Affinage

PRKCSH

Glucosidase 2 subunit beta · UniProt P14314

Round 2 corrected
Length
528 aa
Mass
59.4 kDa
Annotated
2026-04-28
66 papers in source corpus 17 papers cited in narrative 17 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PRKCSH encodes the non-catalytic beta subunit of ER glucosidase II, functioning as an ER-resident regulatory and chaperone-like glycoprotein that integrates N-glycan processing with Ca²⁺ signaling, protein quality control, and the unfolded protein response. Its C-terminal HDEL signal retains the glucosidase II holoenzyme in the ER, while its EF-hand domains sense Ca²⁺ to regulate ion channels including TRPV5 and IP3R1, and it protects client glycoproteins such as TRPP2 from HERP-mediated ERAD (PMID:8910335, PMID:15100231, PMID:18990696, PMID:19801576). PRKCSH selectively promotes IRE1α autophosphorylation and oligomerization, activating the XBP1 branch of the UPR; in cancer contexts this confers ER-stress resistance and modulates tumor immune evasion via cytokine and apoptotic pathways (PMID:31320625, PMID:40189587, PMID:41350724). Germline loss-of-function mutations in PRKCSH cause autosomal dominant polycystic liver disease through a two-hit cystogenesis mechanism (PMID:12577059, PMID:12529853).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 1996 High

    The identity of PRKCSH as the non-catalytic beta subunit of glucosidase II established its core enzymatic partnership and ER-retention mechanism, answering how glucosidase II is localized and assembled in the ER.

    Evidence Biochemical purification from rat liver, peptide sequencing, cDNA cloning, and yeast gene disruption

    PMID:8910335

    Open questions at the time
    • Catalytic contribution of the beta subunit to trimming activity not defined
    • Structural basis of alpha-beta interaction unknown
  2. 1996 Medium

    Parallel findings placed 80K-H as a signaling-competent molecule — a tyrosine-phosphorylated FGF-receptor substrate binding GRB2 and a component of AGE receptor complexes — suggesting roles beyond glucosidase II scaffolding.

    Evidence Phosphotyrosine immunoprecipitation, GST-GRB2 pulldown (FGF signaling); AGE-ligand binding, antibody inhibition assays (AGE receptor)

    PMID:8621453 PMID:8855306

    Open questions at the time
    • FGF/GRB2 interaction not confirmed with reciprocal endogenous IP
    • Physiological relevance of AGE binding not established in vivo
    • Relationship between ER-resident function and cell-surface signaling roles unclear
  3. 2003 High

    Identification of PRKCSH germline mutations in polycystic liver disease families established it as a disease gene and implied that loss of hepatocystin's ER functions drives cystogenesis.

    Evidence Linkage mapping and mutation analysis across multiple Dutch families, independently confirmed by a second group

    PMID:12529853 PMID:12577059

    Open questions at the time
    • Molecular mechanism linking glucosidase II beta loss to cholangiocyte cyst formation not defined
    • Nature of second hit not characterized
  4. 2004 High

    Demonstration that PRKCSH's EF-hand domains sense Ca²⁺ and directly regulate the TRPV5 channel established a Ca²⁺-sensor function independent of its glucosidase II role.

    Evidence Co-IP, Ca²⁺-binding assays with EF-hand mutants, electrophysiology of TRPV5 currents

    PMID:15100231

    Open questions at the time
    • Whether Ca²⁺ sensing and glucosidase II scaffolding are mutually exclusive activities is unknown
    • In vivo renal Ca²⁺ phenotype in PRKCSH-deficient animals not tested
  5. 2005 High

    Discovery of a PKCζ–80K-H–munc18c trimeric complex that promotes GLUT4 translocation revealed PRKCSH as an adaptor in insulin-stimulated glucose uptake.

