Affinage

IRAG1

Inositol 1,4,5-triphosphate receptor associated 1 · UniProt Q9Y6F6

Length
904 aa
Mass
98.0 kDa
Annotated
2026-06-10
29 papers in source corpus 17 papers cited in narrative 17 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

IRAG1 (MRVI1) is an endoplasmic reticulum-anchored membrane protein that serves as the central scaffold of an NO/cGMP signaling module controlling intracellular Ca²⁺ release in smooth muscle and platelets (PMID:10724174). It assembles an obligate trimeric complex with cGMP-dependent protein kinase Iβ (cGKIβ/PKGIβ) and IP3 receptor type I, binding the kinase through an electrostatic interaction between the cGKIβ N-terminal leucine zipper (residues 1–53; acidic residues D26/E31) and basic residues in IRAG1 (residues 152–184), while bridging IP3R-I, which does not contact cGKIβ directly (PMID:11309393, PMID:16166082). This complex is isoform-specific: IRAG1 recruits cGKIβ — but not cGKIα or cGKII — to the ER (PMID:15388327). Upon cGMP activation, cGKIβ phosphorylates IRAG1, and phosphorylation at Ser696 is necessary and sufficient to inhibit IP3-induced Ca²⁺ release (PMID:11309393); in platelets the corresponding sites are Ser664/Ser677 (PMID:16990611). Through this mechanism IRAG1 mediates NO/cGMP-dependent relaxation of hormone receptor-triggered (but not K⁺-induced) smooth muscle contraction (PMID:15483626, PMID:20080989), inhibition of platelet aggregation, granule secretion, fibrinogen-receptor activation and arterial thrombosis (PMID:16990611, PMID:21244222), and NO-dependent inhibition of IP3R-driven TRPM4 channel activity to dilate cerebral arteries (PMID:34734188). Independently of its phosphorylation and Ca²⁺ functions, ER-anchored IRAG1 retains cGKIβ at the ER to prevent its cGMP-induced nuclear translocation and restrict CRE-dependent transcription (PMID:18450420), and is required for PKGIβ protein stability (PMID:34064290). Loss of IRAG1 in mice produces pulmonary hypertension with right ventricular hypertrophy (PMID:33066124) and gastrointestinal bleeding with iron-deficiency anemia (PMID:34064290). C-terminally truncated splice variants lacking the phosphorylation and IP3R-I interaction domains act as dominant-negative modulators of the pathway (PMID:21865585).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2000 High

    Established IRAG as the missing link coupling NO/cGMP signaling to inhibition of IP3-mediated Ca²⁺ release by demonstrating it forms a functional trimeric complex with cGKIβ and IP3R-I.

    Evidence Reciprocal Co-IP from native smooth muscle microsomes plus reconstitution by co-expression in COS-7 cells with calcium-release readout

    PMID:10724174

    Open questions at the time
    • Did not define the binding interfaces or the relevant phosphosite
    • Physiological requirement in vivo not yet tested
  2. 2001 High

    Mapped the molecular architecture of the complex, showing cGKIβ binds IRAG via its leucine zipper while IP3R-I is bridged through IRAG, and pinned the inhibitory function to phosphorylation of a single serine.

    Evidence Yeast two-hybrid, co-precipitation of expressed proteins, and Ser→Ala mutagenesis with calcium-release assays

    PMID:11309393

    Open questions at the time
    • Structural basis of the electrostatic interface not resolved at atomic level
    • Mapping done in heterologous/in vitro context
  3. 2004 High

    Proved IRAG is physiologically required for cGMP-dependent smooth muscle relaxation, and specifically for hormone receptor-triggered rather than depolarization-induced contraction.

    Evidence Exon 12 deletion mouse disrupting IRAG–IP3R-I interaction with contraction/relaxation and Ca²⁺ assays, plus antisense knockdown in human colonic SMCs

    PMID:14729908 PMID:15483626

    Open questions at the time
    • Exon 12 deletion disrupts IP3R-I binding but does not eliminate all IRAG functions
    • Did not address platelet or other tissue roles
  4. 2004 Medium

    Demonstrated IRAG actively targets and recruits cGKIβ to the ER in an isoform-selective manner, explaining how the kinase is positioned at its substrate.

