Affinage

CEND1

Cell cycle exit and neuronal differentiation protein 1 · UniProt Q8N111

Length
149 aa
Mass
15.0 kDa
Annotated
2026-06-09
38 papers in source corpus 19 papers cited in narrative 19 extracted findings
Cross-family judge faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CEND1 (BM88) is a neuron-specific integral membrane protein that couples cell cycle exit to neuronal differentiation during development (PMID:7616611, PMID:16893893, PMID:17971443). It acts as a cell-cycle brake: overexpression arrests cells at the G0/G1 restriction point through elevated p53, accumulation of hypophosphorylated pRb, and downregulation/cytoplasmic relocalization of cyclin D1, while its knockdown accelerates proliferation and impairs differentiation (PMID:16893893). CEND1 operates within the proneural program, lying downstream of Mash1 and being sufficient to drive neural precursors out of the cycle, suppress Notch1, and commit to a neuronal fate (PMID:17971443); it is similarly required for Neurogenin2-driven reprogramming of astrocytes (PMID:26321141). Its expression is controlled at multiple levels—by Sp1 sites and Neurogenin1 at its promoter (PMID:16181419), downstream of HDAC activity (PMID:18258204), by LSD1-dependent H3K4me2 repression (PMID:38226173), and by m6A methylation that governs its mRNA export and translation (PMID:34142067)—and at the protein level through CDK5/p25-mediated phosphorylation and degradation (PMID:35732922) and stabilization by Ahi1 (PMID:23658157). CEND1 modulates cyclin D1 stability within a tripartite complex with RanBPM and Dyrk1B (PMID:24312406) and dampens IP3-dependent calcium mobilization (PMID:19061903). At presynaptic mitochondria, CEND1 homodimerizes through GXXXA transmembrane motifs and interacts with the ATP synthase subunit Atp5f1b to support ATP synthesis, with its loss driving Drp1-mediated fission and mitochondrial dysfunction (PMID:35732922, PMID:41469760). Through these activities CEND1 functions are relevant to cerebellar development and motor coordination (PMID:20153830), cardiac development and heart regeneration where LSD1-dependent CEND1 suppression is required (PMID:38226173, PMID:40521201), glioma growth suppression via AMPK activation and inhibition of oxidative phosphorylation (PMID:41239369), and Alzheimer's-related cognitive deficits, where hippocampal CEND1 overexpression rescues 5xFAD mice (PMID:35732922).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 1991 High

    Established the basic biochemical nature of CEND1 before any function was known: whether it was a surface or intrinsic membrane protein and how it was anchored.

    Evidence Immunopurification, hydrophobic chromatography, Triton X-114 phase separation, and phospholipase C digestion of neuronal protein

    PMID:1704420

    Open questions at the time
    • No topology of the extramembranous domain defined
    • No functional role established
  2. 1995 High

    Defined CEND1 as a ~22 kDa neuron-specific disulfide-linked dimeric membrane protein associated with mitochondria, ER, vesicles, and synaptic densities, anchoring later mitochondrial work.

    Evidence Western blot, immunopurification, electron microscopy, and glycanase/protease digestion in neurons

    PMID:7616611

    Open questions at the time
    • Functional significance of multi-organelle localization unresolved
    • No molecular partners identified
  3. 1995 Medium

    First showed CEND1 has a cellular function by linking its overexpression to neuronal differentiation and slowed division.

    Evidence Stable transfection of Neuro-2a cells with morphological, neurofilament, and growth readouts

    PMID:7775480

    Open questions at the time
    • Mechanism connecting CEND1 to differentiation not defined
    • Single cell line
  4. 2005 Medium

    Resolved how CEND1 transcription is restricted to neurons, identifying the cis-elements and a transactivator.

    Evidence Promoter deletion, Sp1-site mutagenesis, and reporter assays in primary neurons and glia

    PMID:16181419

    Open questions at the time
    • Endogenous role of Neurogenin1 at the locus not tested in vivo
    • Single lab
  5. 2006 High

    Defined the molecular mechanism of CEND1's anti-proliferative effect via the p53/pRb/cyclin D1 axis using reciprocal gain- and loss-of-function.