    Evidence Yeast two-hybrid, reciprocal co-IP from adipocytes and myotubes, GLUT4 translocation and glucose uptake assays

    PMID:15707389

    Open questions at the time
    • Structural basis of trimeric complex assembly unknown
    • Relevance to PCLD pathogenesis not addressed
  6. 2008 High

    Direct enhancement of IP3-induced Ca²⁺ release by purified 80K-H binding to IP3R1 established PRKCSH as a positive modulator of ER Ca²⁺ store mobilization, and ER localization of hepatocystin in cholangiocytes with loss in PCLD cysts supported a two-hit cystogenesis model.

    Evidence In vitro reconstituted Ca²⁺ release assay with purified protein, co-IP, immunohistochemistry of PCLD cyst tissue

    PMID:18224332 PMID:18990696

    Open questions at the time
    • Whether IP3R1 modulation is Ca²⁺-EF-hand-dependent not tested
    • Two-hit mechanism not genetically proven at the somatic level
  7. 2010 High

    PRKCSH was shown to protect TRPP2/polycystin-2 from HERP-mediated ubiquitination and ERAD, and zebrafish epistasis phenocopied polycystin-2 perturbation, providing a mechanistic link between PRKCSH loss and cystic disease.

    Evidence Co-IP, ubiquitination assays, zebrafish morpholino/overexpression with pronephric cyst and laterality phenotypes

    PMID:19801576

    Open questions at the time
    • Whether glucosidase II trimming activity is required for the TRPP2-protective function is unknown
    • Mammalian in vivo confirmation lacking
  8. 2012 Medium

    Identification of TRIM67-mediated proteasomal degradation of 80K-H, with phenotypic consequences for neuritogenesis, revealed upstream regulation of PRKCSH protein levels in neural differentiation.

    Evidence Co-IP, siRNA knockdown, TRIM67 overexpression, proliferation and neuritogenesis assays in neuroblastoma cells

    PMID:22337885

    Open questions at the time
    • Ubiquitin site(s) on 80K-H not mapped
    • In vivo neuronal phenotype of PRKCSH loss not examined
    • Single cell line (N1E-115)
  9. 2019 High

    PRKCSH was established as a selective activator of the IRE1α/XBP1 branch of the UPR through direct interaction with IRE1α and promotion of its autophosphorylation and oligomerization, linking PRKCSH to ER-stress signaling and tumor biology.

    Evidence Co-IP, autophosphorylation and oligomerization assays, PRKCSH knockdown/overexpression, XBP1 target gene profiling, in vivo tumor models

    PMID:31320625

    Open questions at the time
    • Whether IRE1α interaction is glycan-dependent or direct protein–protein is unclear
    • Relationship between glucosidase II activity and UPR regulation not dissected
  10. 2024 Medium

    PRKCSH stabilizes IGF1R protein to boost oncogenic survival signaling, impairing caspase-8 activation and conferring TNFSF resistance, and its loss enhances NK cell-mediated tumor killing, expanding its tumor-promoting functions beyond UPR modulation.

    Evidence Co-IP, protein half-life assay, caspase activation assays, xenograft model with NK cells

    PMID:38200153

    Open questions at the time
    • Whether IGF1R stabilization is glycan-processing-dependent not tested
    • Single cancer type (lung)
    • NK cell killing mechanism not fully dissected
  11. 2025 Medium

    In colorectal and lung cancer cells, PRKCSH inhibition was shown to sensitize tumors to ionizing radiation and ferroptosis through exaggerated IRE1α activation, p53 stabilization, and altered macrophage polarization, consolidating PRKCSH as a multifaceted regulator of tumor-immune and stress-response crosstalk.

