Affinage

CEP57

Centrosomal protein of 57 kDa · UniProt Q86XR8

Length
500 aa
Mass
57.1 kDa
Annotated
2026-06-09
25 papers in source corpus 18 papers cited in narrative 18 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CEP57 (Translokin) is a centrosomal coiled-coil scaffold that organizes the pericentriolar material (PCM) and stabilizes microtubules to safeguard centriole engagement and accurate chromosome segregation (PMID:21552266, PMID:30804344, PMID:30035751). It is built around two functional regions: an N-terminal coiled-coil domain that targets the centrosome internal to gamma-tubulin and mediates self-multimerization, and a C-terminal microtubule-binding domain that directly nucleates and bundles microtubules into nocodazole-resistant cables (PMID:18294141). Self-assembly is driven by liquid-liquid phase separation through its NTD, CTD, and a polybasic LMN motif, and the resulting condensates catalyze microtubule nucleation by concentrating tubulin, an activity restricted by Cep63 (PMID:38857398). At the proximal centriole end CEP57 forms a ring-like torus with Cep63 and Cep152, with its initial recruitment dependent on NuSAP (PMID:23333316, PMID:41616107), and its centrosomal localization additionally requires NEDD1 (PMID:22508265). CEP57 directly binds the PACT domain of pericentrin to bridge the centriole core and PCM, and loss of this organization causes premature centriole disengagement, ectopic MTOC activity, centrosome amplification, and chromosome mis-segregation (PMID:30804344, PMID:30035751); CEP57 and its paralog Cep57L1 act cooperatively to maintain interphase centriole engagement, restraining Plk1-dependent disengaged daughter conversion (PMID:33492359). CEP57 also localizes to kinetochores, where it binds Mis12 and Mad1 to support Mad1-Mad2 loading and spindle assembly checkpoint signaling [#1_kt, #10], and to the central spindle and midbody, where it recruits Tektin 1 and is required for cytokinesis (PMID:23569207). Independently, CEP57 functions as an intracellular trafficking factor that translocates the 18K form of FGF-2 to the nucleus through KIF3A/KIF3B kinesin complexes, links FGF-2 signaling to centriole duplication, and sequesters cyclin D1 in the juxtanuclear region to restrain Cdk4-dependent pRB phosphorylation and S-phase entry (PMID:12717444, PMID:19804566, PMID:21306487, PMID:23243019). Biallelic loss-of-function mutations in CEP57 cause mosaic variegated aneuploidy syndrome (PMID:21552266).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2003 High

    Established the first molecular function of CEP57 as an FGF-2-specific intracellular carrier, explaining how a growth factor reaches the nucleus to exert mitogenic activity.

    Evidence Co-IP, RNAi knockdown, FGF-1/FGF-2 chimera mapping and proliferation assays in cultured cells

    PMID:12717444

    Open questions at the time
    • Did not connect FGF-2 trafficking to centrosomal function
    • Mechanism of microtubule-based transport not resolved
  2. 2007 High

    Showed CEP57 acts at kinetochores and centrosomes to maintain microtubule attachment and spindle bipolarity, broadening its role from trafficking to spindle integrity.

    Evidence Immunodepletion from Xenopus egg extracts with in vitro kinetochore-microtubule binding reconstitution and Co-IP

    PMID:17803911

    Open questions at the time
    • Whether anchorage role is conserved in human cells not established here
    • Direct microtubule-binding domain not yet defined
  3. 2008 High

    Defined the domain architecture, mapping centrosome targeting/multimerization to the N-terminus and direct microtubule nucleation/bundling to the C-terminus.

    Evidence Domain truncation/overexpression with in vitro microtubule nucleation and bundling assays

    PMID:18294141

    Open questions at the time
    • How the two domains are coordinated in vivo unclear
    • Structural basis of microtubule binding not resolved
  4. 2009 Medium

    Resolved how CEP57 partitions FGF-2 between secretion and nuclear import, identifying the kinesin and adaptor partners that build mutually exclusive trafficking complexes.

