Affinage

CAMK1

Calcium/calmodulin-dependent protein kinase type 1 · UniProt Q14012

Length
370 aa
Mass
41.3 kDa
Annotated
2026-06-09
24 papers in source corpus 16 papers cited in narrative 16 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

CAMK1 (CaMKIα) is a Ca2+/calmodulin-dependent serine/threonine kinase that couples intracellular calcium signals to transcriptional, organelle, and behavioral outputs (PMID:21791615, PMID:34766550). Its activity is gated by an autoinhibitory mechanism: crystal structures show that in the autoinhibited state an activation segment adopts a helical conformation that, together with the autoinhibitory segment, constrains the αC/αD helices, sequesters Thr177 from phosphorylation, and occludes the substrate-binding site, whereas ATP binding dissociates the regulatory region from the catalytic core to yield an active conformation (PMID:23028635); deletion of the autoinhibitory domain produces constitutively active, Ca2+-independent kinase with broad substrate specificity (PMID:27207832). Once activated, CAMK1 phosphorylates substrates to control gene expression and cell fusion: downstream of cAMP/Epac1/Rap1 it phosphorylates GCM1 at Ser47 to promote SENP1-dependent desumoylation and activation of GCM1, and it phosphorylates HDAC5 at Ser259/Ser498 to drive nuclear export and de-repress GCM1-driven syncytin-1/2 expression and trophoblast fusion (PMID:21791615, PMID:23867755). CAMK1 also activates the nuclear phosphatase CaMKP-N/PPM1E by phosphorylating Ser480, providing negative feedback on multifunctional CaMK signaling (PMID:22627141), and phosphorylates PINK1 at Ser228 to recruit Parkin and activate mitophagy (PMID:35145192). It contributes to starvation-induced autophagosome formation through WIPI-1 puncta downstream of Ca2+/CaMKK (PMID:21896713) and to granulocyte effector functions including phagocytosis, ROS production, migration, and adhesion (PMID:15840691). In C. elegans, the CaMKI ortholog CMK-1 undergoes Ca2+/CaM-driven, IMA-3 importin-dependent nuclear translocation that underlies experience-dependent gene transcription and behavioral plasticity across thermosensory, chemosensory, and developmental decisions (PMID:34766550, PMID:26335407). CAMK1 has been linked to mitochondrial homeostasis and disease in mammalian tissues, restraining mitochondrial fission to protect against diabetic kidney injury (PMID:38216068) and, when overexpressed, suppressing PI3K/AKT signaling to drive mitochondrial dysfunction and anoikis in colorectal cancer cells (PMID:42175534).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2005 Medium

    Established that a granulocyte-restricted CaMKI-like kinase translates chemoattractant-induced calcium rises into neutrophil effector functions, linking the kinase to innate immune cell behavior.

    Evidence Peptide inhibitor and functional assays (phagocytosis, ROS, migration, adhesion) in primary human granulocytes

    PMID:15840691

    Open questions at the time
    • No direct substrate phosphorylated by CKLiK identified
    • Reliance on a single peptide inhibitor rather than genetic loss-of-function
  2. 2008 Low

    Implicated CaMKI in cAMP-driven transcription by linking it to Nur77 promoter activity, an early hint at a transcriptional regulatory role.

    Evidence Promoter-reporter assays with pharmacological CaMK inhibition in MA-10 Leydig cells

    PMID:18835829

    Open questions at the time
    • Pharmacological inhibition only — no direct CaMKI substrate or knockdown
    • Cannot distinguish CaMKI from other CaMK family members
  3. 2011 High

    Defined a direct CAMK1 substrate by showing the cAMP/Epac1/Rap1 cascade activates CaMKI to phosphorylate GCM1 Ser47, establishing CAMK1 as a regulator of trophoblast fusion through control of SUMO-dependent transcription factor activity.

    Evidence RNAi, phosphomimetic GCM1 mutants, reciprocal co-IP in BeWo placental cells

    PMID:21791615

    Open questions at the time
    • Mechanism of how Ser47 phosphorylation enhances SENP1 recruitment not structurally resolved
    • Direct kinase-substrate phosphorylation shown largely in cells
  4. 2011 Medium

    Distinguished CaMKI from CaMKIV as the calcium-dependent kinase required for early autophagosome membrane formation, placing CAMK1 in starvation-induced autophagy downstream of CaMKK and independent of AMPK.