    Evidence Stable transfection, siRNA, BrdU/FACS, and Western/IF for cell-cycle regulators in Neuro-2a

    PMID:16893893

    Open questions at the time
    • Direct molecular target of CEND1 upstream of p53/cyclin D1 unknown
    • Cell-line based
  6. 2007 High

    Placed CEND1 in the proneural pathway in vivo (Mash1→CEND1→Notch1 suppression), establishing it as a node coupling cell-cycle exit to fate commitment.

    Evidence Gain/loss-of-function in chick spinal cord with neuronal-marker and Notch1 immunohistochemistry

    PMID:17971443

    Open questions at the time
    • How CEND1 suppresses Notch1 mechanistically unknown
    • Direct vs indirect epistasis not resolved
  7. 2008 Medium

    Identified an additional CEND1 activity, dampening IP3-dependent calcium mobilization and ceramide-induced apoptosis.

    Evidence Calcium imaging with P2Y pharmacology and ceramide apoptosis assays in Neuro-2a and HeLa

    PMID:19061903

    Open questions at the time
    • Molecular link between CEND1 and IP3 stores undefined
    • Single lab
  8. 2008 Medium

    Positioned CEND1 downstream of HDAC activity in the neuronal differentiation program.

    Evidence TSA treatment, RT-PCR, and knockdown rescue in neuronal vs non-neuronal cells

    PMID:18258204

    Open questions at the time
    • Specific HDAC and direct chromatin mechanism not identified
    • Single lab
  9. 2010 High

    Demonstrated CEND1's developmental necessity in vivo through a knockout with cerebellar proliferation, migration, differentiation, and behavioral phenotypes.

    Evidence Cend1 knockout mice with histology, BrdU, immunohistochemistry, and motor tests

    PMID:20153830

    Open questions at the time
    • Cell-autonomous vs non-autonomous contributions not fully separated
    • Molecular cause of altered Patched1/reelin/BDNF unclear
  10. 2013 Medium

    Revealed a protein-level mechanism for CEND1's control of cyclin D1 via a tripartite complex with RanBPM and Dyrk1B.

    Evidence Co-immunoprecipitation, transient co-expression, fractionation, and BrdU in cell culture

    PMID:24312406

    Open questions at the time
    • Stoichiometry and direct binding interfaces not defined
    • Single Co-IP-based study
  11. 2013 Medium

    Showed CEND1 protein stability is regulated by Ahi1, linking it to neurite extension.

    Evidence Mass spectrometry of immunoprecipitates, Ahi1 KO mouse analysis, and overexpression rescue of neurite defects

    PMID:23658157

    Open questions at the time
    • Direct vs indirect CEND1-Ahi1 interaction not resolved
    • Mechanism of stabilization unknown
  12. 2015 Medium

    Extended CEND1's role to direct reprogramming, showing it is required for NEUROG2-driven astrocyte-to-neuron conversion within a feedback loop.

    Evidence Lentiviral overexpression, siRNA, and live-cell imaging of reprogramming

    PMID:26321141

    Open questions at the time
    • Molecular basis of the CEND1-NEUROG2 feedback unknown
    • Single lab
  13. 2019 Medium

    Connected CEND1 function to MAPK signaling using cross-species expression.

    Evidence Transgenic Drosophila expression with neuroblast/cell-cycle markers and anti-pMAPK Western blot

    PMID:31079319

    Open questions at the time
    • Whether MAPK is a direct CEND1 target in mammals untested
    • Heterologous system
  14. 2021 Medium

    Identified m6A methylation of CEND1 mRNA as a post-transcriptional control point governing its export and translation during neurogenesis.