    Evidence Co-IP and yeast two-hybrid for SNX6, RanBPM, KIF3A/KIF3B plus trafficking assays

    PMID:19804566

    Open questions at the time
    • Single lab
    • Stoichiometry and regulation of the two complexes not determined
  5. 2011 Medium

    Linked CEP57 to cell-cycle control by showing it sequesters cyclin D1 to keep cells quiescent, connecting its scaffolding role to S-phase entry.

    Evidence Co-IP, siRNA/overexpression with pRB phosphorylation and flow cytometry readouts

    PMID:21306487

    Open questions at the time
    • Single lab
    • Relationship between cyclin D1 sequestration and centrosomal functions unclear
  6. 2011 Medium

    Established CEP57 as a disease gene, demonstrating biallelic loss-of-function causes mosaic variegated aneuploidy and is essential for chromosome number maintenance.

    Evidence Exome sequencing of patients with functional analysis of patient cells

    PMID:21552266

    Open questions at the time
    • Cellular mechanism linking mutations to aneuploidy not yet mechanistically defined
  7. 2012 Medium

    Defined CEP57 as a PCM component requiring NEDD1 for centrosomal localization and showed its depletion fragments the PCM and disrupts spindle assembly.

    Evidence Co-IP (CEP57-NEDD1), siRNA knockdown, immunofluorescence and spindle assays

    PMID:22508265

    Open questions at the time
    • Direction of CEP57-NEDD1 dependency only partially resolved
    • Single lab
  8. 2012 Medium

    Connected FGF-2 trafficking to centriole biology, showing CEP57 promotes daughter centriole stability via tubulin acetylation and links FGF-2 signaling to centriole duplication.

    Evidence RNAi screen, siRNA/overexpression with centriole counting and tubulin acetylation assays

    PMID:23243019

    Open questions at the time
    • Mechanism by which CEP57 modulates tubulin acetylation unknown
    • Single lab
  9. 2013 Medium

    Extended CEP57 function to cytokinesis, showing it organizes the central spindle/midbody and recruits Tektin 1 for successful division.

    Evidence siRNA knockdown, immunofluorescence, live imaging and pull-down for CEP57-Tektin 1

    PMID:23569207

    Open questions at the time
    • Single lab
    • How midbody role integrates with centriole engagement role unclear
  10. 2013 High

    Placed CEP57 structurally within a defined ring-like torus with Cep63 and Cep152 at the proximal centriole end.

    Evidence Selective chemical crosslinking with superresolution STED microscopy

    PMID:23333316

    Open questions at the time
    • Assembly order of the torus not yet established
    • Functional consequence of torus geometry not tested here
  11. 2016 High

    Defined a kinetochore checkpoint role in human cells, showing CEP57 binds Mis12 and Mad1 to control Mad1-Mad2 loading and SAC signaling.

    Evidence Co-IP, siRNA knockdown, kinetochore Mad1-Mad2 imaging, SAC and segregation assays

    PMID:26743940

    Open questions at the time
    • How microtubule-binding triggers Mad1 removal mechanistically unclear
    • Single lab
  12. 2018 High

    Demonstrated in vivo that CEP57 is required for G2 centrosome maturation and acts as a haploinsufficient tumor suppressor, integrating its centrosomal and FGF-2 roles in an animal model.

    Evidence Mouse knock-in model plus patient fibroblasts with centrosome, chromosome and tumor incidence readouts

    PMID:30035751

    Open questions at the time
    • Molecular trigger of maturation failure not fully resolved
  13. 2019 High

    Identified the direct CEP57-pericentrin PACT interface as the bridge between centriole core and PCM, explaining premature disengagement and linking pericentrin disease mutations to this interaction.

    Evidence Pull-down mapping to PACT domain, siRNA depletion, MVA/MOPDII patient cells, live imaging

    PMID:30804344

    Open questions at the time
    • How PCM disorganization mechanistically triggers disengagement not fully resolved
  14. 2021 High

    Resolved that CEP57 and paralog Cep57L1 cooperatively enforce interphase centriole engagement, with disengagement driving Plk1-dependent reduplication.

    Evidence siRNA co-depletion epistasis, live imaging and Plk1 inhibitor rescue

    PMID:33492359

    Open questions at the time
    • Division of labor between CEP57 and Cep57L1 not fully defined
  15. 2024 High

    Provided a biophysical mechanism, showing CEP57 phase-separates via NTD/CTD/LMN motifs to catalyze microtubule nucleation by concentrating tubulin, with Cep63 acting as a brake.

