Affinage

CDK5RAP3

CDK5 regulatory subunit-associated protein 3 · UniProt Q96JB5

Length
506 aa
Mass
56.9 kDa
Annotated
2026-06-09
31 papers in source corpus 24 papers cited in narrative 24 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/6 claims corpus-supported (83%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CDK5RAP3 is a multifunctional adaptor that couples the UFM1 conjugation system to endoplasmic reticulum homeostasis and acts as a signaling and transcriptional modulator across multiple tissues (PMID:30635284, PMID:42045457). Its best-defined biochemical role is as a substrate adaptor for UFMylation: only full-length CDK5RAP3 binds the E3 ligase UFL1, and its loss impairs UFMylation of the substrates RPL26 and UFBP1 while controlling UFL1 phosphorylation, with restoration of full-length protein reversing proteomic and phosphoproteomic dysregulation spanning extracellular matrix, genome-stability, and cytoskeletal programs (PMID:42045457). Through this and related activities, CDK5RAP3 maintains ER and organelle integrity; its deficiency disrupts UFMylation homeostasis and provokes ER stress and unfolded-protein responses in liver (PMID:30635284, PMID:32926856), triggers ER-membrane and lysosomal remodeling in pancreatic acinar cells (PMID:40637352), drives ER stress and encephalo-dysplasia in neurons by allowing accumulation of the N-glycosylation proteins RPN1 and ALG2 that CDK5RAP3 normally targets for degradation (PMID:40188151), and is required for Paneth cell fate specification and rough-ER architecture in the intestine (PMID:33504792). CDK5RAP3 additionally functions in the nucleus and in signaling: it binds the BRCA2 helical domain to negatively regulate double-strand break repair (PMID:35053516), interacts with HSF1 and HSP90 to govern HSF1 nucleocytoplasmic shuttling during heat stress (PMID:33182370), serves as a STAT3 transcriptional co-factor occupying STAT3 target loci (PMID:31765941), and represses Wnt/β-catenin signaling by suppressing AKT and promoting GSK-3β-dependent β-catenin degradation (PMID:27793695, PMID:29540196). It also binds and activates PAK4 (PMID:21385901) and represses p14ARF transcription (PMID:22860085). A disease-linked study established that full-length CDK5RAP3 loss underlies a neurodevelopmental disorder rescuable by antisense-oligonucleotide restoration of the full-length isoform (PMID:42045457).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 2003 Low

    Established the first physical link of CDK5RAP3 to CDK5 regulation by showing it binds the CDK5 activator p35, originally framing the protein as a CDK5 activator-binding protein.

    Evidence In vitro pulldown of CDK5RAP3 (IC53-2) with p35

    PMID:12737517

    Open questions at the time
    • Single in vitro pulldown without mutagenesis or functional follow-up
    • No demonstration that the interaction modulates CDK5 activity in cells
    • Subsequent timeline findings do not develop a CDK5-centric function
  2. 2009 Medium

    Addressed whether CDK5RAP3 has a vascular function in vivo by showing endothelial overexpression suppresses eNOS and raises blood pressure, the first physiological loss/gain-of-function readout.

    Evidence VE-cadherin-driven transgenic mice and HUVEC siRNA with eNOS/NO and blood-pressure assays

    PMID:19541669

    Open questions at the time
    • Molecular mechanism linking CDK5RAP3 to eNOS not defined
    • No binding partner identified in the vascular context
  3. 2012 Medium

    Defined nuclear and signaling roles in cancer, showing CDK5RAP3 binds and activates PAK4 and directly represses the p14ARF promoter to drive invasiveness.

    Evidence Co-IP, kinase assay, ChIP and siRNA epistasis with invasion assays in HCC cells

    PMID:21385901 PMID:22860085

    Open questions at the time
    • Mechanism of CDK5RAP3 recruitment to the p14ARF promoter unknown
    • Whether PAK4 activation and ARF repression are connected is not resolved
  4. 2018 Medium

    Placed CDK5RAP3 in the AKT–GSK-3β–β-catenin axis as a Wnt suppressor, resolving its directionality in gastric cancer signaling.

