glucose/ammonia-induced autophagy, and that they function within an ATG13–FIP200 complex with ATG13 retaining ULK-independent activity, defined the scope and limits of ULK2's canonical autophagy role.

    Evidence Ulk1/Ulk2 double-knockout MEFs; Atg13-deficient cells; multiple autophagy induction conditions

    PMID:21460635 PMID:21690395 PMID:22024743

    Open questions at the time
    • Molecular basis of stimulus-specific autophagy pathway selectivity unknown
    • Relative contribution of ULK2 kinase activity vs. scaffolding unclear
  3. 2011 Medium

    Identification of Kctd12.1 as a ULK2-binding partner that asymmetrically inhibits ULK2 to generate left–right differences in habenular neuropil elaboration revealed a neurodevelopmental function for ULK2 beyond autophagy.

    Evidence Protein interaction screen and morpholino knockdown/overexpression in zebrafish

    PMID:21734278

    Open questions at the time
    • Mechanism by which Kctd12 inhibits ULK2 kinase activity uncharacterized
    • Not confirmed in mammalian neurons at this stage
    • Direct phosphorylation substrate in this context unknown
  4. 2014 High

    Showing that ULK2's kinase activity is required for autophagy-dependent tumor growth inhibition in glioma (via ATG5 epistasis) established that ULK2 can function as a tumor suppressor through its autophagy-initiating activity.

    Evidence Kinase-dead ULK2 mutant; ATG5-null epistasis; in vivo tumor growth assays

    PMID:24923441

    Open questions at the time
    • Downstream targets mediating growth suppression not identified
    • Whether this is ULK2-specific or shared with ULK1 not tested
  5. 2015 High

    Discovery that PKA phosphorylates ULK2 at Ser1027, causing dissociation from ATG13/FIP200 and Kapβ2-dependent nuclear import, revealed a phosphorylation switch governing ULK2 subcellular distribution and autophagy activity.

    Evidence Pull-down, confocal imaging, PY-NLS and Ser1027 mutagenesis, in vitro kinase assay

    PMID:26052940

    Open questions at the time
    • Nuclear function of ULK2 unknown
    • Physiological stimuli that activate PKA-mediated nuclear import uncharacterized
  6. 2017 High

    CNS-specific Ulk1/Ulk2 double knockout in mice produced corpus callosum and axon guidance defects not seen in canonical autophagy knockouts (Atg7, Rb1cc1), establishing a bona fide autophagy-independent neurodevelopmental function for ULK1/2.

    Evidence Nestin-Cre conditional double KO mice compared with Atg7−/− and Rb1cc1−/− mice; neuroanatomical analysis

    PMID:29099309

    Open questions at the time
    • Downstream effectors of ULK1/2 in axon guidance unidentified
    • Individual contributions of ULK1 vs. ULK2 to axon guidance not resolved
  7. 2017 Medium

    Identification of CARMA2sh as a direct ULK2 phosphorylation substrate that, when phosphorylated, promotes BCL10 lysosomal degradation and NF-κB suppression—with psoriasis-associated CARMA2sh mutants escaping this regulation—linked ULK2 to skin inflammatory disease mechanisms.

    Evidence Co-IP, phosphorylation assays, NF-κB reporter assays, disease-associated mutant analysis in keratinocytes

    PMID:28230860

    Open questions at the time
    • Specific phosphorylation sites on CARMA2sh not mapped
    • Not independently replicated
    • In vivo relevance in psoriasis models untested
  8. 2018 High

    Demonstrating that ULK2 haploinsufficiency causes p62 accumulation that sequesters GABARAPL2 and reduces GABAA receptor surface levels in prefrontal cortex neurons, correctable by p62 reduction, established a specific mechanism linking ULK2 to excitatory–inhibitory balance.