    Evidence siRNA knockdown, WIPI-1 puncta high-throughput analysis, LC3 lipidation, pharmacological inhibitors

    PMID:21896713

    Open questions at the time
    • No CAMK1 substrate in the autophagy machinery identified
    • Single lab, single cellular system
  5. 2012 High

    Resolved the structural basis of CAMK1 autoinhibition and activation, explaining how the activation segment and autoinhibitory segment sequester Thr177 and block substrate binding until ATP/regulatory dissociation.

    Evidence X-ray crystallography of apo and ATP-bound CaMKIα truncates

    PMID:23028635

    Open questions at the time
    • Structures do not capture the Ca2+/CaM-bound activation intermediate
    • CaMKK-phosphorylated active full-length state not crystallized
  6. 2012 High

    Identified a negative-feedback substrate, showing CaMKI phosphorylates nuclear CaMKP-N/PPM1E at Ser480 to enhance phosphatase activity and dampen multifunctional CaMK signaling.

    Evidence In vitro kinase assay, S480A/D/E mutagenesis, phosphatase assays, Neuro2a cell transfection

    PMID:22627141

    Open questions at the time
    • Physiological context of CaMKP-N feedback in mammalian neurons not established
    • Demonstrated in vitro and in heterologous cells
  7. 2013 High

    Extended the Epac1/Rap1/CaMKI pathway by showing CaMKI phosphorylates HDAC5 at Ser259/Ser498 to drive its nuclear export, linking the kinase to chromatin de-repression and syncytin-1 expression.

    Evidence Phospho-specific antibodies, reciprocal co-IP, constitutively active Epac1/CaMKI, RNAi, immunofluorescence

    PMID:23867755

    Open questions at the time
    • Direct versus indirect phosphorylation of HDAC5 by CaMKI not fully separated from pathway effects
    • Restricted to placental cell model
  8. 2015 High

    Defined isoform-specific regulation, showing CaMKIδ is phosphatase-resistant via N-terminal residues, allowing a Ca2+-independent 'primed' active state that phosphorylates CREB.

    Evidence In vitro dephosphorylation assays, chimeric/point mutants, CREB phosphorylation assays in 293T cells

    PMID:25994484

    Open questions at the time
    • Physiological consequences of constitutive CaMKIδ activity in vivo unclear
    • Specific to the δ isoform, not CaMKIα
  9. 2015 High

    Demonstrated cell-type-specific and feeding-state-dependent CaMKI signaling, with CMK-1 controlling daf-7 TGF-β and daf-28 insulin-like peptide expression to govern the dauer developmental decision.

    Evidence C. elegans genetics, cell-specific rescue, transcriptional reporters, live subcellular imaging

    PMID:26335407

    Open questions at the time
    • Direct nuclear substrates linking CMK-1 to daf-7/daf-28 transcription not identified
    • Ortholog-based; mammalian relevance inferred
  10. 2016 Medium

    Confirmed by reconstitution that the autoinhibitory domain suppresses basal activity, since an autoinhibitory-domain-deleted CaMKIδ fragment is constitutively active with broad substrate specificity.

    Evidence Recombinant E. coli expression, in vitro kinase and substrate specificity assays

    PMID:27207832

    Open questions at the time
    • Broad in vitro specificity may not reflect cellular substrate selectivity
    • Single study, zebrafish ortholog
  11. 2018 Medium

    Placed CMK-1 downstream of sensory calcium signals in chemosensory learning, showing it is required in ASE neurons for salt-aversive behavioral plasticity.

    Evidence C. elegans cmk-1 loss-of-function, microfluidic calcium imaging, behavioral assays

    PMID:29875264

    Open questions at the time
    • Molecular substrates mediating the learning phenotype not identified
    • Effects on sensory calcium responses described as subtle
  12. 2021 High

    Established the mechanism of calcium-triggered CAMK1 nuclear translocation, showing Ca2+/CaM binding increases CMK-1 affinity for IMA-3 importin to drive slow nuclear import matched to sensory adaptation timescales.