    Evidence Phospho-Western in stable gain/loss-of-function lines plus a 295-sample patient cohort

    PMID:27793695 PMID:29540196

    Open questions at the time
    • Direct molecular target of CDK5RAP3 in the AKT/GSK-3β cascade not identified
    • Whether regulation is direct or indirect is unclear
  5. 2019 Medium

    Identified the central biochemical role of CDK5RAP3 as a UFL1-interacting adaptor of the UFM1 conjugation system whose loss disrupts UFMylation and triggers ER stress.

    Evidence In vivo Co-IP in mouse liver, ufmylation profiling, and liver-specific knockout with partial-hepatectomy ER-stress phenotyping

    PMID:30635284 PMID:32926856

    Open questions at the time
    • Substrate repertoire of the adaptor not fully defined at this stage
    • Direct vs indirect contribution to ER stress not separated
  6. 2019 Medium

    Expanded CDK5RAP3 into transcriptional, stress-response and angiogenic regulation by establishing STAT3 genomic co-occupancy, HSF1/HSP90 binding controlling HSF1 shuttling, and AKT/HIF-1α/VEGFA-dependent angiogenesis suppression.

    Evidence ChIP for STAT3 loci, reciprocal Co-IP and co-IF with HSF1/HSP90, conditional KO heat-stress phenotyping, and angiogenesis/tube-formation assays

    PMID:31728130 PMID:31765941 PMID:33182370

    Open questions at the time
    • Whether CDK5RAP3 binds DNA directly or via partners at STAT3 loci unknown
    • Structural basis of HSF1/HSP90 interaction undefined
  7. 2022 Medium

    Connected CDK5RAP3 to genome maintenance and growth control through BRCA2 helical-domain binding that restrains DSB repair, and RPL26 binding that links it to mTOR signaling, autophagy, and G2/M progression.

    Evidence Domain-specific Co-IP, HR/SSA and genomic-instability assays, and KO MEF/knockdown studies of mTOR and cell-cycle markers

    PMID:35053516 PMID:35509151

    Open questions at the time
    • How CDK5RAP3 mechanistically suppresses HR is not resolved
    • Whether RPL26 binding intersects the UFMylation role is untested
  8. 2021 High

    Demonstrated tissue-essential roles for CDK5RAP3 in secretory cell biology, establishing it as required for Paneth cell fate and rough-ER integrity in vivo.

    Evidence Intestinal- and Paneth-cell-specific and inducible conditional knockout mice with histology, immunofluorescence and Gfi1/Sox9 analysis

    PMID:33504792

    Open questions at the time
    • Molecular link between CDK5RAP3 and Gfi1/Sox9 transcription not defined
    • Whether the ER phenotype is UFMylation-dependent not directly shown
  9. 2025 Medium

    Generalized the ER/organelle-homeostasis function across tissues, showing CDK5RAP3 loss remodels lysosomal and ER membranes in acinar cells and drives glycoprotein accumulation (RPN1, ALG2) and ER stress in neurons.

    Evidence Acinar- and neuron-specific knockout mice with EM, organelle-marker Western blot/IF, and transcriptomics

    PMID:40188151 PMID:40637352

    Open questions at the time
    • Whether RPN1/ALG2 degradation is directly mediated by UFMylation is not established
    • Mechanism of CLIMP63 and lysosomal upregulation unknown
  10. 2026 High

    Resolved the isoform-specific UFMylation-adaptor mechanism and tied it to human disease, showing only full-length CDK5RAP3 binds UFL1, controls RPL26/UFBP1 UFMylation and UFL1 S462 phosphorylation, with ASO rescue reversing the defect.