    Evidence Ulk2 heterozygous mice; biochemical fractionation; peptide interference with p62–GABARAPL2; genetic p62 dosage reduction; behavioral assays

    PMID:29893844

    Open questions at the time
    • Whether full ULK2 KO worsens the phenotype not shown
    • How p62–GABARAPL2 interaction specifically affects GABAA trafficking not fully resolved
  9. 2019 High

    Two studies revealed non-redundant tissue-specific functions: ULK1/2 phosphorylate VCP/p97 to enhance its ATPase activity and stress granule disassembly (with double-KO mice developing inclusion body myopathy), while ULK2 alone is uniquely required in skeletal muscle for selective autophagy of ubiquitinated protein aggregates.

    Evidence In vitro VCP phosphorylation and ATPase assays; Ulk1/2 double-KO myopathy model; skeletal muscle-specific Ulk2 KO with aggregate and force measurements

    PMID:30979586 PMID:31361156

    Open questions at the time
    • Specific VCP phosphosites mediating stress granule disassembly not fully mapped
    • Mechanism of ULK2-specific selective autophagy in muscle uncharacterized
    • Whether ULK2 muscle function is kinase-dependent not directly tested
  10. 2021 High

    Establishing that PKCλ/ι phosphorylates ULK2 to promote its endosomal microautophagic degradation, and that stabilized ULK2 directly phosphorylates and activates TBK1 to drive STING-mediated interferon signaling and anti-tumor immunity, placed ULK2 at the nexus of autophagy, innate immunity, and tumor microenvironment regulation.

    Evidence In vitro kinase assays for PKCλ/ι→ULK2 and ULK2→TBK1; microautophagy degradation assays; PKCλ/ι-KO intestinal tumor model; multiplex imaging

    PMID:34560002

    Open questions at the time
    • Specific phosphosites on ULK2 targeted by PKCλ/ι not fully characterized
    • Whether ULK2→TBK1 axis operates outside intestinal tumors untested
  11. 2022 High

    Perinatal cardiomyocyte-specific deletion showed compensatory upregulation between ULK1 and ULK2, while adult-specific loss of ULK1 but not ULK2 caused acute cardiomyopathy, demonstrating stage-dependent functional differentiation between the paralogs in the heart.

    Evidence Perinatal and inducible adult cardiomyocyte-specific conditional KO mice; autophagy flux; mitochondrial and cardiac function measurements

    PMID:35104184

    Open questions at the time
    • Why adult ULK2 loss is tolerated in heart while ULK1 loss is not remains unexplained at molecular level
  12. 2024 High

    Discovery that ULK1/2 phosphorylate paxillin to antagonize FAK/SRC-mediated tyrosine phosphorylation and inhibit focal adhesion assembly revealed an autophagy-independent role in mechanotransduction and cell migration control.

    Evidence In vitro PXN phosphorylation; phosphosite mutagenesis; focal adhesion imaging; migration assays with ULK1/2 KO

    PMID:38163960

    Open questions at the time
    • Relative contribution of ULK2 vs. ULK1 to PXN phosphorylation in vivo not resolved
    • Structural basis of antagonism between serine and tyrosine phosphorylation on PXN unknown
  13. 2025 Medium

    Identification of ULK2-specific interactions with AMPK α1/γ1 subunits via FIP200, and demonstration that ULK2 knockdown triggers AMPK activation and autophagy-dependent BCR::ABL degradation in CML cells, revealed a ULK2-specific scaffolding role in AMPK regulation with therapeutic implications.

    Evidence Mass spectrometry interactome; co-IP; shRNA knockdown in CML cells; autophagy flux and BCR::ABL degradation assays

    PMID:40664084

    Open questions at the time
    • Direct vs. FIP200-mediated interaction with AMPK subunits not distinguished
    • Whether this mechanism operates in primary CML patient cells unknown
    • Single-lab finding awaiting independent confirmation
  14. 2025 Medium

    Phosphoproteomic identification of c-Jun Ser243 as a direct ULK2 substrate that upon phosphorylation undergoes degradation, suppressing glycolytic gene expression and restoring cisplatin sensitivity in ovarian cancer, expanded ULK2's substrate repertoire to metabolic transcription factors.