    Evidence In vivo live imaging, optogenetic Ca2+ control, genetic manipulation, co-IP of CMK-1 with IMA-3

    PMID:34766550

    Open questions at the time
    • Nuclear targets driving behavioral plasticity not enumerated
    • Conservation of the IMA-3/importin interaction in mammals not tested here
  13. 2022 Medium

    Connected CAMK1 to mitophagy, showing pitavastatin-driven mitochondrial calcium release activates CAMK1 (Thr177), which phosphorylates PINK1 Ser228 to recruit Parkin and activate mitophagy in endothelial progenitor cells.

    Evidence Phospho-CAMK1/PINK1 Western blots, PINK1-KO mice, Atg7 silencing, calcium measurements, pharmacology

    PMID:35145192

    Open questions at the time
    • Direct CAMK1-PINK1 phosphorylation not reconstituted in vitro
    • Single lab, single cell type
  14. 2024 Medium

    Linked CAMK1 to mitochondrial dynamics in cancer, showing CAMK1 overexpression interacts with PI3K, suppresses PI3K/AKT signaling, and induces mitochondrial dysfunction and anoikis in colorectal cancer.

    Evidence Overexpression, co-IP with PI3K, JC-1/ROS/apoptosis assays, mouse tumor models, PI3K-activator rescue

    PMID:42175534

    Open questions at the time
    • Whether CAMK1 directly phosphorylates PI3K unresolved
    • Overexpression context may not reflect endogenous CAMK1 levels
  15. 2024 Medium

    Identified CAMK1 as a regulator of mitochondrial fission and renal protection, with IGF2BP3/m6A stabilizing CAMK1 mRNA and proximal-tubule CAMK1 knockout worsening diabetic kidney injury.

    Evidence Proximal-tubule CAMK1 knockout mice, STZ diabetes, RIP/MeRIP/luciferase, mRNA stability assay, EM of mitochondria

    PMID:38216068

    Open questions at the time
    • Direct fission-machinery substrate of CAMK1 not identified
    • Mechanism connecting kinase activity to fission control unresolved
  16. 2025 Medium

    Began systematic substrate mapping, identifying hundreds of CMK-1 phosphotargets including calcineurin TAX-6, and revealing antagonistic CMK-1/calcineurin control of thermal nociception and adaptation.

    Evidence In vitro kinase assays with MS phosphoproteomics, C. elegans genetics, cell-specific manipulation

    PMID:40305390

    Open questions at the time
    • Direct TAX-6 phosphorylation may not underlie the behavioral phenotype
    • Most identified substrates not individually validated

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CAMK1's distinct outputs — transcriptional control, mitophagy/mitochondrial dynamics, autophagy, and immune effector functions — are selected by upstream calcium-source and isoform context in mammalian cells remains unresolved.
  • No unified substrate-selection logic across tissues established
  • Mammalian nuclear translocation mechanism not directly demonstrated
  • Few direct substrates validated in mammalian systems beyond GCM1, HDAC5, CaMKP-N, and PINK1

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 6 GO:0140096 catalytic activity, acting on a protein 6 GO:0098772 molecular function regulator activity 1 GO:0140657 ATP-dependent activity 1
Localization
GO:0005634 nucleus 2 GO:0005829 cytosol 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-1266738 Developmental Biology 2 R-HSA-74160 Gene expression (Transcription) 2 R-HSA-9612973 Autophagy 2
Partners
GCM1HDAC5IMA-3PI3KPINK1PPM1ETAX-6