    Evidence Immunohistochemistry in murine tissue and heterologous co-expression with confocal microscopy in COS-7 cells

    PMID:15388327

    Open questions at the time
    • Recruitment shown in overexpression system
    • Determinants of isoform selectivity not fully defined
  5. 2005 High

    Defined the acidic residues (D26/E31) within the cGKIβ leucine zipper that mediate electrostatic binding to IRAG, separable from kinase dimerization.

    Evidence Site-directed mutagenesis with in vitro binding and cell-based co-IP

    PMID:16166082

    Open questions at the time
    • Single lab
    • Did not test functional consequence of the interface mutant in vivo
  6. 2006 High

    Extended the IRAG module to platelets, showing it mediates NO/cGMP inhibition of platelet activation and arterial thrombosis and identifying the platelet phosphosites.

    Evidence IRAGΔ12 mouse with intravital microscopy, aggregation/Ca²⁺ assays, and MS phosphosite mapping (Ser664/Ser677)

    PMID:16990611

    Open questions at the time
    • Distinct phosphosites between platelets and smooth muscle not mechanistically reconciled
  7. 2008 Medium

    Revealed a Ca²⁺-independent function of IRAG: ER anchoring of cGKIβ to block its nuclear translocation and restrain cGMP-dependent transcription.

    Evidence WT and binding/phospho-deficient IRAG mutants in BHK cells with CRE-reporter assay and localization imaging

    PMID:18450420

    Open questions at the time
    • Shown in heterologous cells
    • Transcriptional targets and physiological relevance not established
  8. 2010 High

    Confirmed with a complete knockout that IRAG is obligate downstream of cGKIβ for NO/ANP/cGMP-dependent relaxation, ruling out compensation by cGKIβ alone.

    Evidence Exon 3 deletion KO with cGMP affinity chromatography, Ca²⁺ imaging, relaxation assays, blood pressure telemetry, and cGKIβ-transgenic rescue

    PMID:20080989

    Open questions at the time
    • LPS blood-pressure resistance mechanism not dissected
    • Did not address non-vascular phenotypes
  9. 2011 High

    Detailed the breadth of platelet inhibition mediated by IRAG across aggregation, granule secretion, and integrin-dependent adhesion.

    Evidence IRAG KO mouse with aggregation, granule secretion, P-selectin flow cytometry, adhesion, and bleeding-time assays

    PMID:21244222

    Open questions at the time
    • Did not establish whether all readouts are downstream of the same IP3R-Ca²⁺ node
  10. 2011 Medium

    Identified C-terminally truncated IRAG splice variants that act as dominant-negative regulators, adding an endogenous mechanism for tuning the pathway.

    Evidence Splice-variant identification and functional expression of truncated isoforms in human colonic SMCs with Ca²⁺/contractility readouts

    PMID:21865585

    Open questions at the time
    • Endogenous abundance and regulation of variants in vivo unknown
    • Single lab
  11. 2021 High

    Resolved the complex as a nanoscale SR assembly and connected IRAG to a new effector, TRPM4 channel inhibition, extending its role to cerebral artery dilation.

    Evidence Superresolution microscopy, patch-clamp TRPM4 currents, Ca²⁺ imaging, and IRAG knockdown in vascular SMCs

    PMID:34734188

    Open questions at the time
    • Quantitative stoichiometry of the nanocomplex not defined
  12. 2020 Medium

    Linked IRAG1 loss to spontaneous pulmonary hypertension and right ventricular dysfunction, implicating the pathway in pulmonary vascular homeostasis.

    Evidence Global IRAG1 KO with echocardiography, right heart catheterization, and PASMC analysis

    PMID:33066124

    Open questions at the time
    • Pathway placement of downstream PKGIβ candidates not resolved
    • Single lab
  13. 2021 Medium

    Uncovered a non-scaffolding requirement of IRAG1 for PKGIβ protein stability and tied its loss to gastrointestinal bleeding and anemia.