    Evidence m6A-seq, Arhgef2/Mettl14 knockout mice, export assays, and Cend1 overexpression rescue

    PMID:34142067

    Open questions at the time
    • m6A reader mediating CEND1 export not identified
    • Single lab
  15. 2022 High

    Defined CEND1's mitochondrial role at presynaptic mitochondria and its post-translational regulation by CDK5/p25, linking it to Alzheimer's-related cognition.

    Evidence Proteomics, fractionation, KO/OE mice, Drp1 and mitochondrial assays, CDK5/p25 Co-IP and phosphorylation, and 5xFAD rescue

    PMID:35732922

    Open questions at the time
    • How CEND1 restrains Drp1 mechanistically unresolved
    • CDK5 phosphosite mapping incomplete
  16. 2023 High

    Established LSD1-dependent H3K4me2 as the epigenetic mechanism repressing CEND1, with reciprocal genetic epistasis demonstrating CEND1 as the key downstream effector in cardiomyocyte proliferation.

    Evidence Cardiomyocyte Lsd1 KO mice, ChIP for H3K4me2, Lsd1/Cend1 double KO, and iPSC-derived cardiomyocytes

    PMID:38226173

    Open questions at the time
    • Direct recruitment of LSD1 to the Cend1 promoter not detailed
    • Cardiac-specific generality unclear
  17. 2025 High

    Defined the structural basis of CEND1's mitochondrial activity: GXXXA-mediated homodimerization required for ATP-synthase interaction and ATP synthesis enhancement.

    Evidence CEND1 KO mice, Atp5f1b Co-IP, G130P dimerization mutant, ATP/mPTP assays, and Tianeptine stabilization

    PMID:41469760

    Open questions at the time
    • Structure of the CEND1-Atp5f1b interface not solved
    • Single lab
  18. 2025 High

    Extended the LSD1-CEND1 axis to functional heart regeneration, showing CEND1 suppression is required and its deletion rescues Lsd1-loss defects.

    Evidence Cardiomyocyte Lsd1 and Cend1 genetic models, injury models, RNA-seq, echocardiography, and immunostaining

    PMID:40521201

    Open questions at the time
    • Mechanistic link from CEND1 to neovascularization/macrophage activation unclear
    • Adult human relevance untested
  19. 2025 Medium

    Showed CEND1 suppresses glioma growth by activating AMPK and inhibiting oxidative phosphorylation, extending its tumor-suppressive metabolic role.

    Evidence CEND1 overexpression in glioma cells, metabolomics, PDH activity and AMPK Western blots, and orthotopic tumor model

    PMID:41239369

    Open questions at the time
    • Direct molecular target driving AMPK activation undefined
    • Single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CEND1's plasma-membrane/ER cell-cycle activities are mechanistically integrated with its mitochondrial ATP-synthase function, and the direct molecular target through which it triggers p53/cyclin D1 and AMPK changes, remain unresolved.
  • No structural model of CEND1 or its dimer-Atp5f1b interface
  • Direct effector linking CEND1 to p53/cyclin D1 unidentified
  • Unifying mechanism across cell-cycle and metabolic roles unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 3 GO:0098772 molecular function regulator activity 3
Localization
GO:0005739 mitochondrion 3 GO:0005886 plasma membrane 2 GO:0005783 endoplasmic reticulum 1 GO:0031410 cytoplasmic vesicle 1
Pathway
R-HSA-1266738 Developmental Biology 4 R-HSA-1640170 Cell Cycle 3 R-HSA-1430728 Metabolism 2
Partners
AHI1ATP5F1BCDK5DYRK1BRANBPM
Complex memberships
CEND1 homodimerCEND1-RanBPM-Dyrk1B complex