    Evidence PRKCSH knockdown and CRISPR KO, clonogenic survival, apoptosis, DNA repair assays, cytokine profiling, macrophage co-culture, patient-derived organoids, xenograft models

    PMID:40189587 PMID:41350724

    Open questions at the time
    • Therapeutic window for PRKCSH inhibition not defined
    • Contribution of glucosidase II catalytic activity versus non-catalytic functions in these phenotypes not separated

Open questions

Synthesis pass · forward-looking unresolved questions
  • A central unresolved question is whether the diverse functions of PRKCSH — glucosidase II scaffolding, Ca²⁺ sensing, ERAD protection, IRE1α activation, and receptor stabilization — represent independent activities of distinct domains or are mechanistically coupled through its glycan-processing role.
  • No high-resolution structure of the full glucosidase II complex with client substrates
  • Domain-specific separation-of-function mutants for glucosidase II versus signaling roles not systematically generated
  • Conditional knockout mouse model to separate hepatic versus extrahepatic functions not reported

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0060090 molecular adaptor activity 2 GO:0044183 protein folding chaperone 1 GO:0140299 molecular sensor activity 1
Localization
GO:0005783 endoplasmic reticulum 3
Pathway
R-HSA-162582 Signal Transduction 5 R-HSA-1643685 Disease 5 R-HSA-382551 Transport of small molecules 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-8953897 Cellular responses to stimuli 3
Partners
GIIΑ (GANAB)IGF1RIRE1Α (ERN1)ITPR1MUNC18C (STXBP3)PKD2PRKCZTRPV5
Complex memberships
Glucosidase II (alpha-beta heterodimer)PKCζ–80K-H–munc18c complex

