Affinage

CAPN2

Calpain-2 catalytic subunit · UniProt P17655

Round 2 corrected
Length
700 aa
Mass
80.0 kDa
Annotated
2026-04-28
51 papers in source corpus 19 papers cited in narrative 19 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CAPN2 encodes the catalytic large subunit of m-calpain, a calcium-dependent cysteine protease that serves as a context-dependent regulator of cell adhesion, migration, apoptosis, and inflammatory signaling. In the calcium-free state, the catalytic subdomains dIIa and dIIb are misaligned by ~50°, rendering the active site non-functional; calcium binding to a negatively charged electrostatic switch loop in domain dIII realigns the subdomains for catalysis, and ERK-mediated phosphorylation at Ser50 provides a calcium-independent activation route downstream of EGF signaling (PMID:10639123, PMID:14993287). Active CAPN2 cleaves IκBα to activate NF-κB, p35 to generate the neurotoxic p25/CDK5 complex, Bcl-2 family members and Atg5 to trigger mitochondrial apoptosis, and caspases-7/8/9 at non-canonical sites to suppress apoptosis, positioning it as a pivotal switch between cell survival and death programs (PMID:9873017, PMID:10830966, PMID:12000759, PMID:16998475, PMID:10671558). CAPN2 protein stability is regulated by TRIM8-mediated ubiquitination and proteasomal degradation, and its transcription during myogenesis is controlled by MyoD through E-box and MEF-2 elements in the CAPN2 promoter (PMID:40520022, PMID:12559913).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1991 Medium

    Determining where calpain isoforms reside in the cell was necessary before mechanistic studies; fractionation and immunofluorescence established that m-calpain is predominantly membrane-associated in Schwann cells yet cytosolic in brain, revealing tissue-dependent compartmentalization.

    Evidence Subcellular fractionation with activity assays and isoform-specific immunofluorescence in transformed Schwann cells and mouse/human brain

    PMID:1548485 PMID:1656060

    Open questions at the time
    • Mechanism of membrane recruitment unresolved
    • No live-cell imaging to confirm dynamics
    • Tissue-specific regulatory factors not identified
  2. 1995 Medium

    How calcium activates the heterodimer was unclear; biochemical studies showed that Ca²⁺ induces dissociation of the 80-kDa and 30-kDa subunits, with the free large subunit representing the active enzyme.

    Evidence Biochemical dissociation and activity assays on purified calpain heterodimer

    PMID:8561910

    Open questions at the time
    • Structural basis of dissociation not resolved at atomic level
    • In vivo dissociation dynamics not confirmed
    • Single-lab biochemical characterization
  3. 1999 High

    Whether calpain could directly participate in NF-κB signaling was unknown; reconstitution showed that TNFα-activated m-calpain cleaves IκBα independently of the proteasome, enabling NF-κB nuclear translocation.

    Evidence Broken-cell reconstitution with purified m-calpain, calpastatin overexpression, ubiquitin-pathway-deficient cell line

    PMID:9873017

    Open questions at the time
    • Cleavage site on IκBα not mapped
    • Relative contribution of calpain vs. proteasome pathway in vivo not quantified
  4. 2000 High

    The structural basis of calpain autoinhibition was resolved: the 2.3-Å crystal structure of calcium-free m-calpain revealed a ~50° rotation between catalytic subdomains dIIa and dIIb that disrupts the active site, and identified the dIII electrostatic switch loop whose calcium binding would permit realignment.

    Evidence X-ray crystallography at 2.3 Å of recombinant full-length heterodimeric human m-calpain

    PMID:10639123

    Open questions at the time
    • No calcium-bound structure to confirm predicted subdomain movement
    • Role of each individual calcium-binding site not dissected
  5. 2000 High

    Two key substrate classes were identified simultaneously: calpain cleaves caspases-7/8/9 at non-canonical sites to inactivate them (suppressing apoptosis), and cleaves p35 to generate the neurotoxic p25/CDK5 complex driving tau hyperphosphorylation and neurodegeneration.