    Evidence In vitro LLPS and microtubule nucleation assays, domain mutagenesis, SAXS and in-cell rescue

    PMID:38857398

    Open questions at the time
    • In vivo extent of phase separation not quantified
    • How LLPS is regulated through the cell cycle unknown
  16. 2024 Medium

    Provided atomic detail of the C-terminal microtubule-binding domain as a leucine-zipper scaffold accommodating nucleation and tension.

    Evidence X-ray crystallography of the human CEP57 C-terminal domain

    PMID:38699879

    Open questions at the time
    • Functional validation of identified structural elements not reported
    • Microtubule-bound structure not determined
  17. 2026 Medium

    Placed NuSAP upstream of CEP57, identifying it as a direct interactor required for initial torus complex recruitment to procentrioles.

    Evidence TurboID proximity proteomics, Co-IP/biochemistry, super-resolution microscopy and siRNA depletion

    PMID:41616107

    Open questions at the time
    • Single lab
    • How NuSAP triggers torus nucleation mechanistically unclear
  18. 2025 Low

    Suggested additional nuclear and cohesin-related roles for Cep57 in early embryos, interacting with Rad21 and Geminin to influence genome stability and G1 arrest.

    Evidence Zebrafish loss-of-function, Co-IP, immunofluorescence, quantitative proteomics and cell cycle analysis (preprint)

    PMID:bio_10.1101_2025.04.10.648303

    Open questions at the time
    • Preprint, not peer-reviewed
    • Co-IP interactions lack reciprocal/structural validation
    • Conservation in human cells untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CEP57's distinct activities — torus scaffolding, microtubule nucleation, kinetochore checkpoint control, FGF-2 trafficking, and cyclin D1 sequestration — are temporally coordinated and regulated across the cell cycle remains unresolved.
  • No unified regulatory mechanism links the trafficking and centrosomal functions
  • Post-translational control of CEP57 not characterized
  • Whether FGF-2/cyclin D1 roles operate in the same cells as centriole roles unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008092 cytoskeletal protein binding 4 GO:0060090 molecular adaptor activity 4 GO:0005198 structural molecule activity 3 GO:0140313 molecular sequestering activity 1
Localization
GO:0005815 microtubule organizing center 4 GO:0005856 cytoskeleton 3 GO:0005694 chromosome 2 GO:0005634 nucleus 1
Pathway
R-HSA-1640170 Cell Cycle 4 R-HSA-1852241 Organelle biogenesis and maintenance 4 R-HSA-9609507 Protein localization 2
Partners
CEP152CEP63KIF3AMAD1MIS12NEDD1NUSAP1PCNT
Complex memberships
CEP57-CEP63-CEP152 toruskinetochore (KMN network, via Mis12)