    Evidence Phosphoproteomics in ULK2-overexpressing organoids; glycolysis assays; c-Jun overexpression rescue; in vivo experiments

    PMID:41719166

    Open questions at the time
    • In vitro kinase assay directly confirming ULK2 phosphorylation of c-Jun Ser243 not shown
    • Generalizability beyond cisplatin-resistant ovarian cancer untested
    • Single-lab finding

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the identity and function of nuclear ULK2 substrates, the structural basis for substrate selectivity between ULK1 and ULK2, and how ULK2's autophagy-independent functions (axon guidance, focal adhesion regulation, innate immune signaling) are coordinated with its canonical autophagy role in vivo.
  • No nuclear substrates or functions identified despite demonstrated nuclear import
  • No structural model of ULK2 or ULK2-substrate complexes available
  • Mechanism of ULK2 specificity in selective muscle autophagy unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 7 GO:0140657 ATP-dependent activity 2
Localization
GO:0005829 cytosol 2 GO:0005634 nucleus 1 GO:0005856 cytoskeleton 1
Pathway
R-HSA-9612973 Autophagy 9 R-HSA-1266738 Developmental Biology 3 R-HSA-162582 Signal Transduction 3 R-HSA-168256 Immune System 1 R-HSA-5357801 Programmed Cell Death 1
Partners
ATG13FIP200KCTD12PRKCIPXNTBK1TNFRSF14VCP
Complex memberships
ULK2–ATG13–FIP200 complex

