Affinage

NKAP

NF-kappa-B-activating protein · UniProt Q8N5F7

Length
415 aa
Mass
47.1 kDa
Annotated
2026-06-10
32 papers in source corpus 19 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

NKAP is a multifunctional nuclear protein that operates at the interface of transcriptional repression, pre-mRNA splicing, and genome integrity to control hematopoietic and lymphoid development (PMID:19409814, PMID:24353314, PMID:37322264). Its best-defined molecular activity is transcriptional repression through physical association with the histone deacetylase HDAC3 and the Notch corepressor complex; loss of NKAP in T cells derepresses Notch target genes (Hes1, Deltex1, CD25) and blocks alphabeta T cell development (PMID:19409814). The NKAP–HDAC3 interaction, mapped to NKAP residues Y352 and F347, is the essential module for this function: a Y352A point mutant that cannot bind HDAC3 recapitulates NKAP deficiency in T cell maturation, Treg maturation, and iNKT cell development while sparing other cell types, indicating NKAP works in distinct complexes in different lineages (PMID:23481390, PMID:31387873, PMID:30804042). NKAP localizes to nuclear speckles via its basic domain, binds spliced and unspliced RNA and U1/U4/U5 snRNAs, and associates with splicing factors including FUS/TLS through its RS domain, with knockdown increasing unspliced pre-mRNA (PMID:24353314). In complex with HDAC3, NKAP maintains RNA polymerase II pausing and prevents transcription-dependent R-loop accumulation, DNA damage, and replication fork defects, with HDAC3 stabilizing NKAP protein independently of deacetylase activity (PMID:37322264). NKAP is also SUMOylated during mitosis, which is required for it to anchor CENP-E at kinetochores for chromosome alignment downstream of Bub3 (PMID:27694884). At the organismal level NKAP is required for adult hematopoietic stem cell maintenance, post-selection T cell maturation, iNKT development, and peripheral Treg survival (PMID:21624937, PMID:20610818). Missense and C-terminal mutations of NKAP that disrupt HDAC3 binding and intranuclear distribution cause developmental defects in humans and zebrafish, establishing a Mendelian developmental disorder link (PMID:31587868, PMID:38647244).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2009 High

    Established NKAP's core molecular function as a Notch-pathway transcriptional repressor acting through HDAC3, answering how it controls a defined gene-expression program in T cell development.

    Evidence Genetic complementation screen, reciprocal Co-IP, ChIP, and Lck-cre conditional knockout in T cells

    PMID:19409814

    Open questions at the time
    • DNA-binding partner conferring sequence specificity not identified
    • Direct vs indirect Notch target occupancy not fully resolved
  2. 2010 High

    Showed NKAP is cell-intrinsically required for adult hematopoietic stem cell maintenance, linking its loss to CDK-inhibitor upregulation, decreased proliferation, and apoptosis.

    Evidence Mx1-cre conditional knockout, mixed radiation chimeras, gene expression analysis

    PMID:20610818

    Open questions at the time
    • Molecular mechanism connecting NKAP loss to p21/p19 induction unresolved
    • Whether the HSC defect uses the transcriptional or splicing function not separated
  3. 2011 High

    Distinguished a maturation/functional-competency role from survival, showing NKAP-deficient peripheral T cells fail maturation in a manner not rescued by anti-apoptotic Bcl-2.

    Evidence CD4-cre conditional knockout with Bcl-2 transgene rescue, flow cytometry

    PMID:21624937

    Open questions at the time
    • Downstream maturation program controlled by NKAP not defined
  4. 2013 High

    Connected NKAP and HDAC3 genetically in iNKT development and demonstrated NKAP's biochemical engagement with the splicing machinery, broadening its function beyond Notch repression.

    Evidence Parallel NKAP and HDAC3 conditional KOs with TCR transgene rescue; immunofluorescence, CLIP-seq, pull-downs, in vitro splicing assays with FUS/TLS domain mapping

    PMID:23481390 PMID:24353314

    Open questions at the time
    • Direct splicing substrates in lymphocytes not catalogued
    • Relationship between speckle localization and HDAC3-dependent repression unresolved
  5. 2016 High

    Revealed a mitosis-specific role: SUMOylated NKAP anchors CENP-E at kinetochores via Bub3 to drive chromosome alignment, extending NKAP function to mitotic fidelity.