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1995 BM88/CEND1 is a neuron-specific integral membrane protein of approximately 22 kDa, composed of two polypeptide chains linked by disulfide bridges, not glycosylated, and associated with mitochondrial limiting membranes, endoplasmic reticulum, small vesicles, and synaptic densities in neurons. Western blot, immunopurification, electron microscopy, Triton X-114 phase separation, N-glycanase digestion, protease digestion Journal of neuroscience research High 7616611
1991 BM88/CEND1 is an integral membrane protein with at least one small extramembranous domain; it cannot be solubilized by phospholipase C, indicating it is not GPI-anchored, and is anchored via a polypeptide transmembrane chain. Immunopurification, hydrophobic chromatography, Triton X-114 phase separation, phospholipase C digestion, protease digestion, gel filtration, SDS-PAGE Journal of neurochemistry High 1704420
1995 Overexpression of BM88/CEND1 in Neuro-2a neuroblastoma cells promotes morphological differentiation (enhanced process outgrowth), slows cell division, and accelerates differentiation in the presence of agents such as sucrose and retinoic acid, including induction of neurofilament protein expression. Stable transfection, morphological analysis, neurofilament immunostaining, cell growth assays The Journal of biological chemistry Medium 7775480
2006 BM88/CEND1 overexpression in Neuro-2a cells causes cell cycle arrest at the G0/G1 restriction point via increased p53 levels, accumulation of hypophosphorylated retinoblastoma protein (pRb), and decreased/cytoplasmic relocalization of cyclin D1; conversely, BM88 siRNA knockdown accelerates proliferation and impairs retinoic acid-induced differentiation. Stable transfection, BrdU incorporation, FACS, Western blot, immunofluorescence for cyclin D1 localization, RNA interference The Journal of biological chemistry High 16893893
2007 BM88/CEND1 is downstream of the proneural gene Mash1 (forced Mash1 expression induces endogenous BM88), and BM88 is sufficient to drive spinal cord neural precursors to exit the cell cycle, down-regulate Notch1, and commit to neuronal differentiation; BM88 siRNA knockdown enhances cell cycle progression and impairs neuronal differentiation. Gain-of-function overexpression in chick spinal cord, siRNA knockdown, immunohistochemistry for neuronal markers and Notch1, BrdU incorporation Proceedings of the National Academy of Sciences of the United States of America High 17971443
2008 BM88/CEND1 overexpression diminishes P2Y receptor-induced intracellular calcium mobilization from IP3-sensitive stores in both Neuro-2a and HeLa cells, and reduces C2-ceramide-induced calcium release and apoptosis; BM88 knockdown facilitates proliferation under both stimulating and non-stimulating conditions. Calcium imaging, stable transfection, siRNA knockdown, P2Y receptor pharmacology, C2-ceramide apoptosis assay Neuropharmacology Medium 19061903
2008 Trichostatin A (HDAC inhibitor) specifically induces Cend1 transcription in neuronal (Neuro-2a) but not non-neuronal cells, and Cend1 knockdown alleviates both the anti-proliferative and differentiation effects of TSA, placing Cend1 downstream of HDAC activity in the neuronal differentiation program. TSA treatment, RT-PCR, siRNA knockdown, cell proliferation and differentiation assays FEBS letters Medium 18258204
2010 Cend1 knockout mice show increased proliferation of cerebellar granule cell precursors, delayed radial granule cell migration, and impaired Purkinje cell differentiation, with altered expression of Patched1, cyclin D1, reelin, and BDNF, leading to motor coordination deficits. Cend1 knockout mouse generation, histology, BrdU incorporation, immunohistochemistry, motor behavior tests Molecular and cellular neurosciences High 20153830
2013 BM88/Cend1 physically interacts with RanBPM (Ran-binding protein M); this tripartite complex with Dyrk1B affects cyclin D1 levels and cell cycle progression: RanBPM reverses BM88/Cend1-dependent or Dyrk1B-dependent cyclin D1 downregulation by stabilizing cyclin D1 in the nucleus, but co-expression of Cend1 reverts RanBPM-dependent Dyrk1B cytosolic retention and degradation, resulting in cyclin D1 destabilization. Co-immunoprecipitation, transient co-expression, BrdU incorporation, Western blot, subcellular fractionation PloS one Medium 24312406
2013 Full-length Ahi1 (but not N-terminal fragments) binds Hap1A in a phosphorylation-regulated manner, and also binds Cend1 as identified by mass spectrometry of cytosolic Ahi1 immunoprecipitates; Ahi1 loss reduces Cend1 protein levels in hypothalamus of Ahi1 KO mice, and overexpressed Ahi1 stabilizes Cend1 in cultured cells; Cend1 overexpression rescues neurite extension defects in hypothalamic neurons from Ahi1 KO mice. Mass spectrometry of immunoprecipitates, Western blot, overexpression rescue, Ahi1 KO mouse analysis, neurite extension assay The Journal of neuroscience Medium 23658157