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 ULK2 is a serine/threonine kinase that undergoes autophosphorylation in vitro; truncation mutants identified the proline/serine-rich (PS) domain as the site of autophosphorylation. Domain chimera analysis with C. elegans UNC-51 showed that kinase and PS domain functions are conserved across species, while the C-terminal domain acts in a species-specific manner. In vitro autophosphorylation assay with truncation mutants; ULK2/UNC-51 chimeric kinase rescue experiments in C. elegans Oncogene High 10557072
2011 ULK1 and ULK2 are functionally redundant kinases required for autophagy in response to amino acid (nitrogen) deprivation in fibroblasts, but not for autophagy induced by glucose deprivation or ammonia. In cerebellar granule neurons, ULK1 but not ULK2 is required for the autophagic response to low potassium, demonstrating cell-type-specific redundancy. Double knockout MEFs (Ulk1/2-/-) and single knockout analysis; autophagy assays under nutrient deprivation; genetic epistasis Autophagy High 21460635 21690395
2011 Atg13 and FIP200 form a complex with ULK1/2, but Atg13 has autophagy-inducing functions independent of ULK1/2 kinase activity; simultaneous knockout of Ulk1 and Ulk2 did not fully recapitulate the autophagy defect of Atg13 loss, indicating Atg13 acts upstream in a ULK1/2-independent manner as well. Atg13-deficient cells combined with Ulk1/Ulk2 double knockout; autophagy induction assays; identification of Ulk1-dependent phosphorylation sites on Atg13 Autophagy High 22024743
2011 In zebrafish, Ulk2 promotes neuropil elaboration in habenular neurons. Kctd12.1 was identified as a novel binding partner of Ulk2 (via protein interaction screen) that asymmetrically inhibits Ulk2 activity, causing left-right differences in habenular neuropil formation. Knockdown of Ulk2 reduces neuropil elaboration; overexpression causes excess elaboration. Screen for Kctd12.1-interacting proteins uncovering Ulk2 interaction; morpholino knockdown and overexpression in zebrafish; genetic mutation of kctd12 The Journal of Neuroscience Medium 21734278
2013 In 3T3-L1 adipocytes, ULK2 knockdown reduces basal autophagy and mitochondrial respiration, and has opposing effects on fatty acid oxidation and uptake compared to ULK1, demonstrating distinct (non-redundant) roles of ULK1 and ULK2 in lipid metabolism. shRNA knockdown of Ulk1 and Ulk2 in differentiated adipocytes; lipolysis assays, fatty acid oxidation/uptake, mitochondrial respiration measurements Autophagy Medium 24135897
2014 ULK2 overexpression induces autophagy and inhibits glioma cell growth; a kinase-dead mutant of ULK2 fails to induce autophagy and fails to inhibit growth. Growth inhibition requires the autophagy-inducing activity of ULK2 (demonstrated in ATG5+/+ but not ATG5-/- cells). Ectopic overexpression of wild-type vs. kinase mutant ULK2; autophagy assays; ATG5-/- cells; in vivo tumor growth The Journal of Biological Chemistry High 24923441
2015 ULK2 is transported to the nucleus via karyopherin beta 2 (Kapβ2) through a PY-NLS motif ((774)GPGFGSSPPGAEAAPSLRYVPY(795)) in its S/P domain. PKA phosphorylates ULK2 at Ser1027, which promotes dissociation from Atg13 and FIP200, nuclear localization, and reduced autophagic activity. The cytoplasmic-localization mutant (P794A) shows increased autophagy. Pull-down assay (in vitro and in vivo); confocal microscopy co-localization; mutagenesis of PY-NLS (P794A) and Ser1027; transient transfection autophagy assays; in vitro kinase assay PLoS One High 26052940
2017 In zebrafish, Ulk2 positively regulates dendrite branching and elaboration in habenular neurons via interaction with Kctd12 proteins through a proline-serine-rich domain. Loss of Kctd12 results in increased dendritogenesis and decreased anxiety behavior, establishing a Kctd12–Ulk2 regulatory axis in neural circuit development. Genetic loss-of-function (ulk2 morpholino, kctd12 mutants) and gain-of-function in zebrafish; behavioral assays; domain mapping of Ulk2–Kctd12 interaction PLoS One Medium 25329151
2017 ULK1 and ULK2 regulate axon guidance and defasciculation in the developing mouse forebrain via an autophagy-independent mechanism. CNS-specific double knockout mice show corpus callosum, anterior commissure, and thalamocortical axon defects not observed in Atg7 or Rb1cc1 single-KO mice, placing ULK1/2 in a noncanonical pathway for axon guidance. CNS-specific conditional double-knockout mice (Nes-Cre); comparison with Atg7-/- and Rb1cc1-/- mice; neuroanatomical analysis Autophagy High 29099309
2017 ULK2 binds to and phosphorylates CARMA2sh, inhibiting its capacity to activate NF-κB by promoting lysosomal degradation of BCL10 in human keratinocytes. Psoriasis-associated missense mutants of CARMA2sh escape ULK2-mediated phosphorylation and inhibition. Co-immunoprecipitation; phosphorylation assays; lysosomal degradation assays; NF-κB reporter assays; mutant CARMA2sh analysis in keratinocytes Cell Death & Disease Medium 28230860
