Affinage

OCIAD1

OCIA domain-containing protein 1 · UniProt Q9NX40

Length
245 aa
Mass
27.6 kDa
Annotated
2026-06-10
29 papers in source corpus 19 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

OCIAD1 (Asrij) is a conserved, dually localized scaffold protein acting at endosomes and the inner mitochondrial membrane to coordinate organelle function with stem cell maintenance and differentiation (PMID:23972987, PMID:34034859). At endosomes it provides a platform for STAT3 interaction and JAK/STAT-dependent pluripotency signaling (PMID:23972987) and controls Notch receptor trafficking, with loss causing Notch accumulation in sorting endosomes and aberrant blood cell (crystal cell) differentiation (PMID:22110713); this endocytic axis operates downstream of activated ARF1-GTP, which physically binds OCIAD1 and regulates its levels (PMID:24707047, PMID:33433647). At the inner mitochondrial membrane OCIAD1 assembles with supramolecular prohibitin complexes to support Complex III biogenesis by enabling IMMP2L-mediated processing of the catalytic subunit CYC1 (PMID:34034859) and to protect the TIMM17A variant of the TIM23 import translocase from YME1L-mediated degradation (PMID:39630581). It additionally restrains Complex I activity and oxidative phosphorylation to maintain pluripotency, since Complex I inhibition rescues the differentiation defects of OCIAD1 loss (PMID:29937147), and it acts at the mitochondria–peroxisome interface to balance lipid metabolism, with knockout cells losing peroxisomal proteins and ether phospholipids while accumulating mitochondrial β-oxidation enzymes (PMID:40211913). Through its conserved OCIA domain OCIAD1 sequesters the COP9 signalosome subunit CSN5 to block p53 ubiquitination and degradation, thereby sustaining hematopoietic stem cell quiescence (PMID:30952670). Loss of OCIAD1 in HSCs produces convergent organelle dysfunction—damaged mitochondria with elevated ROS, impaired endosomal trafficking, and reduced proteasome activity—that is reversible by pharmacological correction (PMID:35289070). OCIAD1 is cleaved at Cys38 by the HCV NS3-4A protease, a selectivity determined by sequence around the scissile site and the adjacent transmembrane segment (PMID:32697788).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2003 Medium

    Established the existence and basal localization of OCIAD1/Asrij, defining it as a conserved transmembrane protein of the endo-lysosomal system expressed in stem cells and embryos.

    Evidence Subcellular fractionation and localization imaging in mouse ES cells and embryos

    PMID:12889067

    Open questions at the time
    • No functional perturbation
    • Molecular activity undefined
    • Mitochondrial localization not yet detected
  2. 2011 High

    Showed OCIAD1 has a functional role in vesicular trafficking, linking it to Notch receptor sorting and blood cell differentiation rather than being a passive endosomal resident.

    Evidence Drosophila asrij null mutants with endosomal marker imaging and in vitro trafficking assays

    PMID:22110713

    Open questions at the time
    • Direct cargo-binding mechanism unresolved
    • How OCIAD1 selects endosomal subcompartments unknown
  3. 2013 High

    Identified an endosomal signaling scaffold function by showing OCIAD1 binds STAT3 and dose-dependently tunes JAK/STAT signaling for stem cell maintenance.

    Evidence Co-IP, colocalization, and cross-species genetic gain/loss-of-function with rescue in mouse ESCs and Drosophila HSCs

    PMID:23972987

    Open questions at the time
    • Whether OCIAD1 directly activates or just localizes STAT3 is unclear
    • Structural basis of the interaction unknown
  4. 2014 High

    Placed OCIAD1 in a defined signaling hierarchy by showing ARF1-GTP binds OCIAD1 and acts upstream in endocytic control of Notch trafficking and hematopoiesis.

    Evidence Genetic epistasis with ARF1 GEF/GAP manipulation, interaction assay, and Notch trafficking imaging

    PMID:24707047

    Open questions at the time
    • Direct vs indirect ARF1 binding not resolved here
    • Downstream effectors between OCIAD1 and Notch sorting unidentified
  5. 2017 Medium

    Extended the ARF1-Asrij axis to innate immunity, distinguishing OCIAD1-dependent from ARF1-independent control of melanization and antimicrobial peptide pathways.