2015 CEND1 is a key mediator of NEUROG2-driven neuronal reprogramming of mouse cortical astrocytes; knockdown of endogenous CEND1 impairs NEUROG2-driven neuronal conversion, and a reciprocal feedback loop exists between CEND1 and NEUROG2 at mRNA and protein levels. Lentiviral overexpression, siRNA knockdown, live-cell imaging, mRNA and protein expression analysis, immunocytochemistry Stem cell reports Medium 26321141
2019 Expression of mammalian BM88/CEND1 in Drosophila reduces neuroblast and ganglion mother cell markers, impairs MP2 precursor formation, causes disorganized cell-cycle marker expression, disrupts eye disc development, and reduces activated MAP kinase (MAPK) levels, indicating functional interference with the MAPK signaling pathway. Transgenic Drosophila expression, immunohistochemistry for neuroblast/GMC markers, cell-cycle markers, anti-pMAP kinase Western blot Neuroscience bulletin Medium 31079319
2005 The BM88/CEND1 promoter contains four functional Sp1-binding sites that are required for activity; simultaneous mutation of all four Sp1 sites abolishes promoter activity. Neurogenin-1 also transactivates the BM88 promoter. An 88 bp minimal promoter fragment is sufficient for neuron-specific (but not glial) transcriptional activity. Promoter deletion analysis, site-directed mutagenesis of Sp1 sites, transactivation/reporter assays in primary neurons and glia Journal of neurochemistry Medium 16181419
2021 Arhgef2 deficiency reduces Mettl14 expression and total m6A levels, decreasing m6A methylation of Cend1 mRNA; reduced m6A on Cend1 mRNA inhibits its nuclear export and translation, resulting in decreased CEND1 protein and impaired neuronal differentiation; overexpression of Cend1 rescues the neurogenesis defects of Arhgef2 KO mice. m6A sequencing, Arhgef2 knockout mice, mRNA nuclear export assays, Western blot, overexpression rescue iScience Medium 34142067
2022 CEND1 localizes to presynaptic mitochondria in neurons. CEND1 depletion increases mitochondrial fission via upregulation of Drp1, causing abnormal mitochondrial function and cognitive impairment. CDK5/p25 interacts with and phosphorylates CEND1, promoting its degradation. Overexpression of CEND1 in the hippocampus of 5xFAD mice rescues cognitive deficits. Proteomic analysis, subcellular fractionation/localization, Cend1 knockout/overexpression in mice, mitochondrial morphology assays, co-immunoprecipitation of CDK5/p25 with CEND1, phosphorylation assay, behavioral tests Cell death and differentiation High 35732922
2023 LSD1 (a histone demethylase) epigenetically represses Cend1 transcription by maintaining low levels of H3K4me2 at the Cend1 promoter; loss of LSD1 in cardiomyocytes elevates H3K4me2 at the Cend1 promoter and increases Cend1 transcription, causing cell cycle arrest and heart growth defects; Cend1 knockdown rescues the proliferation defect caused by LSD1 inhibition, and genetic deletion of Cend1 rescues embryonic lethality of Lsd1 null mice. Cardiomyocyte-specific Lsd1 KO mice, RNA-seq, ChIP for H3K4me2, siRNA knockdown, Cend1/Lsd1 double KO mice, iPSC-derived cardiomyocytes iScience High 38226173
2025 CEND1 forms homodimers via conserved GXXXA motifs in its transmembrane domain, and this dimerization is required to enhance ATP synthesis; disruption of dimerization (G130P mutation) destabilizes CEND1 and abolishes its ATP-enhancing effects. CEND1 physically interacts with Atp5f1b (mitochondrial ATP synthase subunit beta). The small molecule Tianeptine stabilizes CEND1 dimers and elevates ATP levels in a CEND1-dependent manner. CEND1 KO mice, co-immunoprecipitation/interaction assay for Atp5f1b, mutagenesis (G130P), ATP synthesis assays, mitochondrial membrane potential and mPTP assays, Tianeptine treatment with KO validation Communications biology High 41469760
2025 LSD1-dependent suppression of CEND1 is required for neonatal and adult heart regeneration; cardiomyocyte-specific Cend1 overexpression inhibits heart regeneration, while Cend1 nullizygous mice show enhanced cardiomyocyte proliferation, neovascularization, and macrophage activation; the cardiac regeneration defect from Lsd1 loss is rescued by Cend1 deletion. Cardiomyocyte-specific Lsd1 KO/OE mice, Cend1 null mice, cardiomyocyte-specific Cend1 OE mice, apical resection and LAD ligation injury models, RNA-seq, echocardiography, immunostaining Theranostics High 40521201
2025 CEND1 overexpression in glioma cells activates AMPK signaling, inhibits PDH activity and mitochondrial oxidative phosphorylation (reducing ATP levels), and induces cell cycle arrest and neuron-like morphology; CEND1 overexpression suppresses tumor growth in intracranial orthotopic mouse models. CEND1 overexpression in glioma cells, metabolomics, PDH activity assay, AMPK pathway Western blot, orthotopic tumor model Cell & bioscience Medium 41239369