    Evidence Isoform-specific Co-IP, quantitative proteomics/phosphoproteomics in patient amniocytes, splice-variant RT-PCR and ASO rescue

    PMID:42045457

    Open questions at the time
    • Precise UFL1 region engaged by full-length CDK5RAP3 not structurally defined
    • How CDK5RAP3 controls UFL1 S462 phosphorylation mechanistically is unresolved
  11. 2026 Medium

    Extended CDK5RAP3 to endocrine regulation by showing SMAD4/CEBPB interaction and hCG-driven nuclear translocation place it upstream of BMP signaling in Leydig-cell steroidogenesis.

    Evidence IP-MS, AAV-mediated in vivo knockdown, steroidogenic-enzyme Western blot, testosterone ELISA and Noggin epistasis

    PMID:41596239

    Open questions at the time
    • Direct vs indirect SMAD4/CEBPB binding not dissected
    • Link between BMP regulation and the UFMylation function unexplored

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how CDK5RAP3's core UFL1/UFMylation adaptor activity mechanistically accounts for its diverse transcriptional, DNA-repair, and signaling roles, and whether these represent independent functions or downstream consequences of disrupted UFMylation.
  • No structural model of CDK5RAP3 with any partner
  • Substrate selectivity of the UFMylation adaptor not comprehensively mapped
  • Integration of cytoplasmic vs nuclear functions undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 2 GO:0060090 molecular adaptor activity 2 GO:0098772 molecular function regulator activity 2 GO:0140110 transcription regulator activity 2
Localization
GO:0005634 nucleus 3 GO:0005783 endoplasmic reticulum 3 GO:0005829 cytosol 1
Pathway
R-HSA-8953897 Cellular responses to stimuli 3 R-HSA-162582 Signal Transduction 2 R-HSA-392499 Metabolism of proteins 2 R-HSA-9612973 Autophagy 2 R-HSA-73894 DNA Repair 1
Partners
BRCA2HSF1HSP90PAK4RPL26STAT3UFBP1UFL1
Complex memberships
UFM1 conjugation (UFL1) system