    Evidence Drosophila genetic loss-of-function with AMP/phenoloxidase, ubiquitination, and infection survival assays

    PMID:28273919

    Open questions at the time
    • Molecular link to Cactus ubiquitination unresolved
    • Single model organism
  6. 2018 High

    Defined a mitochondrial function by showing OCIAD1 interacts with Complex I and restrains OXPHOS to preserve pluripotency.

    Evidence Co-IP, live-cell OXPHOS assays, CRISPR knockout, and Complex I inhibitor rescue in human pluripotent stem cells

    PMID:29937147

    Open questions at the time
    • Whether OCIAD1 directly assembles into Complex I unknown
    • Mechanism of activity suppression unresolved
  7. 2019 High

    Resolved a molecular mechanism for stem cell maintenance: OCIAD1 sequesters CSN5 via its OCIA domain to stabilize p53 and enforce HSC quiescence.

    Evidence Domain-specific Co-IP, ubiquitination assay, asrij knockout mouse, Nutlin-3 rescue, and transplantation

    PMID:30952670

    Open questions at the time
    • How endosomal/mitochondrial OCIAD1 pools relate to CSN5 sequestration unclear
    • Structural definition of OCIA-domain binding lacking
  8. 2020 High

    Mapped OCIAD1 as a host substrate of the HCV NS3-4A protease, defining the Cys38 scissile site and the determinants of protease selectivity.

    Evidence SILAC proteomics, replicon and cell-culture HCV systems, patient liver biopsies, and domain-swapping mutagenesis

    PMID:32697788

    Open questions at the time
    • Functional consequence of cleavage for the host not established
    • Fate of cleavage fragments unknown
  9. 2021 High

    Established OCIAD1 as an inner mitochondrial membrane prohibitin-associated factor required for Complex III biogenesis through IMMP2L-mediated CYC1 processing.

    Evidence Genome-wide CRISPRi screen, fractionation, Co-IP, and CYC1 processing/Complex III assembly assays

    PMID:34034859

    Open questions at the time
    • Whether OCIAD1 directly presents CYC1 to IMMP2L unknown
    • Stoichiometry within prohibitin assemblies undefined
  10. 2021 Medium

    Connected OCIAD1 to mitochondrial dynamics, showing its loss elongates mitochondria and that it genetically interacts with Drp1 and Marf to control differentiation.

    Evidence Live imaging of mitochondrial dynamics and genetic epistasis in Drosophila hemocytes and OCIAD1 KO hESCs

    PMID:34295888

    Open questions at the time
    • Direct interaction with fission/fusion machinery untested
    • Causal order between dynamics and Notch defects unclear
  11. 2021 Medium

    Confirmed a direct OCIAD1-ARF1 physical interaction using purified components, validating the in vivo epistasis at the biochemical level.

    Evidence Protein complementation assay with bacterially purified recombinant proteins; sophorolipid-aided solubilization

    PMID:33433647

    Open questions at the time
    • No structure obtained
    • Functional follow-up limited in this study
  12. 2022 High

    Demonstrated that OCIAD1 integrates mitochondrial, endosomal, and proteasomal organelle health in HSCs, with pharmacological and LPA-driven rescue of aging phenotypes.

    Evidence asrij knockout mouse with mitochondrial/ROS, trafficking marker, and proteasome assays plus pharmacological and LPA rescue in aged mice

    PMID:35289070

    Open questions at the time
    • Whether organelle defects are independent or sequential unresolved
    • Primary versus secondary effects not separated
  13. 2024 High

    Refined the mitochondrial role by showing OCIAD1, with prohibitins, protects the TIMM17A variant of the TIM23 import translocase from YME1L proteolysis, with reciprocal regulation by TIM23 status.

    Evidence Co-IP of OCIAD1-prohibitin-TIM23, genetic depletion, YME1L protease assay, and TIM23 stability assays

    PMID:39630581

    Open questions at the time
    • Mechanism distinguishing TIMM17A from TIMM17B protection unclear
    • How TIM23 status feeds back to OCIAD1 levels undefined
  14. 2025 Medium

    Positioned OCIAD1 at the mitochondria-peroxisome interface balancing lipid metabolism, linking its loss to peroxisomal protein loss and shifted ether-lipid and β-oxidation profiles.