Source papers

Stage 0 corpus · 38 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2007 BM88/CEND1 coordinates cell cycle exit and differentiation of neuronal precursors. Proceedings of the National Academy of Sciences of the United States of America 61 17971443
2006 BM88 is a dual function molecule inducing cell cycle exit and neuronal differentiation of neuroblastoma cells via cyclin D1 down-regulation and retinoblastoma protein hypophosphorylation. The Journal of biological chemistry 51 16893893
2022 CEND1 deficiency induces mitochondrial dysfunction and cognitive impairment in Alzheimer's disease. Cell death and differentiation 50 35732922
2019 Cend1, a Story with Many Tales: From Regulation of Cell Cycle Progression/Exit of Neural Stem Cells to Brain Structure and Function. Stem cells international 35 31191667
2010 Transplantation of embryonic neural stem/precursor cells overexpressing BM88/Cend1 enhances the generation of neuronal cells in the injured mouse cortex. Stem cells (Dayton, Ohio) 34 19911428
2004 BM88 is an early marker of proliferating precursor cells that will differentiate into the neuronal lineage. The European journal of neuroscience 33 15548196
2015 CEND1 and NEUROGENIN2 Reprogram Mouse Astrocytes and Embryonic Fibroblasts to Induced Neural Precursors and Differentiated Neurons. Stem cell reports 30 26321141
1995 Characterization and localization of the BM88 antigen in the developing and adult rat brain. Journal of neuroscience research 30 7616611
1995 The BM88 antigen, a novel neuron-specific molecule, enhances the differentiation of mouse neuroblastoma cells. The Journal of biological chemistry 28 7775480
2013 Loss of Ahi1 affects early development by impairing BM88/Cend1-mediated neuronal differentiation. The Journal of neuroscience : the official journal of the Society for Neuroscience 26 23658157
2010 Impaired cerebellar development and deficits in motor coordination in mice lacking the neuronal protein BM88/Cend1. Molecular and cellular neurosciences 24 20153830
1991 Purification and characterization of neuron-specific surface antigen defined by monoclonal antibody BM88. Journal of neurochemistry 22 1704420
2013 Functional Interactions between BM88/Cend1, Ran-binding protein M and Dyrk1B kinase affect cyclin D1 levels and cell cycle progression/exit in mouse neuroblastoma cells. PloS one 21 24312406
2008 BM88/Cend1 is involved in histone deacetylase inhibition-mediated growth arrest and differentiation of neuroblastoma cells. FEBS letters 20 18258204
2005 Characterization of the BM88 promoter and identification of an 88 bp fragment sufficient to drive neurone-specific expression. Journal of neurochemistry 17 16181419
2001 Cloning, expression and localization of human BM88 shows that it maps to chromosome 11p15.5, a region implicated in Beckwith-Wiedemann syndrome and tumorigenesis. The Biochemical journal 16 11311134
2006 Expression pattern of BM88 in the developing nervous system of the chick and mouse embryo. Gene expression patterns : GEP 15 16949349
2019 Increased Anxiety-Related Behavior, Impaired Cognitive Function and Cellular Alterations in the Brain of Cend1-deficient Mice. Frontiers in cellular neuroscience 14 30760981