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 Translokin (CEP57) interacts specifically with the 18K form of FGF-2 (but not FGF-1), colocalizes with the microtubular network, and is required for intracellular translocation of FGF-2 to the nucleus; RNAi knockdown of Translokin reduces FGF-2 translocation without affecting FGF-1 trafficking, and this nuclear translocation is essential for FGF-2 mitogenic activity. Co-immunoprecipitation, RNAi knockdown, FGF-1/FGF-2 chimera mapping, nuclear localization signal rescue, cell proliferation assay Nature cell biology High 12717444
2007 Xenopus Cep57 (xCep57) localizes to kinetochores and interacts with kinetochore proteins Zwint, Mis12, and CLIP-170, as well as gamma-tubulin. Immunodepletion of xCep57 from egg extracts produces weakened bipolar spindles, loss of tension between sister kinetochores, spindle microtubules sensitive to nocodazole, and defective kinetochore-microtubule binding in vitro. At centrosomes, xCep57 is required for maintaining (but not initiating) microtubule anchorage. Immunodepletion from Xenopus egg extracts, in vitro kinetochore-microtubule binding assay, co-immunoprecipitation, spindle assembly assay Cell High 17803911
2008 Cep57 has two functional domains: an N-terminal coiled-coil domain that localizes to the centrosome (internal to gamma-tubulin) and mediates multimerization with other Cep57 molecules, and a C-terminal coiled-coil domain that directly binds microtubules, nucleates and bundles microtubules in vitro, and generates nocodazole-resistant microtubule cables in vivo when overexpressed. Domain truncation/overexpression, in vitro microtubule nucleation/bundling assay, nocodazole resistance assay, immunofluorescence The Biochemical journal High 18294141
2009 Translokin/CEP57 interacts with sorting nexin 6, Ran-binding protein M, and kinesins KIF3A and KIF3B; through these interactions it participates in two exclusive complexes that direct bidirectional trafficking of FGF2, controlling the balance between unconventional secretion and nuclear translocation of FGF2. Co-immunoprecipitation, yeast two-hybrid, functional trafficking assays Traffic (Copenhagen, Denmark) Medium 19804566
2011 Translokin/CEP57 interacts with cyclin D1 (binding to regions also involved in Cdk4 binding), retains a fraction of cyclin D1 in the juxtanuclear region, and prevents its nuclear accumulation in quiescent cells. Knockdown of CEP57 leads to undue nuclear cyclin D1 accumulation and increased Cdk4-dependent pRB phosphorylation; overexpression of CEP57 blocks nuclear cyclin D1 accumulation, inhibits Cdk4-dependent pRB phosphorylation, and impairs S-phase entry. Co-immunoprecipitation, siRNA knockdown, overexpression, immunofluorescence localization, pRB phosphorylation assay, flow cytometry Traffic (Copenhagen, Denmark) Medium 21306487
2011 Biallelic loss-of-function mutations in CEP57, a centrosomal protein involved in nucleating and stabilizing microtubules, cause constitutional mosaic aneuploidies (mosaic variegated aneuploidy syndrome), establishing CEP57 function as essential for correct chromosome number maintenance during cell division. Exome sequencing, identification of loss-of-function variants in patients, cell biology in patient cells Nature genetics Medium 21552266
2012 Cep57 is a pericentriolar material (PCM) component whose centrosomal localization depends on interaction with NEDD1. Depletion of Cep57 causes PCM fragmentation, multipolar spindles, unaligned chromosomes, decreased centrosomal microtubule assembly activity, and reduced spindle length and microtubule density; Cep57 also binds spindle microtubules and is required for proper localization of spindle pole focusing proteins. Co-immunoprecipitation (Cep57–NEDD1), siRNA knockdown, immunofluorescence, spindle assembly assays Cell research Medium 22508265
2012 CEP57 is required for FGF-2-induced centriole overduplication and normal centriole duplication; CEP57 overexpression stimulates centriole overduplication; CEP57 functions by modulating tubulin acetylation to promote daughter centriole stability; CEP57 is an intracellular FGF-2-binding and trafficking factor that links FGF-2 signaling to centrosome duplication. RNAi screen, siRNA knockdown, overexpression, immunofluorescence for centriole number, tubulin acetylation assay Cancer research Medium 23243019
2013 Cep57, Cep63, and Cep152 form a ring-like complex localizing around the proximal end of centrioles, as determined by selective chemical crosslinking combined with superresolution microscopy. Selective chemical crosslinking, superresolution STED microscopy Current biology : CB High 23333316
2013 Cep57 localizes to the central spindle and midbody during cytokinesis and is required for cytokinesis. Depletion of Cep57 disrupts central spindle microtubule assembly and causes abnormal midbody localization of MKLP1, Plk1, and Aurora B, leading to cytokinesis failure and binuclear cell formation. Cep57 directly recruits Tektin 1 to the midbody matrix to regulate microtubule organization. siRNA knockdown, immunofluorescence, co-immunoprecipitation/pull-down for Cep57–Tektin 1 interaction, live imaging The Journal of biological chemistry Medium 23569207