    Evidence Lipidomics and proteomics of OCIAD1 KO cells, proximity-labeling meta-analysis, and peroxisome morphology imaging

    PMID:40211913

    Open questions at the time
    • No direct enzymatic reconstitution with FAR1/ABCD3
    • Mechanism of peroxisomal protein loss unresolved
  15. 2025 Medium

    Implicated OCIAD1 as a driver of neuroinflammatory microglial states in Alzheimer's models via STAT3/NF-κB signaling, with depletion reducing plaque load.

    Evidence asrij knockout in APP/PS1 mice with microglial RNA-seq, flow cytometry, pathway activation assays, and behavioral testing

    PMID:40114191

    Open questions at the time
    • Cell-intrinsic mechanism in microglia not dissected
    • Relationship to mitochondrial/endosomal functions unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How OCIAD1 physically partitions between its endosomal scaffolding and inner-mitochondrial membrane roles, and whether one biochemical activity underlies both, remains unresolved.
  • No structural model of OCIAD1
  • No defined catalytic activity
  • Determinants of dual targeting unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0098772 molecular function regulator activity 3
Localization
GO:0005739 mitochondrion 5 GO:0005768 endosome 4 GO:0005764 lysosome 1 GO:0005777 peroxisome 1
Pathway
R-HSA-1430728 Metabolism 3 R-HSA-162582 Signal Transduction 2 R-HSA-392499 Metabolism of proteins 2 R-HSA-5653656 Vesicle-mediated transport 2
Partners
ARF1BCL2CSN5IMMP2LPHBSTAT3TIMM17AYME1L
Complex memberships
TIM23 translocase (TIMM17A variant)mitochondrial Complex Imitochondrial Complex IIIprohibitin complex