    Evidence In vitro cleavage with N-terminal sequencing for caspases; recombinant p35 cleavage, calpain inhibitor rescue in Aβ-treated primary cortical neurons

    PMID:10671558 PMID:10830966

    Open questions at the time
    • In vivo stoichiometry of caspase inactivation vs. activation pathways not determined
    • Isoform specificity (CAPN1 vs. CAPN2) for p35 cleavage not resolved
  6. 2002 High

    The role of calpain in the intrinsic apoptotic pathway was established when m-calpain was shown to cleave Bcl-2, Bid, and Bcl-xL, generating truncated forms that induce cytochrome c release from mitochondria.

    Evidence In vitro cleavage of recombinant Bcl-2 family proteins, binding studies, cytochrome c release from isolated mitochondria, calpastatin inhibition in cells

    PMID:12000759

    Open questions at the time
    • Relative importance of each Bcl-2 family substrate in different apoptotic contexts unclear
    • Whether calpain-truncated Bid functions identically to caspase-8-truncated tBid not tested
  7. 2003 Medium

    How CAPN2 transcription is controlled during differentiation was unknown; promoter analysis revealed MyoD as the pivotal transactivator of CAPN2 through E-box and MEF-2 elements, linking calpain upregulation to the myogenic program.

    Evidence Promoter deletion/reporter assays, overexpression of myogenic factors, antisense oligonucleotide knockdown of MyoD

    PMID:12559913

    Open questions at the time
    • Chromatin accessibility at the CAPN2 locus during myogenesis not examined
    • Whether other tissues use analogous transcriptional control is unknown
    • Single-lab study
  8. 2004 High

    A calcium-independent activation mechanism was discovered: ERK directly phosphorylates CAPN2 at Ser50 downstream of EGF, and this phosphorylation is necessary and sufficient for calpain activation, cell deadhesion, and motility.

    Evidence In vitro kinase assay, S50A/S50E mutagenesis, intracellular calcium chelation, cell motility assays

    PMID:14993287

    Open questions at the time
    • Structural mechanism by which Ser50 phosphorylation bypasses calcium requirement not resolved
    • Whether other kinases phosphorylate this site in different contexts not tested
  9. 2006 High

    Two studies expanded the functional reach of CAPN2: TRPM7 ion channel activity was shown to regulate cell adhesion through local m-calpain activation at peripheral adhesion complexes, and calpain cleavage of Atg5 was identified as a molecular switch converting autophagy to apoptosis.

    Evidence TRPM7/m-calpain co-localization, epistasis by double knockdown; Atg5 in vitro cleavage, Co-IP with Bcl-xL, siRNA rescue, subcellular fractionation

    PMID:16436382 PMID:16998475

    Open questions at the time
    • Identity of TRPM7-derived ions activating calpain (Ca²⁺ vs. others) not fully dissected
    • Whether Atg5 cleavage is CAPN1- or CAPN2-specific not determined
  10. 2022 Medium

    Beyond apoptosis, CAPN2 was linked to pyroptosis: cisplatin activates CAPN1/CAPN2 to trigger BAK/BAX activation and a caspase-9→caspase-3→GSDME cascade executing pyroptotic cell death in esophageal cancer cells.

    Evidence CAPN1/CAPN2 gene knockout, pharmacological calpain inhibition, LDH release and calpain activity assays

    PMID:35525317

    Open questions at the time
    • Individual contributions of CAPN1 vs. CAPN2 not separated
    • Direct cleavage of BAK/BAX by calpain not demonstrated biochemically
    • Single cancer cell line study
  11. 2023 Medium

    A developmental role for CAPN2 was established when loss-of-function in Xenopus caused hypoplastic ventricle phenotypes, and human CAPN2 hypomorphic variants were identified in individuals with hypoplastic left heart syndrome.