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2011 CDK5RAP3 is a novel binding partner of PAK4 and enhances PAK4 kinase activity; siRNA-mediated knockdown of PAK4 in CDK5RAP3-overexpressing HCC cells reversed the enhanced cell invasiveness, establishing PAK4 as essential for CDK5RAP3-mediated metastatic function. Co-immunoprecipitation (binding partner identification), kinase activity assay (PAK4 activation), siRNA knockdown with cell invasion assay (epistasis) Cancer research Medium 21385901
2012 CDK5RAP3 binds directly to the p14ARF promoter in vivo and represses p14ARF transcription; knockdown of p14ARF in CDK5RAP3-depleted HCC cells rescued invasiveness, placing CDK5RAP3 upstream of p14ARF in a transcriptional repression pathway. Chromatin immunoprecipitation (promoter binding), RT-PCR and Western blot (mRNA/protein levels), siRNA epistasis (cell invasion assay) PloS one Medium 22860085
2003 CDK5RAP3 (IC53-2) physically binds the CDK5 activator p35 in vitro, confirming it as a CDK5 activator-binding protein. In vitro association assay (pulldown) Cell research Low 12737517
2016 CDK5RAP3 suppresses phosphorylation of GSK-3β at Ser9, thereby promoting phosphorylation (Ser37/Thr41) and subsequent proteasomal degradation of β-catenin, reducing Wnt/β-catenin signaling in gastric cancer cells. Western blot (phosphorylation status of GSK-3β, β-catenin), overexpression and knockdown in cell lines with proliferation/invasion assays Cancer letters Medium 27793695 29540196
2018 CDK5RAP3 represses AKT phosphorylation (Ser473), which in turn promotes GSK-3β phosphorylation (Ser9) and β-catenin suppression, placing CDK5RAP3 upstream of AKT in the Wnt/β-catenin cascade in gastric cancer. Western blot in stable CDK5RAP3 overexpression/knockdown gastric cancer cell lines; correlation analysis in 295 patient tumor samples by IHC and Western blot Journal of experimental & clinical cancer research Medium 29540196
2019 CDK5RAP3 interacts with UFL1 (the E3 ligase of the UFM1 conjugation system) in vivo, and loss of CDK5RAP3 alters the ufmylation profile in liver cells, identifying CDK5RAP3 as a substrate adaptor for UFMylation. Co-immunoprecipitation (CDK5RAP3–UFL1 interaction in mouse liver); ufmylation profile analysis in knockout liver cells Development (Cambridge, England) Medium 30635284
2019 CDK5RAP3 inhibits angiogenesis by suppressing the AKT/HIF-1α/VEGFA signaling axis; CDK5RAP3 knockdown in gastric neuroendocrine carcinoma cells increased VEGFA secretion and promoted endothelial cell migration and tube formation, while overexpression had the opposing effect. Knockdown/overexpression with tube formation assay, ELISA (VEGFA), Western blot (AKT, HIF-1α), in vivo xenograft angiogenesis assay Cancer cell international Medium 31728130
2019 CDK5RAP3 functions as a co-factor for the transcription factor STAT3; CDK5RAP3 binds to STAT3-regulated genomic loci in a STAT3-dependent manner, enhancing STAT3-dependent gene expression; silencing CDK5RAP3 reduces STAT3-mediated clonogenesis and migration. RNA-interference screen, ChIP (CDK5RAP3 at STAT3 genomic loci), knockdown with clonogenesis and migration assays Neoplasia (New York, N.Y.) Medium 31765941
2020 CDK5RAP3 expression is regulated by ERK signaling; ERK inhibition phenocopies CDK5RAP3 overexpression in reducing gastric cancer stem cell self-renewal and EMT, placing CDK5RAP3 downstream of ERK. ERK inhibitor treatment with Western blot (CDK5RAP3 levels), spheroid formation and invasion assays in cell lines and mouse organoids British journal of cancer Low 32606358