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 Asrij/OCIAD1 encodes a novel conserved predicted transmembrane protein of 247 amino acids that localizes to lysosomes and endosomes, as determined by subcellular fractionation and localization studies in mouse embryonic stem cells and during development. Subcellular localization (lysosomes/endosomes) by direct imaging/fractionation; expression analysis in ES cells and embryos Developmental dynamics Medium 12889067
2011 Drosophila Asrij localizes to a subset of endocytic vesicles and is required for proper Notch trafficking; loss of asrij causes accumulation of Notch in sorting endosomes and increased crystal cell differentiation, indicating Asrij regulates Notch signaling through endosomal trafficking. Genetic loss-of-function (asrij null mutants), immunostaining of endosomal markers, in vitro fluorescent probe trafficking assay PloS one High 22110713
2013 Asrij/OCIAD1 is an endosomal protein that dose-dependently modulates JAK/STAT signaling to maintain stem cell pluripotency; STAT3 colocalizes with Asrij in endosomes and interacts with it biochemically, suggesting Asrij provides an endosomal scaffold for STAT3 activation. Co-immunoprecipitation (biochemical interaction), colocalization imaging (endosomal compartment), genetic gain/loss-of-function in mouse ESCs and Drosophila HSCs, cross-species rescue Cell reports High 23972987
2014 Activated ARF1 (ARF1-GTP) physically interacts with Asrij and regulates its levels in blood cells; perturbation of ARF1 activation leads to aberrant Notch trafficking with Notch intracellular domain stalled in sorting endosomes, placing ARF1 upstream of Asrij in endocytic control of hematopoiesis. Genetic epistasis (ARF1 knockdown, GEF/GAP manipulation), co-immunoprecipitation/interaction assay, Notch trafficking analysis by immunostaining Proceedings of the National Academy of Sciences High 24707047
2008 OCIAD1 overexpression in ovarian cancer cells increases LPA-induced cell adhesion to collagen I and laminin 10/11, and this effect is not blocked by PKC or PI3K inhibitors, indicating OCIAD1 promotes cell adhesion through a PKC/PI3K-independent mechanism. Overexpression and knockdown in HEY ovarian cancer cells, cell adhesion assay with pharmacological inhibitors (LY294002, GF109203X) Gynecologic oncology Medium 18328549
2010 LPA induces OCIAD1 serine phosphorylation within 2 hours and upregulates OCIAD1 expression via the MKK6/p38 MAPK pathway; OCIAD1 knockdown inhibits LPA-induced adhesion to collagen I and laminin 10/11 and specifically to alpha2, alpha5, alphaV, and beta1 integrins; proteomic studies show OCIAD1 is physically associated with alpha-actin 4 and beta-actin, indicating a role in cytoskeletal regulation. LPA stimulation assay, serine phosphorylation detection, p38 inhibitor (pharmacological), MKK6 transfection, knockdown, integrin-specific adhesion assay, co-immunoprecipitation/proteomics (OCIAD1–actin interaction) Molecular cancer therapeutics Medium 20515946
2017 The ARF1-Asrij endosomal axis regulates the cellular immune response by controlling crystal cell melanization and phenoloxidase activity, and suppresses Toll pathway anti-microbial peptides by regulating ubiquitination of the Toll inhibitor Cactus; Asrij (but not ARF1) is required for Imd pathway AMP production. Genetic loss-of-function (ARF1 and asrij mutants), AMP and phenoloxidase activity assays, ubiquitination analysis, infection survival assay Scientific reports Medium 28273919
2018 OCIAD1 interacts with mitochondrial Complex I and regulates its activity; OCIAD1 depletion in human pluripotent stem cells increases oxidative phosphorylation (OXPHOS), and pharmacological inhibition of Complex I rescues the differentiation defects caused by OCIAD1 loss, placing OCIAD1 as a regulator of mitochondrial Complex I activity to maintain pluripotency. Co-immunoprecipitation (OCIAD1-Complex I interaction), energy metabolic assays (live cell OXPHOS), CRISPR/Cas9 knockout, pharmacological rescue (Complex I inhibitor) Stem cell reports High 29937147
2019 Asrij/OCIAD1 sequesters CSN5 (COP9 signalosome subunit 5) via its conserved OCIA domain, preventing CSN5-mediated p53 ubiquitination and degradation; loss of Asrij in mouse HSCs leads to increased polyubiquitinated proteins and p53 degradation, and Nutlin-3 treatment (p53 stabilization) restores normal HSPC frequencies in asrij knockout mice. Co-immunoprecipitation (Asrij-CSN5 interaction via OCIA domain), ubiquitination assay, asrij knockout mouse model, pharmacological rescue (Nutlin-3), transplantation assays Blood High 30952670
2019 OCIAD1 regulates ATM expression/function in pancreatic ductal adenocarcinoma cells to promote cell migration; OCIAD1 downregulation inhibits migration and is associated with increased ATM. Knockdown/overexpression in PDAC cell lines, migration assay, gene chip correlation analysis Pancreatology Low 31221523