    Evidence Morpholino knockdown in Xenopus laevis, cardiac phenotyping, exome sequencing of human HLHS cohort, functional variant validation in vivo

    PMID:37663545

    Open questions at the time
    • Cardiac substrate(s) of CAPN2 responsible for ventricle morphogenesis unknown
    • Mouse knockout cardiac phenotype not reported
    • Small human cohort, not yet independently replicated
  12. 2025 Medium

    Post-translational regulation of CAPN2 stability was uncovered: the E3 ubiquitin ligase TRIM8 directly ubiquitinates CAPN2 for proteasomal degradation, and ITLN1 antagonizes this process to stabilize CAPN2 and drive ZBP1-dependent PANoptosis in Crohn's disease intestinal epithelium.

    Evidence Reciprocal Co-IP/MS, TRIM8 ubiquitination assays, shRNA/overexpression rescue, IL-10 KO mouse model

    PMID:40520022

    Open questions at the time
    • Ubiquitination site(s) on CAPN2 not mapped
    • Whether TRIM8 regulation of CAPN2 operates outside intestinal epithelium is unknown
    • Single-lab study

Open questions

Synthesis pass · forward-looking unresolved questions
  • A calcium-bound crystal structure of full-length m-calpain that confirms the predicted subdomain realignment has not been reported, and the isoform-specific (CAPN1 vs. CAPN2) substrate selectivity and in vivo redundancy remain poorly defined.
  • No calcium-bound full-length m-calpain structure
  • Isoform-specific substrate repertoire not systematically delineated
  • In vivo mouse knockout phenotype for CAPN2 incompletely characterized

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 6 GO:0016787 hydrolase activity 5
Localization
GO:0005829 cytosol 2 GO:0005886 plasma membrane 2
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-1266738 Developmental Biology 2 R-HSA-9612973 Autophagy 2
Partners
CAPNS1CASTITLN1TRIM8TRPM7
Complex memberships
m-calpain heterodimer (CAPN2/CAPNS1)