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1996 Glucosidase II is a two-subunit enzyme; the beta subunit (encoded by PRKCSH, then called 80K-H) is a non-catalytic, HDEL-containing subunit tightly associated with the catalytic alpha subunit. The beta subunit contains a C-terminal HDEL ER-retention signal and is responsible for ER localization of the enzyme complex. Biochemical purification of glucosidase II from rat liver, peptide sequencing, cDNA identification, and yeast gene disruption experiments The Journal of Biological Chemistry High 8910335
1996 80K-H (PRKCSH protein) was identified as a tyrosine-phosphorylated substrate (p90) in FGF-stimulated fibroblasts and was found to bind specifically to the SH2/SH3 adaptor protein GRB-2, placing 80K-H in the FGF receptor signaling pathway. 2D-PAGE microsequencing, anti-phosphotyrosine immunoprecipitation, GST-GRB2 pulldown, Western blotting The Journal of Biological Chemistry Medium 8621453
1996 The AGE-receptor component p90 is identical to 80K-H (PRKCSH protein); OST-48 (p60) and 80K-H (p90) together mediate AGE binding on cell surfaces. Immunoprecipitated OST-48 from rough ER fractions exhibited AGE binding, and immune IgG to recombinant 80K-H inhibited AGE-BSA binding to cell membranes. N-terminal sequencing, AGE-ligand binding assays, Western blotting, immunoprecipitation, flow cytometry, immunostaining, antibody inhibition assays Proceedings of the National Academy of Sciences of the United States of America Medium 8855306
2003 Germline loss-of-function mutations in PRKCSH (splice-site mutations) cause autosomal dominant polycystic liver disease (PCLD), establishing PRKCSH as a disease gene. The protein, named hepatocystin, is predicted to localize to the ER. Genetic linkage mapping, mutation analysis by sequencing, disease segregation analysis in four Dutch families Nature Genetics High 12529853 12577059
2003 PRKCSH encodes the noncatalytic beta-subunit of glucosidase II, a protein highly conserved across tissues, containing an LDLa domain, two EF-hand domains, and a C-terminal HDEL ER-retention sequence, with proposed roles in N-glycosylation regulation and FGF receptor signal transduction. Sequence analysis, DHPLC heteroduplex analysis, direct sequencing for mutation detection, domain annotation American Journal of Human Genetics Medium 12529853
2004 80K-H (PRKCSH protein) acts as a Ca2+ sensor that directly interacts with and regulates the epithelial Ca2+ channel TRPV5. Ca2+ binding via two EF-hand domains in 80K-H modulates TRPV5 channel activity; inactivation of the EF-hands abolished Ca2+ binding and altered TRPV5-mediated Ca2+ current and sensitivity to intracellular Ca2+. The HDEL and acidic glutamic stretch domains are also required for full TRPV5 regulation. Both proteins co-localize in kidney. cDNA microarray identification, co-immunoprecipitation, co-localization (immunofluorescence), Ca2+-binding assay, electrophysiology with domain mutants The Journal of Biological Chemistry High 15100231
2005 80K-H (PRKCSH protein) interacts with PKCzeta and munc18c in an insulin-dependent manner, forming a trimeric complex (PKCzeta–80K-H–munc18c) that promotes GLUT4 vesicle translocation to the plasma membrane. Overexpression of 80K-H mimicked insulin's effect on glucose uptake and GLUT4 translocation, proportional to its ability to associate with munc18c. Yeast two-hybrid screen, GST pulldown, endogenous co-immunoprecipitation from adipocytes and myotubes, glucose uptake assay, GLUT4 translocation assay The Biochemical Journal High 15707389
2008 80K-H (PRKCSH protein) directly interacts with the C-terminal tail of IP3 receptor type 1 (IP3R1), co-localizes with IP3R1 in COS-7 cells and hippocampal neurons, and directly enhances IP3-induced Ca2+ release from ER microsomes. 80K-H also regulates ATP-induced Ca2+ release in living cells. Yeast two-hybrid screen, in vitro direct binding assay, co-immunoprecipitation, immunocytochemistry/immunohistochemistry, Ca2+ release assay with purified recombinant 80K-H The Journal of Biological Chemistry High 18990696
2008 Hepatocystin (PRKCSH protein) localizes predominantly to the ER in liver cells (both hepatocytes and bile duct epithelia). In PCLD patients with PRKCSH mutations, cyst epithelium lacks hepatocystin expression (consistent with a two-hit/loss-of-function mechanism), while Sec63p is still expressed in all cysts. Hepatocystin and Sec63p do not interact with each other. Cell fractionation, immunofluorescence, immunohistochemistry in fetal and adult liver and PCLD cyst tissue Histochemistry and Cell Biology Medium 18224332