2020 HCV NS3-4A protease cleaves OCIAD1 at Cys38, near a predicted transmembrane segment; cleavage occurs in heterologous systems, HCV replicons, cell-culture HCV, and human liver biopsies from chronic HCV patients; domain-swapping experiments show that the sequence surrounding Cys38 and the transmembrane segment determine substrate selectivity for NS3-4A. Quantitative proteomics (SILAC-MS), heterologous expression cleavage assay, replicon system, cell culture HCV system, patient liver biopsies, domain-swapping mutagenesis PloS one High 32697788
2020 Elevated OCIAD1 interacts with BCL-2 to impair mitochondrial function in neurons; OCIAD1 levels are increased by Aβ/GSK-3β signaling, and elevated OCIAD1 increases neuronal susceptibility to AD pathological challenges. Co-immunoprecipitation (OCIAD1-BCL-2 interaction), mitochondrial function assays, overexpression in neuronal cells, bioinformatics-guided candidate identification EBioMedicine Medium 31931285
2021 OCIAD1 is an inner mitochondrial membrane protein that forms a complex with supramolecular prohibitin assemblies and is required for normal steady-state levels of mitochondrial Complex III and for proteolytic processing of the catalytic subunit cytochrome c (CYC1) by the IMMP2L protease; in OCIAD1-depleted mitochondria, unprocessed CYC1 is hemylated and incorporated into Complex III. Genome-wide CRISPRi screen, CRISPRi depletion, mitochondrial fractionation, co-immunoprecipitation (OCIAD1-prohibitin complex), Complex III assembly assay, CYC1 processing assay, proteomics eLife High 34034859
2021 Asrij/OCIAD1 localizes to mitochondria of larval blood cells and its depletion causes elongated mitochondria and reduced mitochondrial dynamics; genetic interaction studies show Asrij synergizes with fission regulator Drp1 and fusion regulator Marf/Mitofusin to control crystal cell differentiation and Notch signaling in Drosophila progenitors. Live imaging of mitochondrial dynamics (knockdown hemocytes and OCIAD1 KO hESCs), genetic epistasis (Drp1 and Marf knockdown with asrij depletion), Notch signaling readout Frontiers in cell and developmental biology Medium 34295888
2021 Asrij/OCIAD1 physically interacts with ARF1 as confirmed by a protein complementation assay using bacterially expressed purified proteins; sophorolipids improve solubility and monodispersibility of purified Asrij membrane protein. Protein complementation assay (in vitro with purified recombinant proteins), heterologous expression and purification, crystallization trials The Journal of membrane biology Medium 33433647
2022 In asrij knockout mouse HSCs, organelle dysfunction occurs: damaged mitochondria with elevated ROS, impaired endosomal trafficking (increased cleaved Notch1, reduced Rab5), and reduced 26S proteasome activity; pharmacological correction of mitochondrial and proteasome activity restores HSC and myeloid cell frequencies, and LPA-induced Asrij upregulation in aged mice rescues these organelle functions. asrij knockout mouse, mitochondrial function assay, ROS measurement, endosomal trafficking markers (Notch1, Rab5), proteasome activity assay, pharmacological rescue, LPA stimulation in aged mice Aging cell High 35289070
2024 OCIAD1 assembles with the prohibitin complex to protect the TIMM17A variant of the mitochondrial TIM23 translocase from degradation by the YME1L protease; prohibitins are required to stabilize both TIMM17A- and TIMM17B-containing TIM23 variants; OCIAD1 expression is in turn regulated by TIM23 complex status. Co-immunoprecipitation (OCIAD1-prohibitin-TIM23 complex), genetic depletion of OCIAD1 and prohibitins, protease (YME1L) activity assay, TIM23 stability assay Cell reports High 39630581
2025 OCIAD1 knockout cells show extensive lipidome rearrangement including decreased ether phospholipids and phospholipids with odd numbers of carbons, associated with global loss of peroxisomal proteins and aberrant peroxisomal morphology, and increased mitochondrial fatty acid β-oxidation proteins; OCIAD1 is proposed to act at the mitochondria-peroxisome interface to balance lipid metabolism, with direct impact on FAR1 and ABCD3 enzymes. Mass spectrometry-based lipidomics and proteomics (mitochondrial fraction and whole cell) of OCIAD1 KO cells, proximity labeling meta-analysis, peroxisome morphology imaging Journal of cell science Medium 40211913
2025 Asrij depletion in APP/PS1 AD mice reduces STAT3 and NF-κB activation in microglia, increases mitochondrial activity, and impedes acquisition of the pro-inflammatory disease-associated microglia (DAM) state; loss of Asrij reduces proinflammatory cytokine levels and Aβ plaque load, positioning Asrij as a promoter of neuroinflammatory DAM signaling. asrij knockout in APP/PS1 mice, flow cytometry, RNA sequencing of AD microglia, confocal microscopy, immunohistochemistry, STAT3/NF-κB activation assay, mitochondrial activity assay, behavioral testing Journal of neuroinflammation Medium 40114191