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 The 2.3-Å crystal structure of full-length heterodimeric human m-calpain (CAPN2 large subunit + small subunit) in the absence of calcium reveals that the two catalytic subdomains (dIIa+dIIb) are rotated ~50° relative to one another, disrupting the active site and substrate-binding site, explaining calcium-dependent inactivation. An extremely negatively charged loop in domain dIII was identified as an 'electrostatic switch' whose calcium binding could allow subdomain dIIb to move toward dIIa, forming a functional catalytic center. X-ray crystallography at 2.3 Å resolution of recombinant heterodimeric human m-calpain Proceedings of the National Academy of Sciences of the United States of America High 10639123
2004 EGF activates m-calpain (CAPN2) through ERK-mediated direct phosphorylation at serine 50 of the large subunit, independent of intracellular calcium elevation. Phosphorylation at S50 is required for EGF-induced calpain activation, cell deadhesion, and motility; an S50A substitution limits activation, while an S50E substitution confers constitutive activity in vivo. In vitro kinase assay (ERK phosphorylates m-calpain), site-directed mutagenesis (S50A/S50E), intracellular calcium chelation, cell motility and deadhesion assays Molecular and cellular biology High 14993287
1999 TNF-α activates cytosolic m-calpain (CAPN2), which directly cleaves IκBα in a proteasome-independent manner, allowing NF-κB nuclear translocation. This calpain-dependent pathway for IκBα proteolysis operates in parallel to the ubiquitin-proteasome pathway; calpastatin overexpression partially blocks TNF-α-induced NF-κB activity. Fluorescent calpain activity assay, broken-cell reconstitution with purified m-calpain, calpastatin transfection, ubiquitin-pathway-deficient cell line (ts20b), subcellular fractionation The Journal of biological chemistry High 9873017
2000 Calpain (including m-calpain/CAPN2) directly cleaves caspase-7, caspase-8, and caspase-9 at sites distinct from those used by upstream caspases, generating proteolytically inactive fragments. Calpain cleavage of caspase-9 blocks dATP/cytochrome c-induced caspase-3 activation, identifying calpain as a negative regulator of caspase processing and apoptosis. In vitro cleavage assays with purified calpain and recombinant caspases, N-terminal sequencing of cleavage products, cell-free caspase-3 activation assay The Journal of biological chemistry High 10671558
2002 Ionomycin-activated calpains (mu- and m-calpain/CAPN2) cleave Bcl-2, Bid, and Bcl-xL in vitro at single sites truncating their N-terminal regions. Calpain-truncated Bcl-2 and Bid exhibit diminished interactions with intact Bcl-2 family proteins and induce cytochrome c release from isolated mitochondria, triggering the intrinsic apoptotic pathway. In vitro cleavage assays with recombinant Bcl-2 family proteins, binding studies with immobilized proteins, cytochrome c release assay from isolated mitochondria, calpastatin inhibitor pretreatment in LCLC103H cells The Journal of biological chemistry High 12000759
2006 Calpain (m-calpain/CAPN2) cleaves Atg5 at a site generating a truncated ~24 kDa N-terminal fragment that translocates from cytosol to mitochondria, associates with Bcl-xL, and triggers cytochrome c release and caspase activation, converting autophagy to apoptosis. Forced expression and siRNA of Atg5 in tumor cells, calpain inhibitor treatment, subcellular fractionation, co-immunoprecipitation with Bcl-xL, in vitro calpain cleavage assay Nature cell biology High 16998475
2006 TRPM7 co-localizes with m-calpain (CAPN2) at peripheral adhesion complexes and regulates cell adhesion by controlling local calpain activity. TRPM7 overexpression causes cell rounding and loss of adhesion dependent on its ion channel activity; knockdown of m-calpain blocks TRPM7-induced cell detachment, and TRPM7 silencing increases peripheral adhesion complexes. Co-localization imaging, TRPM7 overexpression and RNAi knockdown, m-calpain RNAi rescue epistasis, cell adhesion and morphology assays The Journal of biological chemistry High 16436382
1991 In transformed Schwann cells, >75% of m-calpain (mCANP/CAPN2) activity is membrane-associated while ~80% of mu-calpain is cytosolic. Immunofluorescence with distinct antibodies showed mCANP distributed throughout the intracellular space (sparing the perinuclear region) in permeabilized cells, while anti-cytosolic mCANP antibody stained most intensely in the perinuclear region, establishing distinct subcellular compartmentalization of the two isoforms. DEAE and phenyl Sepharose column chromatography for isoform separation, activity assays on subcellular fractions, immunofluorescence with isoform-specific antibodies on live vs. permeabilized cells Journal of neuroscience research Medium 1656060
1992 In mouse and human brain, >95% of total immunoreactive m-calpain (mCANP/CAPN2) is located in the soluble (cytosolic) fraction after 15,000 g centrifugation, with caseinolytic activity detectable only in fractions from the supernatant. Triton X-100 extraction does not alter this distribution, establishing mCANP as a predominantly cytosolic enzyme in brain. Western blot immunoassay with two independent mCANP-specific antibodies, [14C]azocasein activity assay after DEAE-cellulose removal of endogenous inhibitor, differential centrifugation, Triton X-100 extraction Journal of neurochemistry Medium 1548485