2009 C38, equivalent to BM88, is developmentally expressed in maturing retinal neurons and enhances neuronal maturation. Journal of neurochemistry 10 20002527
2014 Downregulation of BM88 after optic nerve injury. Investigative ophthalmology & visual science 9 24526440
1998 Overexpression of the neuron-specific molecule BM88 in mouse neuroblastoma cells: altered responsiveness to growth factors. Journal of neuroscience research 9 9452316
2023 Reperfusion-induced injury and the effects of the dithioacetate type hydrogen sulfide donor ibuprofen derivative, BM-88, in isolated rat hearts. European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences 8 37076051
2022 Cend1 and Neurog2 efficiently reprogram human cortical astrocytes to neural precursor cells and induced-neurons. The International journal of developmental biology 8 34549796
2021 Arhgef2 regulates neural differentiation in the cerebral cortex through mRNA m6A-methylation of Npdc1 and Cend1. iScience 8 34142067
2008 BM88/Cend1 regulates stimuli-induced intracellular calcium mobilization. Neuropharmacology 8 19061903
2000 Early expression of the BM88 antigen during neuronal differentiation of P19 embryonal carcinoma cells. International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience 8 10715587
2023 Epigenetic repression of Cend1 by lysine-specific demethylase 1 is essential for murine heart development. iScience 5 38226173
2022 CEND1 and miR885 methylation changes associated with successful cognitive aging in community-dwelling older adults. Experimental gerontology 5 35045349
2020 Interaction of CEND1 gene and life events in susceptibility to depressive symptoms in Chinese Han college students. Journal of affective disorders 5 33027701
2019 Expression of Mammalian BM88/CEND1 in Drosophila Affects Nervous System Development by Interfering with Precursor Cell Formation. Neuroscience bulletin 5 31079319
2001 Cellular localization of BM88 mRNA in paraffin-embedded rat brain sections by combined immunohistochemistry and non-radioactive in situ hybridization. Brain research. Brain research protocols 4 11356378
2023 Down-Regulation of CEND1 Expression Contributes to The Progression and Temozolomide Resistance of Glioma. Cell journal 3 37210647
2025 Regulation of heart regeneration by LSD1 through suppressing CEND1. Theranostics 1 40521201
2022 Research on the function of the Cend1 regulatory mechanism on p75NTR signaling in spinal cord injury. Neuropeptides 1 35728483
2026 Astragalus polysaccharide protects against neuron degeneration and mitochondrial dysfunction in Parkinson's disease by upregulating CEND1. Histology and histopathology 0 41537354
2025 Neuronal differentiation regulator CEND1 coordinately suppresses tumor growth and energetics via AMPK signaling in brain glioma. Cell & bioscience 0 41239369
2025 [68Ga]Ga-DOTA-CEND1: A Novel PET Cyclic Peptide Tracer for Noninvasive Imaging of Neuropilin-1 Expression in Pan-Tumors. Molecular pharmaceutics 0 41324177
2025 Targeting Cend1-Atp5f1b interaction rescues mitochondrial dysfunction and ameliorates ischemic brain injury. Communications biology 0 41469760

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