2018 ULK2 deficiency in pyramidal neurons leads to p62 accumulation and selective reduction of GABAA receptor surface expression, causing excitatory-inhibitory imbalance in the prefrontal cortex. Reducing p62 levels or blocking p62-GABARAPL2 (GABARAP-associated protein) interaction restored GABAA receptor surface expression and behavioral deficits. Ulk2 heterozygous mouse model; biochemical fractionation; immunofluorescence; behavioral assays; peptide interference with p62-GABARAPL2 interaction; genetic p62 dosage reduction Human Molecular Genetics High 29893844
2019 ULK1 and ULK2 localize to stress granules and phosphorylate VCP/p97, increasing VCP's ATPase activity and its ability to disassemble stress granules. Loss of ULK1/2 in mice causes vacuolar myopathy with ubiquitin and TDP-43-positive inclusions resembling IBM caused by VCP mutations. Co-localization by imaging; in vitro phosphorylation assay of VCP by ULK1/2; VCP ATPase activity assay; Ulk1/2-/- mouse model with myopathy characterization; ULK1/2 agonist treatment Molecular Cell High 30979586
2019 ULK2 (but not ULK1) is highly enriched in skeletal muscle and is uniquely required for basal selective autophagy of insoluble ubiquitinated protein aggregates associated with p62/SQSTM1 and NBR1. ULK2 deficiency causes myofiber atrophy, degeneration, and impaired muscle force without globally impairing autophagosome formation or lysosomal function. Skeletal muscle-specific Ulk2 KO mice compared to Ulk1 KO; ubiquitinated protein aggregate accumulation assays; p62/NBR1 co-localization; muscle force measurements; autophagy flux assays FASEB Journal High 31361156
2021 PKCλ/ι directly phosphorylates and represses ULK2, promoting its degradation via endosomal microautophagy through a ubiquitin-dependent mechanism. Loss of PKCλ/ι increases enzymatically active ULK2, which directly phosphorylates and activates TBK1 to stimulate STING-mediated interferon signaling and enhance anti-tumor CD8+ T cell recruitment. In vitro kinase assay (PKCλ/ι phosphorylating ULK2); co-immunoprecipitation; ULK2 in vitro phosphorylation of TBK1; endosomal microautophagy degradation assays; PKCλ/ι-KO mouse intestinal tumor model; single-cell multiplex imaging Molecular Cell High 34560002
2022 Perinatal loss of both ULK1 and ULK2 in cardiomyocytes impairs autophagy and causes age-related cardiomyopathy; perinatal loss of either alone enhances basal autophagy via compensatory upregulation of the remaining paralog. Adult-specific loss of ULK1 (but not ULK2) causes rapidly developing cardiomyopathy and heart failure with mitochondrial defects, indicating developmental-stage-specific functional differentiation. Cardiomyocyte-specific conditional KO mice (perinatal and inducible adult); autophagy flux assays; mitochondrial respiration; cardiac function measurements; trehalose rescue Autophagy High 35104184
2024 ULK1 and ULK2 inhibit focal adhesion assembly and F-actin formation by phosphorylating the adhesion protein paxillin (PXN), preventing breast cancer cell migration in an autophagy-independent manner. ULK1/2-mediated serine phosphorylation of PXN counteracts PTK2 (FAK) and SRC-mediated tyrosine phosphorylation at adjacent residues, gatekeeping mechanotransduction. In vitro phosphorylation assay of PXN; mutational analysis of PXN phosphosites; focal adhesion assembly imaging; F-actin quantification; cell migration assays with ULK1/2 KO/KD Autophagy High 38163960
2025 ULK2 forms a stable complex with FIP200, which interacts specifically with AMPK α1 and γ1 subunits (identified by mass spectrometry). ShRNA-mediated knockdown of ULK2 in CML cells induces AMPK activation, promotes cytoplasmic accumulation of ULK1 and FIP200, and triggers autophagy-dependent degradation of BCR::ABL, leading to cell death. Mass spectrometry interactome analysis; co-immunoprecipitation; shRNA knockdown of ULK2 in 293FT and CML cells; autophagy flux and BCR::ABL degradation assays Biochemical and Biophysical Research Communications Medium 40664084
2025 METTL3-mediated N6-methyladenosine (m6A) modification upregulates ULK2 mRNA expression in hypertrophic scar fibroblasts, promoting autophagy and fibroblast-to-myofibroblast differentiation; silencing METTL3 impairs ULK2-driven autophagic flux and reduces scar formation in vivo. MeRIP-seq (m6A RNA immunoprecipitation sequencing); qRT-PCR; Western blotting; METTL3 siRNA knockdown; transmission electron microscopy; rabbit ear scar model International Journal of Biological Macromolecules Medium 40409645
2025 ULK2 overexpression in cisplatin-resistant ovarian cancer organoids suppresses glycolysis and restores chemosensitivity. Phosphoproteomics revealed ULK2 phosphorylates c-Jun at Ser243, promoting c-Jun degradation and reducing glycolytic gene expression; c-Jun overexpression counteracts ULK2-induced chemosensitivity and glycolysis suppression. Phosphoproteomics in ULK2-overexpressing organoids; CCK-8 and in vivo experiments; glycolysis assays; c-Jun overexpression rescue Science Progress Medium 41719166