    Evidence Global IRAG1 KO with western blotting, RT-PCR (protein vs mRNA), histology, and hematology

    PMID:34064290

    Open questions at the time
    • Molecular mechanism of stabilization (degradation pathway) not defined
    • Single lab
  14. 2025 Low

    Began probing the broader IRAG1/MRVI1 interactome and a possible apoptosis/oncogenesis-related role distinct from the canonical Ca²⁺ pathway.

    Evidence TurboID proximity labeling and quantitative proteomics with NPM-ALK co-expression

    PMID:41078212

    Open questions at the time
    • Proximity labeling is not direct binding validation
    • Functional interpretation inferential
    • Single lab
  15. 2026 Low

    Provided first functional evidence for a growth-suppressive (tumor suppressor-like) role of MRVI1 in colorectal cancer cells.

    Evidence Stable MRVI1 overexpression in HCT116 cells with proliferation and viability assays

    PMID:41905951

    Open questions at the time
    • Single overexpression experiment with no molecular mechanism
    • p53 association asserted but not directly tested
    • Single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • How IRAG1's canonical NO/cGMP Ca²⁺-regulatory scaffolding role mechanistically relates to its emerging roles in PKGIβ stability, apoptosis networks, and tumor suppression remains unresolved.
  • No structural model of the trimeric complex
  • Degradation pathway controlling PKGIβ stability unidentified
  • No direct binding validation or mechanism for proposed tumor-suppressor function

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 3 GO:0140313 molecular sequestering activity 1
Localization
GO:0005783 endoplasmic reticulum 3
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-397014 Muscle contraction 3 R-HSA-109582 Hemostasis 2
Partners
ITPR1PRKG1TRPM4
Complex memberships
IRAG1–cGKIβ–IP3R-I trimeric complex