2020 CDK5RAP3 physically interacts with HSF1 (heat shock factor 1) and HSP90, co-localizes with HSF1 in cytoplasm and nucleus, and its deletion impairs nucleoplasmic translocation and trimer formation of HSF1 during heat stress, identifying CDK5RAP3 as a nucleoplasmic shuttle regulating HSF1-mediated heat stress response. Co-immunoprecipitation and co-immunofluorescence (CDK5RAP3–HSF1, CDK5RAP3–HSP90 interactions), conditional knockout mice and MEFs with heat stress phenotyping, Western blot (HSP expression, ER stress markers) International journal of molecular sciences Medium 33182370
2021 Cdk5rap3 deficiency in intestinal epithelial cells causes near-complete loss of Paneth cells with downregulation of transcription factors Gfi1 and Sox9, establishing Cdk5rap3 as essential for Paneth cell fate specification; inducible acute deletion in mature Paneth cells leads to disassembly of the rough endoplasmic reticulum and abnormal zymogen granules. Intestinal epithelial cell-specific and Paneth cell-specific conditional knockout mice; inducible deletion; histology; immunofluorescence; Western blot (Gfi1, Sox9) Cell death & disease High 33504792
2022 CDK5RAP3 interacts with RPL26 (ribosomal protein L26); loss of CDK5RAP3 or RPL26 inhibits mTOR/p-mTOR signaling and induces autophagy, linking CDK5RAP3 to regulation of the mTOR pathway through RPL26. CDK5RAP3 deficiency also blocks the cell cycle at G2/M by downregulating CDK1 and Cyclin B1. Co-immunoprecipitation (CDK5RAP3–RPL26), MEFs from conditional knockout mice, MCF7 knockdown; Western blot (mTOR, CDK1, CCNB1); flow cytometry (cell cycle, apoptosis); autophagy markers Cell proliferation Medium 35509151
2022 CDK5RAP3 is a novel BRCA2 helical domain-interacting protein; CDK5RAP3 depletion upregulates homologous recombination and single-strand annealing, and reduces spontaneous and DNA damage-induced genomic instability, indicating that CDK5RAP3 negatively regulates double-strand break repair in S-phase. Co-immunoprecipitation (CDK5RAP3–BRCA2 helical domain), HR/SSA repair assays, genomic instability assays after CDK5RAP3 depletion Cancers Medium 35053516
2024 CDK5RAP3 deficiency interferes with the UFMylation system and triggers ER-phagy (endoplasmic reticulum-selective autophagy); CDK5RAP3 also maintains the stability of the master transcription factor MEIS2 in neuroblastoma. Knockdown/overexpression in NB cell lines and xenografts, Western blot (UFMylation components, MEIS2), ER-phagy assays Cancer letters Low 38636893
2024 TSPAN6 promotes glioblastoma progression by interacting with CDK5RAP3 and activating the STAT3 signaling pathway. Co-immunoprecipitation (TSPAN6–CDK5RAP3 interaction), overexpression/knockdown with proliferation, migration and STAT3 pathway readouts International journal of biological sciences Low 38725860
2024 CDK5RAP3 inhibits p38MAPK phosphorylation and activity via mediating a p38 interaction with wild-type p53-induced phosphatase 1 (Wip1); under hypoxia, CDK5RAP3 expression decreases in endothelial cells, releasing this inhibition and promoting p38MAPK-dependent angiogenesis. CDK5RAP3 knockdown in HUVECs under hypoxia, Western blot (p38MAPK phosphorylation), tube formation, migration and proliferation assays, VEGF ELISA International heart journal Low 39085114
2025 NXF3 facilitates nuclear export of CDK5RAP3 mRNA, thereby increasing CDK5RAP3 protein levels and promoting cell cycle progression in gastric cancer cells. RNA immunoprecipitation sequencing (RIP-Seq), nuclear-cytoplasmic transcriptomics, NXF3 knockdown with Western blot (CDK5RAP3 protein) and cell cycle assays Cellular and molecular life sciences Low 40032765