Source papers

Stage 0 corpus · 29 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 ARF1-GTP regulates Asrij to provide endocytic control of Drosophila blood cell homeostasis. Proceedings of the National Academy of Sciences of the United States of America 43 24707047
2013 Conserved regulation of the Jak/STAT pathway by the endosomal protein asrij maintains stem cell potency. Cell reports 42 23972987
2011 Asrij maintains the stem cell niche and controls differentiation during Drosophila lymph gland hematopoiesis. PloS one 36 22110713
2021 Genome-wide CRISPRi screening identifies OCIAD1 as a prohibitin client and regulatory determinant of mitochondrial Complex III assembly in human cells. eLife 33 34034859
2019 Asrij/OCIAD1 suppresses CSN5-mediated p53 degradation and maintains mouse hematopoietic stem cell quiescence. Blood 30 30952670
2018 OCIAD1 Controls Electron Transport Chain Complex I Activity to Regulate Energy Metabolism in Human Pluripotent Stem Cells. Stem cell reports 24 29937147
2008 Ovarian cancer immuno-reactive antigen domain containing 1 (OCIAD1), a key player in ovarian cancer cell adhesion. Gynecologic oncology 21 18328549
2012 Increased expression of OCIA domain containing 2 during stepwise progression of ovarian mucinous tumor. Pathology international 19 22726067
2011 Expression of NCAM and OCIAD1 in well-differentiated thyroid carcinoma: correlation with the risk of distant metastasis. Journal of clinical pathology 19 22081784
2017 Differential modulation of the cellular and humoral immune responses in Drosophila is mediated by the endosomal ARF1-Asrij axis. Scientific reports 18 28273919
2010 Role of the 18:1 lysophosphatidic acid-ovarian cancer immunoreactive antigen domain containing 1 (OCIAD1)-integrin axis in generating late-stage ovarian cancer. Molecular cancer therapeutics 18 20515946
2020 OCIAD1 contributes to neurodegeneration in Alzheimer's disease by inducing mitochondria dysfunction, neuronal vulnerability and synaptic damages. EBioMedicine 16 31931285
2003 Embryonic stem cell and tissue-specific expression of a novel conserved gene, asrij. Developmental dynamics : an official publication of the American Association of Anatomists 14 12889067
2024 OCIAD1 and prohibitins regulate the stability of the TIM23 protein translocase. Cell reports 13 39630581
2021 A Conserved Role for Asrij/OCIAD1 in Progenitor Differentiation and Lineage Specification Through Functional Interaction With the Regulators of Mitochondrial Dynamics. Frontiers in cell and developmental biology 12 34295888
2022 Organelle dysfunction upon asrij depletion causes aging-like changes in mouse hematopoietic stem cells. Aging cell 11 35289070
2025 Asrij/OCIAD1 depletion reduces inflammatory microglial activation and ameliorates Aβ pathology in an Alzheimer's disease mouse model. Journal of neuroinflammation 8 40114191
2003 Drosophila asrij is expressed in pole cells, trachea and hemocytes. Development genes and evolution 8 12690451
2020 OCIAD1 is a host mitochondrial substrate of the hepatitis C virus NS3-4A protease. PloS one 7 32697788
2016 Generation of a heterozygous knockout human embryonic stem cell line for the OCIAD1 locus using CRISPR/CAS9 mediated targeting: BJNhem20-OCIAD1-CRISPR-39. Stem cell research 5 27345991
2019 Proteomics of Asrij Perturbation in Drosophila Lymph Glands for Identification of New Regulators of Hematopoiesis. Molecular & cellular proteomics : MCP 4 30923041
2019 OCIAD1 promoted pancreatic ductal adenocarcinoma migration by regulating ATM. Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] 3 31221523
2016 Generation of a heterozygous knockout human embryonic stem cell line for the OCIAD1 locus using CRISPR/CAS9 mediated targeting: BJNhem20-OCIAD1-CRISPR-20. Stem cell research 3 27345969
2021 Expression, Purification and Crystallization of Asrij, A Novel Scaffold Transmembrane Protein. The Journal of membrane biology 2 33433647
2025 Integrated proteome and lipidome analyses place OCIAD1 at the mitochondria-peroxisome intersection balancing lipid metabolism. Journal of cell science 1 40211913
2016 Generation of transgenic human embryonic stem cell line BJNhem20-OCIAD1-OV. Stem cell research 1 27345812
2025 Asrij/OCIAD1 expression delineates functionally distinct hematopoietic stem cells in the bone marrow. Experimental hematology 0 41043641
2016 Generation of OCIAD1 inducible overexpression human embryonic stem cell line: BJNhem20-OCIAD1-Tet-On. Stem cell research 0 27345976
2016 Generation of a transgenic human embryonic stem cell line ectopically expressing the endosomal protein Asrij that regulates pluripotency in mouse embryonic stem cells: BJNhem20-Asrij. Stem cell research 0 27345997

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