2000 Calpain, activated by calcium influx or amyloid-β peptide, directly cleaves p35 (the CDK5 activator) to generate p25, causing prolonged CDK5 activation and mislocalization, tau hyperphosphorylation, and neuronal apoptosis. Specific calpain inhibitors block calcium-induced p35 cleavage in brain lysates and reduce neuronal death in Aβ-treated cortical neurons. In vitro calpain cleavage assay with recombinant p35, calpain inhibitor treatment in primary cortical neurons, brain lysate calcium stimulation, N-terminal sequencing of cleavage product Nature High 10830966
1995 Ca2+ binding causes dissociation of the calpain heterodimer (large 80-kDa subunit encoded by CAPN2 and small 30-kDa subunit), with the free 80-kDa subunit being the active form of the enzyme; this dissociation mechanism corresponds to calpain activation. Biochemical dissociation studies and activity assays Biological chemistry Hoppe-Seyler Medium 8561910
2003 The capn2 promoter contains five consensus E-box binding sites for myogenic regulatory factors and one MEF-2 binding site. MyoD (and, with lesser efficiency, myogenin) transactivates capn2 expression specifically through these elements, particularly the MEF-2/E4-box region. Antisense oligonucleotides against MyoD specifically suppress capn2 upregulation during myogenesis, establishing MyoD as the pivotal regulator of capn2 transcription during myoblast fusion. Promoter deletion analysis, transient transfection with reporter constructs, overexpression of myogenic factors, antisense oligonucleotide knockdown of individual MRFs Journal of molecular biology Medium 12559913
2022 Cisplatin activates CAPN1/CAPN2 calpain activity in esophageal cancer cells, which in turn activates BAK/BAX, triggering a caspase-9→caspase-3→GSDME signaling cascade that executes pyroptosis. Calpain inhibition or CAPN1/CAPN2 knockout suppresses cisplatin-induced pyroptosis and LDH release. Western blotting, LDH release assay, calpain activity assay, cell viability assay, CAPN1/CAPN2 knockout by gene editing, pharmacological calpain inhibition Chemico-biological interactions Medium 35525317
2012 Proteomic profiling of hepatocellular carcinoma cell lines with different metastatic potential identified a CAPN2-centered proteolytic subnetwork including SPTBN1, ATP5B, and VIM that is more active in the highly metastatic cell line, with persistent proteolytic fragments of these substrates detected preferentially in the high-metastasis line. PROTOMAP platform (gel separation + mass spectrometry peptide mapping), bioinformatics network analysis comparing two HCC cell lines Proteomics Low 22623320
2019 CAPN2 knockdown in HBV-induced hepatic fibrosis cells suppresses expression of fibrosis markers α-SMA, COL3A1, COL1A1, and MAPK1, placing CAPN2 upstream of MAPK1 signaling in HBV-driven hepatic fibrosis. siRNA knockdown of CAPN2, western blot for fibrosis markers and MAPK1, RT-qPCR, immunohistochemistry in patient tissues Journal of cellular biochemistry Low 31680308
2017 Silencing CAPN2 in castration-resistant prostate cancer cells induces G1 cell cycle arrest, reduces migration and invasion by decreasing MMP-2 and MMP-9 activation, and suppresses phosphorylation of AKT and mTOR, placing CAPN2 upstream of the AKT/mTOR signaling axis in CRPC. siRNA knockdown of CAPN2, cell cycle analysis, transwell migration/invasion assay, western blot for pAKT, pmTOR, MMP-2, MMP-9 BioMed research international Low 28280729
2025 ITLN1 binds directly to CAPN2 (via Co-IP/MS), enhancing CAPN2 protein stability by antagonizing the E3 ubiquitin ligase TRIM8, which directly ubiquitinates CAPN2 to promote its proteasomal degradation. The ITLN1-TRIM8-CAPN2 axis drives ZBP1-dependent PANoptosis in intestinal epithelial cells in Crohn's disease. Co-immunoprecipitation combined with mass spectrometry, western blot, RNA-seq, rescue experiments with shRNA and overexpression, IL-10 KO mouse model in vivo International journal of biological sciences Medium 40520022
2024 CAPN2 promotes apalutamide resistance in prostate cancer by inhibiting FOXO1 degradation and promoting its nuclear translocation, which then transcriptionally upregulates ATG5 to activate protective autophagy. ATF3 transcriptionally activates CAPN2 to drive this axis. RNA sequencing, western blotting, immunofluorescence, transmission electron microscopy, dual-fluorescence autophagy assay, nucleoplasmic protein isolation, shRNA knockdown Journal of translational medicine Medium 38844946
2023 CAPN2 loss-of-function in Xenopus laevis causes hypoplastic ventricle phenotypes, establishing that CAPN2 is essential for cardiac ventricle morphogenesis. Human CAPN2 variants (p.707C>T and p.1112C>T) found in multiple individuals with isolated hypoplastic left heart syndrome behave as hypomorphic alleles in this vertebrate model. Xenopus laevis morpholino-based loss-of-function, cardiac morphology phenotyping, exome sequencing of human HLHS cohort, functional hypomorph validation in vivo HGG advances Medium 37663545