2010 PRKCSH (hepatocystin) functions as a chaperone-like molecule that binds the C-terminal domain of TRPP2/polycystin-2 within the ER and protects TRPP2 from HERP-mediated ubiquitination and ER-associated degradation (ERAD). PRKCSH interacts with Herp and inhibits Herp-mediated ubiquitination of TRPP2. Over-expression or depletion of PRKCSH in zebrafish embryos phenocopies TRPP2 perturbation (pronephric cysts, body curvature, situs inversus), indicating a shared signaling pathway. Co-immunoprecipitation, co-localization, zebrafish overexpression/morpholino knockdown, ubiquitination assay, genetic epistasis in zebrafish Human Molecular Genetics High 19801576
2012 TRIM67 E3 ubiquitin ligase interacts with 80K-H (PRKCSH protein) and promotes its proteasomal degradation. Ectopic TRIM67 expression reduces endogenous 80K-H levels, attenuates cell proliferation, and enhances neuritogenesis in N1E-115 neuroblastoma cells; 80K-H knockdown phenocopies TRIM67 overexpression, indicating 80K-H is a downstream effector of TRIM67 in Ras-mediated signaling and neural differentiation. Co-immunoprecipitation, Western blot, siRNA knockdown, overexpression, cell proliferation assay, neuritogenesis assay The Journal of Biological Chemistry Medium 22337885
2013 Hepatocystin (PRKCSH protein) interacts with HBx protein of hepatitis B virus via its mannose 6-phosphate receptor homology domain (aa 419–525) binding to HBx C-terminus (aa 110–154). Hepatocystin overexpression accelerates HBx degradation via a ubiquitin-independent proteasome pathway, inhibiting HBV DNA replication and HBs antigen expression. Affinity purification/mass spectrometry, co-immunoprecipitation, Western blot, immunocytochemistry, domain mapping, proteasome/translation inhibitor assays, HBV replication assay Biochimica et Biophysica Acta Medium 23644164
2019 PRKCSH functions as a selective regulator of the IRE1α branch of the unfolded protein response (UPR). PRKCSH directly interacts with IRE1α and boosts its ER stress-mediated autophosphorylation and oligomerization, leading to selective activation of IRE1α/XBP1 signaling. This promotes expression of tumor-promoting factors and confers tumor cell resistance to ER stress. Co-immunoprecipitation, autophosphorylation assay, oligomerization assay, PRKCSH knockdown/overexpression, XBP1 target gene expression analysis, in vivo tumor models Nature Communications High 31320625
2024 PRKCSH interacts with IGF1R and extends its protein half-life (stabilizes it), thereby boosting IGF1R oncogenic signaling in lung cancer cells. The PRKCSH-IGF1R axis impairs caspase-8 activation, increases Mcl-1 expression, and inhibits caspase-9, promoting TNFSF resistance. PRKCSH deficiency augments NK cell-mediated antitumor killing in a xenograft model. Co-immunoprecipitation, protein half-life assay, caspase activation assay, Mcl-1 expression analysis, siRNA knockdown, tumor xenograft model with NK cells Experimental & Molecular Medicine Medium 38200153
2025 PRKCSH inhibition in colorectal cancer cells sensitizes them to ionizing radiation by reducing clonogenic survival, promoting apoptosis, and impairing DNA damage repair. Mechanistically, PRKCSH inhibition reduces p53 ubiquitination and degradation by activating the ER stress IRE1α/XBP1s pathway after radiation, impairing DNA repair and thus reducing radioresistance. PRKCSH knockdown, clonogenic survival assay, apoptosis assay, DNA damage repair assay, p53 ubiquitination assay, IRE1α/XBP1s pathway analysis, patient-derived organoids, tumor xenograft Cell Death & Disease Medium 40189587
2025 PRKCSH deficiency in lung adenocarcinoma cells leads to exaggerated IRE1α activation under ER stress (increased XBP1s and p-JNK), suppresses IL-6 and IL-8 secretion, promotes M1 macrophage polarization (increased CD86+ macrophages), and enhances susceptibility to ER stress-induced apoptosis and ferroptosis while impairing autophagy. CRISPR/Cas9 KO, cytokine profiling, macrophage co-culture, flow cytometry, zebrafish xenograft, clinical pleural effusion sample analysis Cancer Cell International Medium 41350724
2024 Myoclonin1 (EFHC1 protein) interacts with PRKCSH (80K-H), which itself interacts with IP3R1, placing PRKCSH at the intersection of a myoclonin1–PRKCSH–IP3R complex that modulates ER Ca2+ homeostasis and IP3-induced Ca2+ release. Co-immunoprecipitation, Ca2+ measurement in Efhc1-deficient mouse cells, IP3-induced Ca2+ release assay bioRxivpreprint Low bio_10.1101_2024.07.01.601633