2016 Cep57 localizes to kinetochores in human cells and binds Mis12 (a KMN network component). Cep57 also interacts with Mad1. Depletion of Cep57 decreases kinetochore localization of Mad1-Mad2, reduces spindle assembly checkpoint (SAC) signaling, and increases chromosome segregation errors. The microtubule-binding activity of Cep57 is involved in the timely removal of Mad1 from kinetochores upon microtubule attachment. Co-immunoprecipitation, siRNA knockdown, immunofluorescence for kinetochore Mad1-Mad2 localization, SAC signaling assay, chromosome segregation analysis Nature communications High 26743940
2019 Cep57 is required for PCM organization to regulate centriole engagement; depletion of Cep57 causes PCM disorganization and precocious centriole disengagement during mitosis, leading to ectopic MTOC activity of disengaged daughter centrioles and chromosome mis-segregation. Cep57 directly binds the PACT domain of pericentrin, providing a critical interface between the centriole core and PCM. Microcephaly osteodysplastic primordial dwarfism (MOPDII)-associated pericentrin mutations impair the Cep57–pericentrin interaction and cause PCM disorganization. siRNA depletion, pull-down assay (Cep57–pericentrin PACT domain), patient-derived cells (MVA and MOPDII), immunofluorescence, live imaging Nature communications High 30804344
2018 Cep57 mutant (truncating frameshift) mouse embryonic fibroblasts and patient-derived fibroblasts fail to undergo centrosome maturation in G2 phase, causing premature centriole disjunction, centrosome amplification, aberrant spindle formation, and high chromosome missegregation rates. In vivo, Cep57 is required for Fgf2-mediated bone formation, and Cep57 haploinsufficiency predisposes to cancer (tumor suppressor role). Mouse knockout/knock-in model, patient-derived fibroblasts, immunofluorescence for centrosome maturation, chromosome analysis, tumor incidence measurement The Journal of clinical investigation High 30035751
2021 Cep57 and its paralog Cep57L1 cooperatively maintain centriole engagement during interphase. Co-depletion induces precocious centriole disengagement in interphase; the disengaged daughter centrioles convert into centrosomes in a Plk1-dependent manner, leading to centriole reduplication, increased centriole number, and chromosome segregation errors. siRNA co-depletion, immunofluorescence, live imaging, Plk1 inhibitor rescue experiment The Journal of cell biology High 33492359
2024 Cep57 undergoes liquid-liquid phase separation (LLPS) driven by three critical domains (NTD, CTD, and polybasic LMN motif). In vitro Cep57 condensates catalyze microtubule nucleation via LMN motif-mediated tubulin concentration. In cells, the LMN motif is required for centrosomal microtubule aster formation. Cep63 restricts Cep57 assembly, expansion, and microtubule polymerization activity. Overexpression of competitive multivalent-interaction constructs (including an MVA mutation) leads to excessive centrosome duplication. Self-assembly mutants of Cep57 fail to rescue centriole disengagement and PCM disorganization in Cep57-depleted cells. In vitro LLPS assay, in vitro microtubule nucleation assay, domain mutagenesis, overexpression, rescue experiments in Cep57-depleted cells, SAXS (small-angle X-ray scattering) Proceedings of the National Academy of Sciences of the United States of America High 38857398
2024 Crystal structure of the human Cep57 C-terminal microtubule-binding domain reveals a leucine zipper with an adjacent possible microtubule-binding region, forming a stabilizing scaffold proposed to accommodate microtubule nucleation and tension. Conserved structural features are maintained across evolution. X-ray crystallography Proteins Medium 38699879
2026 NuSAP localizes to centrioles, and its depletion disrupts centriole tubulin architecture and premature centriole disengagement, as well as disrupting the spatial organization of the CEP57-CEP63-CEP152 torus assembly. CEP57 is identified as a direct interactor of NuSAP by TurboID-based proteomics and biochemical assays. NuSAP is essential for the initial recruitment of the CEP57-CEP63-CEP152 complex to the proximal end of procentrioles, placing NuSAP upstream of CEP57 in torus complex assembly. TurboID-based proximity proteomics, co-immunoprecipitation/biochemical assays, super-resolution microscopy, siRNA depletion Advanced science (Weinheim, Baden-Wurttemberg, Germany) Medium 41616107
2025 In early zebrafish embryos, Cep57 localizes to both the nucleus and centrosomes. Cep57 interacts with Rad21 (cohesin), and its loss causes Rad21 depletion, supernumerary nuclei, and PCM disorganization. Cep57 also interacts with Geminin and induces Rb1-dependent G1 arrest; loss of Cep57 leads to G1/S cell cycle defects, genome instability, and increased apoptosis. Quantitative proteomics in Cep57-deficient embryos reveals induction of DNA damage response and checkpoint pathways. Zebrafish morpholino/loss-of-function, co-immunoprecipitation (Cep57–Rad21, Cep57–Geminin), immunofluorescence localization, quantitative proteomics, cell cycle analysis bioRxivpreprint Low bio_10.1101_2025.04.10.648303