Source papers

Stage 0 corpus · 51 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1997 Caspases: the executioners of apoptosis. The Biochemical journal 3881 9337844
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2015 The BioPlex Network: A Systematic Exploration of the Human Interactome. Cell 1118 26186194
2006 Calpain-mediated cleavage of Atg5 switches autophagy to apoptosis. Nature cell biology 1087 16998475
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2015 A human interactome in three quantitative dimensions organized by stoichiometries and abundances. Cell 1015 26496610
2000 Neurotoxicity induces cleavage of p35 to p25 by calpain. Nature 915 10830966
2018 VIRMA mediates preferential m6A mRNA methylation in 3'UTR and near stop codon and associates with alternative polyadenylation. Cell discovery 829 29507755
2003 Complete sequencing and characterization of 21,243 full-length human cDNAs. Nature genetics 754 14702039
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2008 Large-scale proteomics and phosphoproteomics of urinary exosomes. Journal of the American Society of Nephrology : JASN 607 19056867
2011 Analysis of the myosin-II-responsive focal adhesion proteome reveals a role for β-Pix in negative regulation of focal adhesion maturation. Nature cell biology 490 21423176
2003 Exploring proteomes and analyzing protein processing by mass spectrometric identification of sorted N-terminal peptides. Nature biotechnology 485 12665801
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2005 Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes. Genome research 409 16344560
2015 Panorama of ancient metazoan macromolecular complexes. Nature 407 26344197
2007 Systematic analysis of the protein interaction network for the human transcription machinery reveals the identity of the 7SK capping enzyme. Molecular cell 367 17643375
2000 The crystal structure of calcium-free human m-calpain suggests an electrostatic switch mechanism for activation by calcium. Proceedings of the National Academy of Sciences of the United States of America 301 10639123
2012 A high-throughput approach for measuring temporal changes in the interactome. Nature methods 273 22863883
1996 The Ced-3/interleukin 1beta converting enzyme-like homolog Mch6 and the lamin-cleaving enzyme Mch2alpha are substrates for the apoptotic mediator CPP32. The Journal of biological chemistry 268 8900201
2022 Tau interactome maps synaptic and mitochondrial processes associated with neurodegeneration. Cell 256 35063084
2009 Proteomic analysis of human parotid gland exosomes by multidimensional protein identification technology (MudPIT). Journal of proteome research 237 19199708
2004 Epidermal growth factor activates m-calpain (calpain II), at least in part, by extracellular signal-regulated kinase-mediated phosphorylation. Molecular and cellular biology 235 14993287
2000 Direct cleavage by the calcium-activated protease calpain can lead to inactivation of caspases. The Journal of biological chemistry 234 10671558
1999 Tumor necrosis factor-alpha-inducible IkappaBalpha proteolysis mediated by cytosolic m-calpain. A mechanism parallel to the ubiquitin-proteasome pathway for nuclear factor-kappab activation. The Journal of biological chemistry 213 9873017
2015 ∆F508 CFTR interactome remodelling promotes rescue of cystic fibrosis. Nature 209 26618866
1995 Calpain: novel family members, activation, and physiologic function. Biological chemistry Hoppe-Seyler 190 8561910
2006 TRPM7 regulates cell adhesion by controlling the calcium-dependent protease calpain. The Journal of biological chemistry 189 16436382