2025 Cdk5rap3 deficiency in pancreatic acinar cells increases lysosomal hydrolase cathepsin B and LAMP1, elevating lysosomal activity; it also causes substantial changes to rough ER structure and increases selective ER membrane protein CLIMP63, identifying Cdk5rap3 as a regulator of lysosomal and ER membrane homeostasis essential for acinar cell survival. Acinar cell-specific knockout mice, tissue histology, Western blot and immunofluorescence (cathepsin B, LAMP1, CLIMP63), electron microscopy (ER structure), primary cell culture American journal of physiology. Cell physiology Medium 40637352
2025 CDK5RAP3 deficiency in neurons increases N-glycosylase proteins RPN1 and ALG2 as well as total glycoprotein levels, causing ER stress and encephalo-dysplasia; CDK5RAP3 normally promotes proteolytic and autophagic degradation of RPN1 and ALG2 to maintain glycoprotein balance. Neuron-specific CDK5RAP3 knockout mice (Nestin-Cre), transcriptome sequencing, Western blot (RPN1, ALG2, glycoproteins, ER stress markers), MEF in vitro deletion (ROSA26-ERT2Cre) Cell death discovery Medium 40188151
2026 Only full-length CDK5RAP3 (but not C-terminal alternative isoforms) binds UFL1; CDK5RAP3 deficiency impairs UFMylation of known substrates RPL26 and UFBP1, and CDK5RAP3 acts as an upstream regulator of UFL1 S462 phosphorylation (linked to ATM signaling). Antisense oligonucleotide-mediated restoration of full-length CDK5RAP3 reversed proteomic/phosphoproteomic dysregulation including extracellular matrix organisation, mitotic/genome stability, and cytoskeletal pathways. Co-immunoprecipitation (full-length vs. C-terminal isoforms with UFL1), Western blot, proteomics and phosphoproteomics in patient amniocytes, RT-PCR (splice variant), ASO rescue experiment Acta neuropathologica High 42045457
2026 CDK5RAP3 interacts with SMAD4 and CEBPB in Leydig cells; hCG stimulation triggers CDK5RAP3 nuclear translocation; CDK5RAP3 knockdown reduces expression of steroidogenic regulators STAR, CYP11A1, CYP17A1, and HSD3B and impairs testosterone production; BMP pathway inhibition (Noggin) rescues the testosterone deficit caused by CDK5RAP3 loss, placing CDK5RAP3 upstream of BMP signaling in steroidogenesis. Immunoprecipitation-mass spectrometry (IP-MS, interaction identification), AAV2/9-mediated in vivo knockdown, primary Leydig cell culture, Western blot (STAR, CYP enzymes), serum testosterone ELISA, Noggin epistasis experiment International journal of molecular sciences Medium 41596239
2009 Endothelium-specific overexpression of IC53 (CDK5RAP3) in transgenic mice decreases eNOS expression and activity, reduces NO production, impairs endothelium-dependent vasodilation, and elevates systolic blood pressure; inhibition of IC53 in HUVECs upregulates eNOS activity. VE-cadherin promoter-driven transgenic mouse model, blood pressure measurement, eNOS activity assay, NO measurement, IC53 siRNA knockdown in HUVECs Cardiovascular research Medium 19541669
2019 CDK5RAP3 depletion in liver cells disrupts UFMylation homeostasis and triggers endoplasmic reticulum stress with activation of unfolded protein responses; this ER stress is exacerbated after partial hepatectomy in liver-specific Cdk5rap3 knockout mice and is associated with impaired hepatocyte proliferation and delayed liver regeneration. Liver-specific CKO mice, partial hepatectomy model, Western blot (ER stress/UPR markers, ufmylation substrates), hepatocyte proliferation assays (BrdU/Ki67) Development (Cambridge, England) / The American journal of pathology Medium 30635284 32926856
2023 CDK5RAP3 knockdown in bovine mammary epithelial cells inhibits autophagolysosome degradation, activates the NF-κB pathway and NLRP3 inflammasome (upregulating NLRP3, IL-1β, IL-6, cleaved caspase-1), and triggers pyroptosis; accumulation of LC3B and p62 confirms the autophagy block. CDK5RAP3 knockdown in BMECs, Western blot (NLRP3, IL-1β, caspase-1, LC3B, p62, NF-κB), cytokine measurement, cell death assays International journal of biological macromolecules Low 36806767