Evidence

Reading pass · 16 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2012 Crystal structures of human CaMKIα (apo form and ATP-bound complexes) revealed that in the autoinhibited state, the activation segment adopts a helical conformation that together with the autoinhibitory segment constrains helices αC and αD in inactive conformations, sequesters Thr177 from phosphorylation, and occludes the substrate-binding site. In an ATP-bound active structure, the regulatory region is dissociated from the catalytic core and the catalytic site assumes an active conformation. X-ray crystallography of four structures of three CaMKIα truncates in apo and ATP-bound forms PloS one High 23028635
2011 CaMKI (but not CaMKIV) contributes to stimulation of WIPI-1 puncta formation at the onset of autophagy downstream of Ca2+/CaMKK signaling; siRNA-mediated knockdown of CaMKI reduced starvation-induced autophagosomal membrane formation independently of AMPKα1/α2. siRNA knockdown of CaMKI, automated high-throughput WIPI-1 puncta analysis, LC3 lipidation assays, pharmacological inhibitors (STO-609, KN-93) Molecular pharmacology Medium 21896713
2011 Epac1 and Rap1, in response to cAMP, activate CaMKI to phosphorylate Ser47 of GCM1; this phosphorylation facilitates interaction between GCM1 and the desumoylating enzyme SENP1, leading to GCM1 desumoylation and activation, thereby promoting syncytin-1/2 expression and trophoblast cell fusion. RNAi knockdown, phosphomimetic/non-phosphorylatable GCM1 mutants, co-immunoprecipitation, transient expression assays in BeWo placental cells Molecular and cellular biology High 21791615
2013 The Epac1/Rap1/CaMKI signaling cascade phosphorylates HDAC5 on Ser259 and Ser498 in a Rap1- and CaMKI-dependent manner, causing nuclear export of HDAC5, thereby relieving HDAC5-mediated deacetylation and transcriptional repression of GCM1 and promoting syncytin-1 expression and placental cell fusion. Co-immunoprecipitation, immunofluorescence microscopy, phospho-specific antibodies against HDAC5, transient expression of constitutively active Epac1 and CaMKI, RNAi Molecular human reproduction High 23867755
2012 CaMKI phosphorylates nuclear CaMK phosphatase (CaMKP-N/PPM1E; zebrafish ortholog zCaMKP-N) at Ser-480 in vitro; phosphorylation-mimic mutants (S480D/S480E) showed higher phosphatase activity and more potently attenuated CaMKII autophosphorylation in cells, indicating CaMKI activates CaMKP-N to provide negative feedback on multifunctional CaMKs. In vitro kinase assay with activated CaMKI, site-directed mutagenesis (S480A, S480D, S480E), solution-based phosphatase assay, co-transfection in Neuro2a cells with ionomycin treatment Biochemical and biophysical research communications High 22627141
2015 CaMKIδ isoform is phosphatase-resistant compared to CaMKIα due to its N-terminal region structure (residues Pro-57, Lys-62, Ser-66, Ile-68, and Arg-76); CaMKP/PPM1F barely dephosphorylates CaMKIδ, allowing it to remain in a 'primed' phosphorylated, active state under low-Ca2+ conditions and to phosphorylate CREB without Ca2+ stimulation. Transient expression in 293T cells, in vitro dephosphorylation assay with CaMKP/PPM1F, chimeric and point mutants of CaMKIδ and CaMKIα, CREB phosphorylation assay Biochemistry High 25994484
2022 Pitavastatin promotes mitochondrial calcium release into the cytoplasm, which phosphorylates CAMK1 (at Thr177); phosphorylated CAMK1 in turn phosphorylates PINK1 at Ser228, which recruits PARK2 (Parkin) and phosphorylates its Ser65 to activate mitophagy, improving endothelial progenitor cell proliferation. CAMK1 phosphorylation assays in EPCs, PINK1-KO mice, Atg7 silencing, intracellular calcium measurements, Western blot for phospho-CAMK1 (Thr177) and phospho-PINK1 (Ser228), pharmacological inhibition Communications biology Medium 35145192
2021 In C. elegans thermosensory neurons, elevation of intracellular Ca2+ is necessary and sufficient for CMK-1 (CaMKI ortholog) nuclear import; Ca2+/CaM binding to CMK-1 increases its affinity for IMA-3 importin, driving nuclear translocation with slow kinetics that matches the timescale of sensory adaptation and is essential for experience-dependent behavioral plasticity and gene transcription control. In vivo live imaging in C. elegans, genetic manipulation (loss-of-function, constitutively active CMK-1), optogenetics to control Ca2+, co-immunoprecipitation of CMK-1 with IMA-3 importin eLife High 34766550