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 IRAG forms a trimeric signaling complex with cGKIβ and IP3 receptor type I (IP3R-I) at endoplasmic reticulum membranes in smooth muscle. In microsomal smooth muscle membranes, cGKIβ phosphorylated IRAG and IP3R. Co-expression of IRAG and cGKIβ in COS-7 cells, in the presence of cGMP, inhibited bradykinin-stimulated calcium release, identifying IRAG as an essential NO/cGKI-dependent regulator of IP3-induced calcium release. Co-immunoprecipitation with antibodies against cGKI, IP3R, and IRAG; heterologous expression in COS-7 cells; calcium release assays; mass spectrometry protein identification Nature High 10724174
2001 The N-terminal leucine zipper (amino acids 1–53) of cGKIβ (but not cGKIα or cGKII) interacts with amino acids 152–184 of IRAG via electrostatic interaction. cGKIβ does not directly interact with IP3R-I but co-precipitates IP3R-I through IRAG. cGKIβ phosphorylates up to four serines in IRAG; phosphorylation specifically of Ser696 is necessary and sufficient to decrease IP3-dependent calcium release. Yeast two-hybrid; co-precipitation of expressed proteins; site-directed mutagenesis (four Ser→Ala mutants); calcium release assays in transfected cells The Journal of biological chemistry High 11309393
2004 Targeted deletion of exon 12 of IRAG (encoding the N-terminus of the coiled-coil domain) disrupts the IRAG–IP3R-I interaction in vivo, abolishing cGMP-dependent relaxation of carbachol- and phenylephrine-contracted smooth muscle from colon and aorta and preventing cGMP-mediated decrease in norepinephrine-induced [Ca2+]i in aortic smooth muscle cells. cGMP-induced relaxation of K+-contracted smooth muscle was unaffected, indicating IRAG is specifically required for hormone receptor–triggered cGMP relaxation. Genetic knockout (exon 12 deletion); smooth muscle contraction/relaxation assays; intracellular calcium measurements (Fura-2); gastrointestinal motility assessment The EMBO journal High 15483626
2004 Endogenous IRAG in human colonic smooth muscle cells is required for NO/cGKI-dependent inhibition of IP3-dependent Ca2+ release. Antisense knockdown of IRAG abolished sodium nitroprusside- and 8-pCPT-cGMP-mediated inhibition of bradykinin-induced calcium transients. Antisense oligonucleotide knockdown of IRAG in cultured human colonic smooth muscle cells; calcium imaging; RT-PCR The Journal of biological chemistry Medium 14729908
2004 IRAG co-localizes with cGKI in smooth muscle of aorta and colon. Upon co-expression in COS-7 cells, IRAG recruits cGKIβ (but not cGKIα) to the endoplasmic reticulum, demonstrating isoform-specific targeting by IRAG. Immunofluorescence/immunohistochemistry in murine tissues; heterologous co-expression in COS-7 cells with confocal microscopy FEBS letters Medium 15388327
2005 Acidic residues in the N-terminal leucine zipper dimerization domain of PKGIβ (D26 and E31) mediate binding to both TFII-I and IRAG via electrostatic interaction with basic residues in alpha-helical regions of IRAG. Mutation D26K/E31R in PKGIβ completely abrogated binding to IRAG without disrupting PKG dimerization. Site-directed mutagenesis; in vitro binding assays; co-immunoprecipitation in intact cells The Journal of biological chemistry High 16166082
2006 IRAG is abundantly expressed in platelets and assembles in a macrocomplex with cGKIβ and IP3R-I. PKGIβ phosphorylates IRAG at Ser664 and Ser677 in intact platelets. Targeted disruption of the IRAG–IP3R-I interaction (IRAGΔ12/Δ12 mice) abolishes NO/cGMP-dependent inhibition of fibrinogen-receptor activation, platelet aggregation, and intracellular calcium transients, and prevents NO-mediated inhibition of arterial thrombosis in vivo. IRAG exon 12 deletion mouse model; intravital microscopy; platelet aggregation assays; calcium imaging; phosphorylation site mapping by mass spectrometry Blood High 16990611
2008 IRAG anchors PKGIβ to the endoplasmic reticulum, preventing cGMP-induced nuclear translocation of PKGIβ and thereby reducing cGMP/PKGIβ-mediated transcriptional activation of a CRE-reporter gene. This effect required the PKGIβ–IRAG binding interface and was specific to PKGIβ (PKGIα was unaffected). A phosphorylation-deficient IRAG mutant still suppressed PKGIβ transcriptional activity, indicating the mechanism is independent of IRAG phosphorylation or changes in intracellular calcium. Co-expression of wild-type and binding-incompetent/phosphorylation-deficient IRAG mutants in baby hamster kidney cells; CRE-reporter gene assay; subcellular localization by imaging Cellular signalling Medium 18450420