Source papers

Stage 0 corpus · 31 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 Overexpression of a novel activator of PAK4, the CDK5 kinase-associated protein CDK5RAP3, promotes hepatocellular carcinoma metastasis. Cancer research 76 21385901
2019 CDK5RAP3, a UFL1 substrate adaptor, is crucial for liver development. Development (Cambridge, England) 75 30635284
2007 Usefulness of CDK5RAP3, CCNB2, and RAGE genes for the diagnosis of lung adenocarcinoma. The International journal of biological markers 61 17549666
2018 CDK5RAP3 suppresses Wnt/β-catenin signaling by inhibiting AKT phosphorylation in gastric cancer. Journal of experimental & clinical cancer research : CR 42 29540196
2016 CDK5RAP3 acts as a tumor suppressor in gastric cancer through inhibition of β-catenin signaling. Cancer letters 39 27793695
2021 Cdk5rap3 is essential for intestinal Paneth cell development and maintenance. Cell death & disease 28 33504792
2012 CDK5RAP3 is a novel repressor of p14ARF in hepatocellular carcinoma cells. PloS one 28 22860085
2020 CDK5RAP3 Deficiency Restrains Liver Regeneration after Partial Hepatectomy Triggering Endoplasmic Reticulum Stress. The American journal of pathology 26 32926856
2002 A novel gene IC53 stimulates ECV304 cell proliferation and is upregulated in failing heart. Biochemical and biophysical research communications 19 12054757
2020 CDK5RAP3 as tumour suppressor negatively regulates self-renewal and invasion and is regulated by ERK1/2 signalling in human gastric cancer. British journal of cancer 18 32606358
2019 CDK5RAP3 is a co-factor for the oncogenic transcription factor STAT3. Neoplasia (New York, N.Y.) 17 31765941
2011 A functional variant of IC53 correlates with the late onset of colorectal cancer. Molecular medicine (Cambridge, Mass.) 17 21394385
2022 CDK5RAP3, an essential regulator of checkpoint, interacts with RPL26 and maintains the stability of cell growth. Cell proliferation 16 35509151
2019 CDK5RAP3 inhibits angiogenesis in gastric neuroendocrine carcinoma by modulating AKT/HIF-1α/VEGFA signaling. Cancer cell international 15 31728130
2019 CDK5RAP3 Participates in Autophagy Regulation and Is Downregulated in Renal Cancer. Disease markers 13 31061682
2020 CDK5RAP3, a Novel Nucleoplasmic Shuttle, Deeply Regulates HSF1-Mediated Heat Stress Response and Protects Mammary Epithelial Cells from Heat Injury. International journal of molecular sciences 12 33182370
2023 CDK5RAP3, a key defender of udder, modulates NLRP3 inflammasome activation by regulating autophagolysosome degradation in S. agalactiae-infected mastitis. International journal of biological macromolecules 11 36806767
2024 CDK5RAP3 is a novel super-enhancer-driven gene activated by master TFs and regulates ER-Phagy in neuroblastoma. Cancer letters 10 38636893
2003 Cloning and characterization of human IC53-2, a novel CDK5 activator binding protein. Cell research 10 12737517
2024 TSPAN6 reinforces the malignant progression of glioblastoma via interacting with CDK5RAP3 and regulating STAT3 signaling pathway. International journal of biological sciences 8 38725860
2009 Endothelium-specific overexpression of human IC53 downregulates endothelial nitric oxide synthase activity and elevates systolic blood pressure in mice. Cardiovascular research 7 19541669
2022 CDK5RAP3 acts as a putative tumor inhibitor in papillary thyroid carcinoma via modulation of Akt/GSK-3β/Wnt/β-catenin signaling. Toxicology and applied pharmacology 6 35219640
2022 CDK5RAP3, a New BRCA2 Partner That Regulates DNA Repair, Is Associated with Breast Cancer Survival. Cancers 5 35053516
2025 Neuronal CDK5RAP3 deficiency leads to encephalo-dysplasia via upregulation of N-glycosylases and glycogen deposition. Cell death discovery 4 40188151
2025 Nuclear translocation of CDK5RAP3 regulated by NXF3 promotes the progression of gastric cancer. Cellular and molecular life sciences : CMLS 1 40032765
2025 CDK5RAP3 Deficiency Is Associated with Hepatic Inflammation and Increased Expression of NLRP3 Inflammasome Components. Biomedicines 1 40868283
2024 CDK5RAP3 Inhibition by Hypoxia Activates P38MAPK to Facilitate Angiogenesis. International heart journal 1 39085114
2026 Sex-Specific Downregulation of CDK5RAP3 Exacerbates ER Stress-Mediated Inflammation and Apoptosis in CCl4-Induced Acute Liver Injury. Genes 0 41595493
2026 CDK5RAP3 Regulates Testosterone Production in Mouse Leydig Cells. International journal of molecular sciences 0 41596239
2026 A severe neurodevelopmental syndrome linked to a South Asian founder variant in the UFMylation adaptor CDK5RAP3. Acta neuropathologica 0 42045457
2025 Cdk5rap3-mediated regulation of lysosomal and ER membrane proteins is pivotal for the survival and function of pancreatic acinar cells. American journal of physiology. Cell physiology 0 40637352

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