Source papers

Stage 0 corpus · 44 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 Ammonia-induced autophagy is independent of ULK1/ULK2 kinases. Proceedings of the National Academy of Sciences of the United States of America 292 21690395
2019 ULK1 and ULK2 Regulate Stress Granule Disassembly Through Phosphorylation and Activation of VCP/p97. Molecular cell 151 30979586
2017 Long noncoding RNA Malat1 is a potent autophagy inducer protecting brain microvascular endothelial cells against oxygen-glucose deprivation/reoxygenation-induced injury by sponging miR-26b and upregulating ULK2 expression. Neuroscience 151 28433650
2011 The requirement of uncoordinated 51-like kinase 1 (ULK1) and ULK2 in the regulation of autophagy. Autophagy 151 21460635
2011 Atg13 and FIP200 act independently of Ulk1 and Ulk2 in autophagy induction. Autophagy 116 22024743
2013 Distinct functions of Ulk1 and Ulk2 in the regulation of lipid metabolism in adipocytes. Autophagy 86 24135897
2014 Methylation silencing of ULK2, an autophagy gene, is essential for astrocyte transformation and tumor growth. The Journal of biological chemistry 79 24923441
1999 Mouse ULK2, a novel member of the UNC-51-like protein kinases: unique features of functional domains. Oncogene 76 10557072
2017 The autophagy-inducing kinases, ULK1 and ULK2, regulate axon guidance in the developing mouse forebrain via a noncanonical pathway. Autophagy 66 29099309
2016 MiR-26b inhibits autophagy by targeting ULK2 in prostate cancer cells. Biochemical and biophysical research communications 56 26920049
2018 Ulk2 controls cortical excitatory-inhibitory balance via autophagic regulation of p62 and GABAA receptor trafficking in pyramidal neurons. Human molecular genetics 43 29893844
2020 ULK1 and ULK2 are less redundant than previously thought: computational analysis uncovers distinct regulation and functions of these autophagy induction proteins. Scientific reports 35 32616830
2019 ULK2 is essential for degradation of ubiquitinated protein aggregates and homeostasis in skeletal muscle. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 35 31361156
2021 PKCλ/ι inhibition activates an ULK2-mediated interferon response to repress tumorigenesis. Molecular cell 27 34560002
2022 Perinatal versus adult loss of ULK1 and ULK2 distinctly influences cardiac autophagy and function. Autophagy 23 35104184
2017 Downregulation of miRNA-26b inhibits cancer proliferation of laryngeal carcinoma through autophagy by targeting ULK2 and inactivation of the PTEN/AKT pathway. Oncology reports 23 28713931
2011 Asymmetric inhibition of Ulk2 causes left-right differences in habenular neuropil formation. The Journal of neuroscience : the official journal of the Society for Neuroscience 20 21734278
2019 Sensory Neuropathy Affects Cardiac miRNA Expression Network Targeting IGF-1, SLC2a-12, EIF-4e, and ULK-2 mRNAs. International journal of molecular sciences 19 30823517
2018 miR-26a suppresses autophagy in swine Sertoli cells by targeting ULK2. Reproduction in domestic animals = Zuchthygiene 18 29761550
2017 Intratumoral Heterogeneity of Somatic Mutations for NRIP1, DOK1, ULK1, ULK2, DLGAP3, PARD3 and PRKCI in Colon Cancers. Pathology oncology research : POR 15 28844109
2021 LncRNA GAS5 Suppressed Proliferation and Promoted Apoptosis in Laryngeal Squamous Cell Carcinoma by Targeting MiR-26a-5p and Modifying ULK2. Cancer management and research 13 33551645
2021 Ulk1, Not Ulk2, Is Required for Exercise Training-Induced Improvement of Insulin Response in Skeletal Muscle. Frontiers in physiology 12 34658916