2010 Global IRAG knockout (exon 3 deletion) prevents stable interaction of IP3R-I with cGKIβ (shown by cGMP affinity chromatography) and abolishes NO-, ANP-, and cGMP-dependent relaxation of hormone-contracted aortic and colonic smooth muscle. cGKIβ/α subcellular localization in VSMCs was unchanged by IRAG loss. IRAG-deficient VSMCs failed to suppress hormone-induced Ca2+ increases in response to cGMP. Selective cGKIβ re-expression in smooth muscle from cGKIβ-transgenic mice did not rescue relaxation, confirming IRAG is obligate downstream of cGKIβ. IRAG-deficient mice showed resistance to LPS-induced blood pressure reduction. Targeted exon 3 deletion mouse model; cGMP affinity chromatography; confocal microscopy; Fura-2 calcium imaging; smooth muscle relaxation assays; telemetric blood pressure measurement; transgenic rescue experiment Cardiovascular research High 20080989
2011 IRAG-deficient murine platelets show enhanced aggregability to collagen, thrombin, and TxA2. NO/cGMP-dependent inhibition of ATP and 5-HT secretion from dense granules, P-selectin secretion from alpha granules, and GPIIb/IIIa-mediated adhesion to fibrinogen were all severely impaired in IRAG-deficient platelets, and bleeding time was reduced. IRAG knockout mouse model; platelet aggregation assays; granule secretion assays (ATP, 5-HT); flow cytometry (P-selectin); adhesion assays; bleeding time measurement Platelets High 21244222
2011 C-terminally truncated IRAG variants lacking the cGKI phosphorylation site and IP3R-I interaction site act as dominant-negative modulators, counteracting cGMP-mediated inhibition of calcium transients and relaxation of human colonic smooth muscle cells. Four unique first-exon variants driven by individual promoters and extensive alternative splicing generate multiple truncated IRAG isoforms. Identification of splice variants by RT-PCR/sequencing; functional expression of truncated IRAG variants in colonic smooth muscle cells; calcium imaging; contractility assays American journal of physiology. Cell physiology Medium 21865585
2021 IRAG, PKGIβ, and IP3Rs form a nanoscale signaling complex on the SR of vascular smooth muscle cells, identified by superresolution microscopy. PKG phosphorylation of IRAG inhibits IP3R-mediated Ca2+ release; IRAG knockdown diminished NO-mediated inhibition of TRPM4 channel activity and vasodilation. Thus, IRAG mediates NO/cGMP/PKG inhibition of IP3R-dependent TRPM4 activation to dilate cerebral arteries. IRAG knockdown in vascular SMCs; patch-clamp electrophysiology (TRPM4 currents); Ca2+ imaging; superresolution microscopy of IRAG/PKG/IP3R nanoscale complex; pharmacological inhibition of guanylyl cyclase and PKG Function (Oxford, England) High 34734188
2020 IRAG1 knockout mice spontaneously develop right ventricular hypertrophy, elevated RV systolic pressure, RV dysfunction, and pulmonary hypertension under normoxic conditions. IRAG1 is expressed in PASMCs and is downregulated under hypoxia. Absence of IRAG1 reduces PKGIβ expression in lung and RV and dysregulates downstream PKGIβ candidates in the RV. Global IRAG1 KO mouse model; echocardiography; right heart catheterization; immunostaining; western blotting; PASMC isolation Cells Medium 33066124
2021 Global IRAG1 KO mice develop gastrointestinal bleeding, iron-deficiency anemia, and anemia-associated splenomegaly. Loss of IRAG1 strongly decreases PKGIβ protein levels (but not mRNA) in colon, spleen, and stomach, indicating IRAG1 is required for PKGIβ protein stability. Global IRAG1 KO mouse model; western blotting; RT-PCR; histology; hematological analysis International journal of molecular sciences Medium 34064290
1999 Mrvi1 (IRAG1 ortholog) encodes a protein with homology to Jaw1, a lymphoid-restricted type II membrane protein localizing to the endoplasmic reticulum. Within hematopoietic cells, Mrvi1 expression is restricted to megakaryocytes and some myeloid leukemias, and is downregulated during monocytic differentiation. Retroviral insertional mutagenesis screen; sequence homology analysis; Northern blot expression analysis Oncogene Low 10321731
2025 TurboID-based proximity labeling identified >700 candidate MRVI1-interacting proteins in mammalian cells, including ER-localized factors and intracellular trafficking components. Co-expression of NPM-ALK oncogenic kinase selectively enhanced MRVI1 association with signaling-related proteins and reduced association with anti-apoptotic regulators (DDB1, PHB2, NOTCH2), suggesting MRVI1 participates in apoptosis-related networks disrupted during oncogenic transformation. TurboID proximity labeling; quantitative proteomics; co-expression of NPM-ALK Journal of biochemistry Low 41078212
2026 Stable overexpression of MRVI1 in HCT116 colorectal cancer cells markedly reduces cell proliferation without increasing cell death (cytostatic effect), providing direct evidence that MRVI1 suppresses colorectal cancer cell growth when overexpressed, consistent with a p53-associated tumor suppressor role. Stable overexpression of V5-TurboID-MRVI1 fusion protein; cell proliferation assays; trypan blue viability staining Biological & pharmaceutical bulletin Low 41905951