Source papers

Stage 0 corpus · 66 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 A human protein-protein interaction network: a resource for annotating the proteome. Cell 1704 16169070
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
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2018 VIRMA mediates preferential m6A mRNA methylation in 3'UTR and near stop codon and associates with alternative polyadenylation. Cell discovery 829 29507755
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2012 A census of human soluble protein complexes. Cell 689 22939629
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2011 Global landscape of HIV-human protein complexes. Nature 593 22190034
2021 Multilevel proteomics reveals host perturbations by SARS-CoV-2 and SARS-CoV. Nature 532 33845483
1994 Oligo-capping: a simple method to replace the cap structure of eukaryotic mRNAs with oligoribonucleotides. Gene 492 8125298
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
2015 A Dynamic Protein Interaction Landscape of the Human Centrosome-Cilium Interface. Cell 433 26638075
2016 Widespread Expansion of Protein Interaction Capabilities by Alternative Splicing. Cell 423 26871637
2010 Systematic analysis of human protein complexes identifies chromosome segregation proteins. Science (New York, N.Y.) 421 20360068
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
1998 Cell activation by glycated proteins. AGE receptors, receptor recognition factors and functional classification of AGEs. Cellular and molecular biology (Noisy-le-Grand, France) 344 9846883
2021 A proximity-dependent biotinylation map of a human cell. Nature 339 34079125
1996 Molecular identity and cellular distribution of advanced glycation endproduct receptors: relationship of p60 to OST-48 and p90 to 80K-H membrane proteins. Proceedings of the National Academy of Sciences of the United States of America 299 8855306
2020 Virus-Host Interactome and Proteomic Survey Reveal Potential Virulence Factors Influencing SARS-CoV-2 Pathogenesis. Med (New York, N.Y.) 291 32838362
2012 A high-throughput approach for measuring temporal changes in the interactome. Nature methods 273 22863883
2011 A directed protein interaction network for investigating intracellular signal transduction. Science signaling 258 21900206
2008 Getting in and out from calnexin/calreticulin cycles. The Journal of biological chemistry 242 18303019
2015 ∆F508 CFTR interactome remodelling promotes rescue of cystic fibrosis. Nature 209 26618866
2011 Toward an understanding of the protein interaction network of the human liver. Molecular systems biology 207 21988832
2018 An AP-MS- and BioID-compatible MAC-tag enables comprehensive mapping of protein interactions and subcellular localizations. Nature communications 201 29568061
1996 Endoplasmic reticulum glucosidase II is composed of a catalytic subunit, conserved from yeast to mammals, and a tightly bound noncatalytic HDEL-containing subunit. The Journal of biological chemistry 197 8910335
2004 Mutations in SEC63 cause autosomal dominant polycystic liver disease. Nature genetics 196 15133510
2020 Systems analysis of RhoGEF and RhoGAP regulatory proteins reveals spatially organized RAC1 signalling from integrin adhesions. Nature cell biology 194 32203420
2003 Germline mutations in PRKCSH are associated with autosomal dominant polycystic liver disease. Nature genetics 175 12577059
2003 Mutations in PRKCSH cause isolated autosomal dominant polycystic liver disease. American journal of human genetics 141 12529853
2006 Changing distribution of norovirus genotypes and genetic analysis of recombinant GIIb among infants and children with diarrhea in Japan. Journal of medical virology 92 16721850
1996 Identification of p90, a prominent tyrosine-phosphorylated protein in fibroblast growth factor-stimulated cells, as 80K-H. The Journal of biological chemistry 60 8621453
2004 80K-H as a new Ca2+ sensor regulating the activity of the epithelial Ca2+ channel transient receptor potential cation channel V5 (TRPV5). The Journal of biological chemistry 57 15100231
2006 Extensive mutational analysis of PRKCSH and SEC63 broadens the spectrum of polycystic liver disease. Human mutation 45 16835903
2012 TRIM67 protein negatively regulates Ras activity through degradation of 80K-H and induces neuritogenesis. The Journal of biological chemistry 44 22337885
2005 Identification of 80K-H as a protein involved in GLUT4 vesicle trafficking. The Biochemical journal 42 15707389