2002 Ionomycin-activated calpain triggers apoptosis. A probable role for Bcl-2 family members. The Journal of biological chemistry 182 12000759
2005 Identification and molecular characterization of the rainbow trout calpains (Capn1 and Capn2): their expression in muscle wasting during starvation. Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology 47 15621511
2022 Cisplatin-induced pyroptosis is mediated via the CAPN1/CAPN2-BAK/BAX-caspase-9-caspase-3-GSDME axis in esophageal cancer. Chemico-biological interactions 44 35525317
2021 hnRNPK-regulated LINC00263 promotes malignant phenotypes through miR-147a/CAPN2. Cell death & disease 30 33731671
1991 Calcium-activated neutral proteinase (CANP; calpain) activity in Schwann cells: immunofluorescence localization and compartmentation of mu- and mCANP. Journal of neuroscience research 24 1656060
2017 Silencing CAPN2 Expression Inhibited Castration-Resistant Prostate Cancer Cells Proliferation and Invasion via AKT/mTOR Signal Pathway. BioMed research international 23 28280729
1992 Immunoassay and activity of calcium-activated neutral proteinase (mCANP): distribution in soluble and membrane-associated fractions in human and mouse brain. Journal of neurochemistry 22 1548485
2017 Overexpression of CAPN2 promotes cell metastasis and proliferation via AKT/mTOR signaling in renal cell carcinoma. Oncotarget 21 29228653
2012 Global profiling of proteolytically modified proteins in human metastatic hepatocellular carcinoma cell lines reveals CAPN2 centered network. Proteomics 21 22623320
2010 Characterisation of capn1, capn2-like, capn3 and capn11 genes in Atlantic halibut (Hippoglossus hippoglossus L.): Transcriptional regulation across tissues and in skeletal muscle at distinct nutritional states. Gene 17 20093171
2003 Transactivation of capn2 by myogenic regulatory factors during myogenesis. Journal of molecular biology 17 12559913
2020 Promotive effect of Talin-1 protein on gastric cancer progression through PTK2-PXN-VCL-E-Cadherin-CAPN2-MAPK1 signaling axis. Journal of clinical laboratory analysis 16 32951272
2020 miR-124 Intensified Oxaliplatin-Based Chemotherapy by Targeting CAPN2 in Colorectal Cancer. Molecular therapy oncolytics 15 32382656
2016 The CAPN2/CAPN8 Locus on Chromosome 1q Is Associated with Variation in Serum Alpha-Carotene Concentrations. Journal of nutrigenetics and nutrigenomics 9 28002826
2025 ITLN1 exacerbates Crohn's colitis by driving ZBP1-dependent PANoptosis in intestinal epithelial cells through antagonizing TRIM8-mediated CAPN2 ubiquitination. International journal of biological sciences 8 40520022
2019 CAPN2 acts as an indicator of hepatitis B virus to induce hepatic fibrosis. Journal of cellular biochemistry 8 31680308
2024 CAPN2 promotes apalutamide resistance in metastatic hormone-sensitive prostate cancer by activating protective autophagy. Journal of translational medicine 7 38844946
2024 METTL16 inhibits pancreatic cancer proliferation and metastasis by promoting MROH8 RNA stability and inhibiting CAPN2 expression - experimental studies. International journal of surgery (London, England) 6 39434688
2024 CAPN2 correlates with insulin resistance states in PCOS as evidenced by multi-dataset analysis. Journal of ovarian research 4 38610028
2024 Amentoflavone regulates the miR-124-3p/CAPN2 axis to promote mitochondrial autophagy in HCC cells. Toxicology research 3 39050595
2023 Rare variants in CAPN2 increase risk for isolated hypoplastic left heart syndrome. HGG advances 3 37663545
2011 [Beta-carotene regulates the expression of proapoptotic BAX and CAPN2 in HL-60, U-937 and TF-1 - human acute myeloid leukemia cell lines; microarray, RQ-PCR and Western Blot analysis]. Przeglad lekarski 2 21961413