Source papers

Stage 0 corpus · 25 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 Mutations in CEP57 cause mosaic variegated aneuploidy syndrome. Nature genetics 101 21552266
2013 Selective chemical crosslinking reveals a Cep57-Cep63-Cep152 centrosomal complex. Current biology : CB 100 23333316
2003 Translokin is an intracellular mediator of FGF-2 trafficking. Nature cell biology 60 12717444
2019 The Cep57-pericentrin module organizes PCM expansion and centriole engagement. Nature communications 55 30804344
2007 Xenopus Cep57 is a novel kinetochore component involved in microtubule attachment. Cell 44 17803911
2008 Cep57, a multidomain protein with unique microtubule and centrosomal localization domains. The Biochemical journal 36 18294141
2012 Cep57, a NEDD1-binding pericentriolar material component, is essential for spindle pole integrity. Cell research 30 22508265
2016 Cep57 is a Mis12-interacting kinetochore protein involved in kinetochore targeting of Mad1-Mad2. Nature communications 27 26743940
2013 CEP57 mutation in a girl with mosaic variegated aneuploidy syndrome. American journal of medical genetics. Part A 21 24259107
2012 FGF-2 disrupts mitotic stability in prostate cancer through the intracellular trafficking protein CEP57. Cancer research 21 23243019
2009 Pivotal role of translokin/CEP57 in the unconventional secretion versus nuclear translocation of FGF2. Traffic (Copenhagen, Denmark) 20 19804566
2018 Mosaic-variegated aneuploidy syndrome mutation or haploinsufficiency in Cep57 impairs tumor suppression. The Journal of clinical investigation 19 30035751
2021 Cep57 and Cep57L1 maintain centriole engagement in interphase to ensure centriole duplication cycle. The Journal of cell biology 16 33492359
2018 Mosaic variegated aneuploidy syndrome caused by a CEP57 mutation diagnosed by whole exome sequencing. Clinical case reports 13 30147898
2013 Cep57 protein is required for cytokinesis by facilitating central spindle microtubule organization. The Journal of biological chemistry 12 23569207
2020 Double homozygosity in CEP57 and DYNC2H1 genes detected by WES: Composite or expanded phenotype? Molecular genetics & genomic medicine 10 31943948
2011 Translokin (Cep57) interacts with cyclin D1 and prevents its nuclear accumulation in quiescent fibroblasts. Traffic (Copenhagen, Denmark) 10 21306487
2021 Mosaic Variegated Aneuploidy syndrome 2 caused by biallelic variants in CEP57, two new cases and review of the phenotype. European journal of medical genetics 9 34500087
2018 A homozygous CEP57 c.915_925dupCAATGTTCAGC mutation in a patient with mosaic variegated aneuploidy syndrome with rhizomelic shortening in the upper and lower limbs and a narrow thorax. European journal of medical genetics 9 30010053
2024 Cep57 regulates human centrosomes through multivalent interactions. Proceedings of the National Academy of Sciences of the United States of America 7 38857398
2023 Mosaic variegated aneuploidy syndrome 2 with biallelic novel CEP57 splice site variation in Indian siblings: Expanding the clinical and molecular spectrum. Clinical genetics 6 36635612
2003 Tsp57: a novel gene induced during a specific stage of spermatogenesis. Biology of reproduction 5 12954732
2026 NuSAP Safeguards Centriole Integrity to Mediate CEP57-CEP152 Torus Recruitment for Proper Engagement. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 0 41616107
2026 A novel CEP57 gene mutation in mosaic variegated aneuploidy syndrome 2: case report. Journal of pediatric endocrinology & metabolism : JPEM 0 41700350
2024 Crystal structure of human Cep57 C-terminal domain reveals the presence of leucine zipper and the potential microtubule binding region. Proteins 0 38699879

Missed literature

Know a paper Affinage missed for CEP57? Flag it for the maintainers and the community.

No submissions yet.