2017 CARMA2sh and ULK2 control pathogen-associated molecular patterns recognition in human keratinocytes: psoriasis-linked CARMA2sh mutants escape ULK2 censorship. Cell death & disease 12 28230860
2022 Mesangial Cell-Derived Exosomal miR-4455 Induces Podocyte Injury in IgA Nephropathy by Targeting ULK2. Oxidative medicine and cellular longevity 11 36388165
2021 CircARHGAP12 Triggers Mesenchymal Stromal Cell Autophagy to Facilitate its Effect on Repairing Diabetic Wounds by Sponging miR-301b-3p/ATG16L1 and miR-301b-3p/ULK2. The Journal of investigative dermatology 11 34933019
2024 An autophagy-independent role of ULK1/ULK2 in mechanotransduction and breast cancer cell migration. Autophagy 10 38163960
2018 Overexpression of Ulk2 inhibits proliferation and enhances chemosensitivity to cisplatin in non-small cell lung cancer. Oncology letters 10 30655741
2015 ULK2 Ser 1027 Phosphorylation by PKA Regulates Its Nuclear Localization Occurring through Karyopherin Beta 2 Recognition of a PY-NLS Motif. PloS one 10 26052940
2020 Association of asparaginase-associated pancreatitis and ULK2 gene polymorphism. International journal of clinical and experimental pathology 7 32269672
2021 Methylation silencing of ULK2 via epithelial-mesenchymal transition causes transformation to poorly differentiated gastric cancers. Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association 6 34554345
2017 Androgen receptor antagonist bicalutamide induces autophagy and apoptosis via ULK2 upregulation in human bladder cancer cells. International journal of clinical and experimental pathology 6 31966605
2024 Exosome-Transmitted miR-224-5p Promotes Colorectal Cancer Cell Proliferation via Targeting ULK2 in p53-Dependent Manner. Biomedical and environmental sciences : BES 5 38326722
2024 ULK2 Is a Key Pro-Autophagy Protein That Contributes to the High Chemoresistance and Disease Relapse in FLT3-Mutated Acute Myeloid Leukemia. International journal of molecular sciences 4 38203816
2024 ULK2 suppresses ovarian cancer cell migration and invasion by elevating IGFBP3. PeerJ 4 38952983
2014 Kctd12 and Ulk2 partner to regulate dendritogenesis and behavior in the habenular nuclei. PloS one 4 25329151
2025 T-lymphocytes suppression by CD14+ monocytes with high expression of ULK2 in patients with multiple myeloma. Journal of translational medicine 3 40336101
2021 Immunosurveillance, interferon, and autophagic networking in cancer: the PRKCI-ULK2 paradigm. Autophagy 3 34895031
2025 METTL3-dependent epigenetic regulation of ULK2 autophagy in hypertrophic scarring. International journal of biological macromolecules 2 40409645
2025 ULK2 promotes migration and invasion of colorectal cancer cells via MCT4-mediated lactate export. Medical oncology (Northwood, London, England) 1 40696241
2026 ULK2 suppresses glycolysis to attenuate cisplatin resistance in ovarian cancer organoid via c-Jun phosphorylation. Science progress 0 41719166
2025 The 2-aminoadipic acid (2-AAA) regulates grass carp ULK2 to inhibit GCRV replication. Fish & shellfish immunology 0 39753154
2025 ULK2 deficiency stratifies autophagy-driven molecular subtypes and exacerbates trophoblasts apoptosis in preeclampsia. Placenta 0 40319799
2025 Novel insights into the ULK2-FIP200-AMPK-mediated regulation of autophagy and BCR::ABL degradation in chronic myeloid leukemia. Biochemical and biophysical research communications 0 40664084
2025 In silico identification of bilobetin and ginsenoside as dual CK2 and ULK2 inhibitors targeting triple-negative breast cancer. Scientific reports 0 41469454