2015 CMK-1 (CaMKI ortholog in C. elegans) regulates the dauer developmental decision as a function of feeding state; CMK-1 acts cell-autonomously in ASI neurons to regulate daf-7 TGF-β expression and non-cell-autonomously in AWC neurons to regulate daf-28 insulin-like peptide expression; food availability dynamically regulates subcellular localization of CMK-1 in AWC neurons. C. elegans genetics (cmk-1 mutants), cell-specific rescue experiments, transgenic reporters for daf-7 and daf-28, live imaging of CMK-1 subcellular localization eLife High 26335407
2018 CMK-1 (CaMKI ortholog) is required in ASE chemosensory neurons for salt-aversive learning in C. elegans; loss of cmk-1 has subtle effects on sensory-evoked calcium responses in ASE axons and their modulation by salt conditioning, placing CMK-1 as a regulator of behavioral plasticity downstream of sensory calcium signals. C. elegans genetics (cmk-1 loss-of-function), microfluidics-based calcium imaging in ASE neurons, behavioral assays The Journal of neuroscience Medium 29875264
2025 In C. elegans, CMK-1 (CaMKI ortholog) and calcineurin TAX-6 have antagonistic roles in modulating thermal nociception and adaptation to repeated stimuli; in vitro kinase assay combined with phosphoproteomics identified hundreds of CMK-1 substrates including the calcineurin A subunit TAX-6 (phosphorylated in its conserved regulatory domain); cell-specific analysis placed CMK-1 in AFD and ASER neurons and TAX-6 in FLP neurons and interneurons. In vitro kinase assays, mass-spectrometry-based phosphoproteomics, C. elegans genetics, pharmacological analyses, cell-specific genetic manipulations eLife Medium 40305390
2008 Ca2+/calmodulin kinase I regulates Nur77 (Nr4a1) promoter activity in MA-10 Leydig cells; cAMP-mediated induction of Nur77 expression involves a CaMK-dependent pathway with distinct regulatory elements for basal and cAMP-induced Nur77 transcription. Promoter-reporter assays, pharmacological CaMK inhibition, transient transfection in MA-10 cells Journal of andrology Low 18835829
2005 CKLiK (CaMKI-like kinase restricted to granulocytes) activity is induced by fMLP and PAF stimulation in parallel with intracellular Ca2+ rise; inhibition of CKLiK with a cell-permeable peptide inhibitor reduced phagocytosis, fMLP-induced ROS production, neutrophil migration, and β2-integrin-mediated adhesion. CKLiK peptide inhibitor (CKLiK297-321), kinase activity assays, phagocytosis assay, ROS/respiratory burst assay, migration assay, adhesion assay in primary human granulocytes Blood Medium 15840691
2016 A constitutively active fragment of zebrafish CaMKIδ (zCaMKIδ(1-299)) lacking the autoinhibitory domain showed high, Ca2+-independent kinase activity comparable to CaMKK-activated wild-type CaMKIδ, confirming that the autoinhibitory domain suppresses basal kinase activity; the fragment exhibited broad substrate specificity similar to full-length activated CaMKIδ. Recombinant protein expression in E. coli, in vitro kinase activity assays, substrate specificity profiling, comparison with PKAc and CaMKII Biochemical and biophysical research communications Medium 27207832
2024 CAMK1 overexpression in colorectal cancer cells inhibits PI3K phosphorylation and downstream AKT pathway activation; CAMK1 interacts with PI3K (by co-immunoprecipitation), and this interaction induces mitochondrial dysfunction (membrane potential depolarization, increased ROS), elevated Bax/Bcl-2 ratio, and Caspase-3 activation to promote anoikis; PI3K activator 740Y-P reversed these effects. CAMK1 overexpression in CRC cell lines, co-immunoprecipitation of CAMK1 with PI3K, phosphorylation assays, mitochondrial membrane potential (JC-1), ROS measurement, apoptosis assays, mouse tumor and metastasis models, rescue with PI3K activator FASEB journal Medium 42175534
2024 IGF2BP3 promotes stability of CAMK1 mRNA through m6A modification, increasing CAMK1 protein levels; CAMK1 inhibits mitochondrial fission, and conditional knockout of CAMK1 in proximal tubules aggravates kidney injury and promotes mitochondrial fission in diabetic mice. Proximal tubule-specific CAMK1 knockout mice, STZ-induced diabetes model, RIP assay, dual-luciferase reporter assay, MeRIP (m6A), actinomycin D mRNA stability assay, electron microscopy of mitochondria, JC-1 staining Biochimica et biophysica acta. Molecular basis of disease Medium 38216068