Source papers

Stage 0 corpus · 29 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2000 Regulation of intracellular calcium by a signalling complex of IRAG, IP3 receptor and cGMP kinase Ibeta. Nature 378 10724174
2001 Molecular determinants of the interaction between the inositol 1,4,5-trisphosphate receptor-associated cGMP kinase substrate (IRAG) and cGMP kinase Ibeta. The Journal of biological chemistry 113 11309393
2006 IRAG mediates NO/cGMP-dependent inhibition of platelet aggregation and thrombus formation. Blood 109 16990611
2004 IRAG is essential for relaxation of receptor-triggered smooth muscle contraction by cGMP kinase. The EMBO journal 103 15483626
2004 Distribution of IRAG and cGKI-isoforms in murine tissues. FEBS letters 79 15388327
2019 The MRVI1-AS1/ATF3 signaling loop sensitizes nasopharyngeal cancer cells to paclitaxel by regulating the Hippo-TAZ pathway. Oncogene 50 31273338
2011 IRAG and novel PKG targeting in the cardiovascular system. American journal of physiology. Heart and circulatory physiology 48 21666108
2010 IRAG determines nitric oxide- and atrial natriuretic peptide-mediated smooth muscle relaxation. Cardiovascular research 43 20080989
1999 Mrvi1, a common MRV integration site in BXH2 myeloid leukemias, encodes a protein with homology to a lymphoid-restricted membrane protein Jaw1. Oncogene 38 10321731
2004 InsP3R-associated cGMP kinase substrate (IRAG) is essential for nitric oxide-induced inhibition of calcium signaling in human colonic smooth muscle. The Journal of biological chemistry 35 14729908
1997 IRAG working group 4. Cell cytotoxicity assays. Interagency Regulatory Alternatives Group. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association 35 9100816
2008 cGMP-dependent protein kinase anchoring by IRAG regulates its nuclear translocation and transcriptional activity. Cellular signalling 32 18450420
2019 miR-940 potentially promotes proliferation and metastasis of endometrial carcinoma through regulation of MRVI1. Bioscience reports 29 31085718
2005 Identification of the interface between cGMP-dependent protein kinase Ibeta and its interaction partners TFII-I and IRAG reveals a common interaction motif. The Journal of biological chemistry 28 16166082
2021 Nitric Oxide Signals Through IRAG to Inhibit TRPM4 Channels and Dilate Cerebral Arteries. Function (Oxford, England) 25 34734188
2018 Whole exome sequencing identifies MRVI1 as a susceptibility gene for moyamoya syndrome in neurofibromatosis type 1. PloS one 25 30001348
2011 Signaling via IRAG is essential for NO/cGMP-dependent inhibition of platelet activation. Platelets 20 21244222
1997 Practical application of non-whole animal alternatives: summary of IRAG workshop on eye irritation testing. Interagency Regulatory Alternatives Group. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association 19 9100821
2023 Hypoxia-induced lncRNA MRVI1-AS1 accelerates hepatocellular carcinoma progression by recruiting RNA-binding protein CELF2 to stabilize SKA1 mRNA. World journal of surgical oncology 10 36973749
2022 MRVI1 and NTRK3 Are Potential Tumor Suppressor Genes Commonly Inactivated by DNA Methylation in Cervical Cancer. Frontiers in oncology 10 35141152
2020 P53-induced MRVI1 mediates carcinogenesis of colorectal cancer. Scandinavian journal of gastroenterology 9 32589066
1997 IRAG working group 3. Cell function-based assays. Interagency Regulatory Alternatives Group. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association 9 9100815
2023 Novel Functional Features of cGMP Substrate Proteins IRAG1 and IRAG2. International journal of molecular sciences 6 37372987
2020 IRAG1 Deficient Mice Develop PKG1β Dependent Pulmonary Hypertension. Cells 6 33066124
2011 Truncated IRAG variants modulate cGMP-mediated inhibition of human colonic smooth muscle cell contraction. American journal of physiology. Cell physiology 6 21865585
2021 Loss of PKGIβ/IRAG1 Signaling Causes Anemia-Associated Splenomegaly. International journal of molecular sciences 5 34064290
2025 Selected PEAR1 and MRVI1 Gene Polymorphisms in Patients with Migraine and Sticky Platelet Syndrome. Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis 1 40696876
2025 Identification of MRVI1-interacting proteins by biotin-based proximity labelling reveals NPM-ALK-dependent interaction dynamics. Journal of biochemistry 1 41078212
2026 Multifaceted MRVI1 Serves as a Tumor Suppressor in HCT116 Colorectal Cancer Cells. Biological & pharmaceutical bulletin 0 41905951

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