2010 PRKCSH/80K-H, the protein mutated in polycystic liver disease, protects polycystin-2/TRPP2 against HERP-mediated degradation. Human molecular genetics 41 19801576
2008 80K-H interacts with inositol 1,4,5-trisphosphate (IP3) receptors and regulates IP3-induced calcium release activity. The Journal of biological chemistry 40 18990696
2019 PRKCSH contributes to tumorigenesis by selective boosting of IRE1 signaling pathway. Nature communications 34 31320625
2010 Secondary and tertiary structure modeling reveals effects of novel mutations in polycystic liver disease genes PRKCSH and SEC63. Clinical genetics 32 20095989
2022 Down-regulating Circular RNA Prkcsh suppresses the inflammatory response after spinal cord injury. Neural regeneration research 31 34100450
2004 Abnormal hepatocystin caused by truncating PRKCSH mutations leads to autosomal dominant polycystic liver disease. Hepatology (Baltimore, Md.) 28 15057895
2018 A newly isolated Chinese virulent genotype GIIb porcine epidemic diarrhea virus strain: Biological characteristics, pathogenicity and immune protective effects as an inactivated vaccine candidate. Virus research 27 30342075
2019 Evaluation and comparison of immunogenicity and cross-protective efficacy of two inactivated cell culture-derived GIIa- and GIIb-genotype porcine epidemic diarrhea virus vaccines in suckling piglets. Veterinary microbiology 26 30827401
2000 Vacuolar system-associated protein-60: a protein characterized from bovine granulosa and luteal cells that is associated with intracellular vesicles and related to human 80K-H and murine beta-glucosidase II. Biology of reproduction 22 10684806
2008 Cysts of PRKCSH mutated polycystic liver disease patients lack hepatocystin but express Sec63p. Histochemistry and cell biology 19 18224332
2003 Immunolocalization of vacuolar system-associated protein-60 (VASAP-60). Histochemistry and cell biology 17 12750905
2003 Elevated 80K-H protein in breast cancer: a role for FGF-1 stimulation of 80K-H. The International journal of biological markers 17 12841677
2013 Hepatocystin/80K-H inhibits replication of hepatitis B virus through interaction with HBx protein in hepatoma cell. Biochimica et biophysica acta 14 23644164
2007 Genotyping of GII.4 and GIIb norovirus RT-PCR amplicons by RFLP analysis. Journal of virological methods 14 17953996
1998 XV454, a novel nonpeptide small-molecule platelet GIIb/IIIa antagonist with comparable platelet alpha(IIb)beta3-binding kinetics to c7E3. Journal of cardiovascular pharmacology 14 9821847
1996 A 3-Mb region for the familial hemiplegic migraine locus on 19p13.1-p13.2: exclusion of PRKCSH as a candidate gene. Dutch Migraine Genetic Research Group. European journal of human genetics : EJHG 13 9043864
2023 Recombinant human adenovirus type 5 based vaccine candidates against GIIa- and GIIb-genotype porcine epidemic diarrhea virus induce robust humoral and cellular response in mice. Virology 12 37201320
2020 PRKCSH Alternative Splicing Involves in Silica-Induced Expression of Epithelial-Mesenchymal Transition Markers and Cell Proliferation. Dose-response : a publication of International Hormesis Society 11 32425726
2005 Autosomal dominant polycystic liver disease in a family without polycystic kidney disease associated with a novel missense protein kinase C substrate 80K-H mutation. World journal of gastroenterology 8 16437702
2024 Navigating PRKCSH's impact on cancer: from N-linked glycosylation to death pathway and anti-tumor immunity. Frontiers in oncology 7 38571496
2024 PRKCSH contributes to TNFSF resistance by extending IGF1R half-life and activation in lung cancer. Experimental & molecular medicine 5 38200153
2009 PRKCSH genetic mutation was not found in Taiwanese patients with polycystic liver disease. Digestive diseases and sciences 4 19308730
2025 PRKCSH enhances colorectal cancer radioresistance via IRE1α/XBP1s-mediated DNA repair. Cell death & disease 2 40189587
2015 Severe Polycystic Liver Disease Is Not Caused by Large Deletions of the PRKCSH Gene. Journal of clinical laboratory analysis 2 26365003
2019 Publisher Correction: PRKCSH contributes to tumorigenesis by selective boosting of IRE1 signaling pathway. Nature communications 1 31420557
2025 Acute Febrile Illness Associated with an Emerging Dengue 4 GIIb Variant Causing Epidemic in León, Nicaragua 2022. Viruses 0 40872827
2025 PRKCSH deficiency promotes an anti-tumor immune microenvironment via UPR activation and M1 macrophage polarization. Cancer cell international 0 41350724