Source papers

Stage 0 corpus · 24 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 Ca2+/calmodulin-dependent kinase (CaMK) signaling via CaMKI and AMP-activated protein kinase contributes to the regulation of WIPI-1 at the onset of autophagy. Molecular pharmacology 71 21896713
2011 A novel cyclic AMP/Epac1/CaMKI signaling cascade promotes GCM1 desumoylation and placental cell fusion. Molecular and cellular biology 44 21791615
2005 Characterization of the role of CaMKI-like kinase (CKLiK) in human granulocyte function. Blood 43 15840691
2008 cAMP-induced expression of the orphan nuclear receptor Nur77 in MA-10 Leydig cells involves a CaMKI pathway. Journal of andrology 42 18835829
2020 Expression of CAMK1 and its association with clinicopathologic characteristics in pancreatic cancer. Journal of cellular and molecular medicine 36 33342045
2015 Feeding state-dependent regulation of developmental plasticity via CaMKI and neuroendocrine signaling. eLife 32 26335407
2015 Capsicum annuum transcription factor WRKYa positively regulates defense response upon TMV infection and is a substrate of CaMK1 and CaMK2. Scientific reports 30 25613640
2022 Pitavastatin activates mitophagy to protect EPC proliferation through a calcium-dependent CAMK1-PINK1 pathway in atherosclerotic mice. Communications biology 26 35145192
2018 Loss of CaMKI Function Disrupts Salt Aversive Learning in C. elegans. The Journal of neuroscience : the official journal of the Society for Neuroscience 26 29875264
2020 Exosomal miR-211 contributes to pulmonary hypertension via attenuating CaMK1/PPAR-γaxis. Vascular pharmacology 25 33238205
2013 Involvement of Epac1/Rap1/CaMKI/HDAC5 signaling cascade in the regulation of placental cell fusion. Molecular human reproduction 23 23867755
2014 CAMK1 phosphoinositide signal-mediated protein sorting and transport network in human hepatocellular carcinoma (HCC) by biocomputation. Cell biochemistry and biophysics 17 24825433
2021 Ca2+/CaM binding to CaMKI promotes IMA-3 importin binding and nuclear translocation in sensory neurons to control behavioral adaptation. eLife 16 34766550
2024 IGF2BP3-stabilized CAMK1 regulates the mitochondrial dynamics of renal tubule to alleviate diabetic nephropathy. Biochimica et biophysica acta. Molecular basis of disease 14 38216068
2012 Crystal structures of human CaMKIα reveal insights into the regulation mechanism of CaMKI. PloS one 12 23028635
2018 1800 MHz radiofrequency fields inhibits testosterone production via CaMKI /RORα pathway. Reproductive toxicology (Elmsford, N.Y.) 11 30125682
2022 Characterization and Functional Analysis of a New Calcium/Calmodulin-Dependent Protein Kinase (CaMK1) in the Citrus Pathogenic Fungus Penicillium italicum. Journal of fungi (Basel, Switzerland) 10 35887424
2014 Negative feedback regulation of calcineurin-dependent Prz1 transcription factor by the CaMKK-CaMK1 axis in fission yeast. Nucleic acids research 10 25081204
2012 Phosphorylation and activation of nuclear Ca2+/calmodulin-dependent protein kinase phosphatase (CaMKP-N/PPM1E) by Ca2+/calmodulin-dependent protein kinase I (CaMKI). Biochemical and biophysical research communications 10 22627141
2015 The Phosphatase-Resistant Isoform of CaMKI, Ca²⁺/Calmodulin-Dependent Protein Kinase Iδ (CaMKIδ), Remains in Its "Primed" Form without Ca²⁺ Stimulation. Biochemistry 9 25994484
2016 High-performance CaMKI: A highly active and stable form of CaMKIδ produced by high-level soluble expression in Escherichia coli. Biochemical and biophysical research communications 5 27207832
2025 Antagonist actions of CMK-1/CaMKI and TAX-6/calcineurin along the C. elegans thermal avoidance circuit orchestrate adaptation of nociceptive response to repeated stimuli. eLife 3 40305390
2026 CAMK1 Suppresses Anoikis Resistance and Liver Metastasis in Colorectal Cancer. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 0 42175534
2025 Dysregulation of Protein Kinase CaMKI Leads to Autism-Related Phenotypes in Synaptic Connectivity, Sleep, Sociality, and Aging-Dependent Degeneration in Drosophila. Biology 0 41007373

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