    Evidence Knockdown, SUMOylation-deficient mutant rescue, reciprocal Co-IP, live imaging, kinetochore fractionation

    PMID:27694884

    Open questions at the time
    • SUMO E3 ligase and acceptor lysines not defined
    • Relationship between nuclear/splicing pools and mitotic kinetochore pool unclear
  6. 2016 Medium

    Placed NKAP upstream of PLZF in NKT17 differentiation, separating a proliferation defect (Bcl-xL-independent) from a differentiation defect (PLZF-rescuable).

    Evidence Conditional knockout with Bcl-xL and PLZF transgene rescue, flow cytometry

    PMID:27183586

    Open questions at the time
    • Mechanism linking NKAP to PLZF expression not defined
    • Single-lab finding
  7. 2019 High

    Pinpointed NKAP residues Y352/F347 as the HDAC3-binding interface essential for lymphoid lineage functions, establishing that NKAP acts in cell-type-specific complexes.

    Evidence Alanine scanning, in vivo conditional deletion/re-expression of NKAP(Y352A), Co-IP

    PMID:30804042 PMID:31387873

    Open questions at the time
    • Whether the same interface mediates R-loop suppression and splicing not tested
    • Structure of the NKAP–HDAC3 interface not solved
  8. 2019 Medium

    Reframed peripheral T cell loss away from complement as the primary cause and implicated lipid-peroxide accumulation/ferroptosis in NKAP-deficient T cells.

    Evidence Complement-pathway genetic ablation (MBL1/MBL2/C4 KO), complement deposition assays, lipid peroxide measurement; companion Foxp3-cre Treg study

    PMID:29366602 PMID:31175160

    Open questions at the time
    • Mechanism linking NKAP loss to lipid peroxidation not established here
    • Relative contribution of ferroptosis vs complement not quantified
  9. 2019 Medium

    Extended NKAP's transcriptional role to oncogenesis, showing it directly transactivates Notch1 to drive a glioma tumor-microenvironment program.

    Evidence ChIP, luciferase reporter, RNA-seq, siRNA, xenografts

    PMID:31277684

    Open questions at the time
    • Activating (vs repressive) mode of NKAP at Notch1 promoter mechanistically unexplained
    • Single-lab finding
  10. 2019 Medium

    Resolved part of the HSC phenotype mechanism, showing NKAP loss drives senescence via p16/p21 and that CDKI ablation shifts but does not rescue the failure.

    Evidence Inducible Mx1-cre KO, double CDKI-deficient mice, ex vivo cultures, senescence assays

    PMID:31632967

    Open questions at the time
    • Upstream trigger of CDKI induction unknown
    • In vivo vs ex vivo discordance unexplained
  11. 2019 Medium

    Linked NKAP to a human developmental disorder, showing C-terminal mutations disrupt HDAC3/spliceosomal interactions and produce a long-gene downregulation transcriptome signature.

    Evidence Zebrafish C-terminal truncation model, patient transcriptomics, domain-interaction mapping

    PMID:31587868

    Open questions at the time
    • Causal link from splicing defect to long-gene downregulation not mechanistically dissected
  12. 2021 Medium

    Identified a cytoplasmic/signaling regulatory input, showing MARCKS binds NKAP and that smoke-induced MARCKS phosphorylation releases NKAP to activate NF-κB in lung cancer.

    Evidence MARCKS interactome proteomics, Co-IP, phosphomimetic mutants, NF-κB reporters

    PMID:33754052

    Open questions at the time
    • Direct molecular step from freed NKAP to NF-κB activation undefined
    • Single-lab finding
  13. 2022 Medium

    Defined an RNA-level ferroptosis-suppressor mechanism: NKAP binds m6A-modified SLC7A11 transcript and recruits SFPQ to promote productive last-exon splicing and SLC7A11 upregulation.

    Evidence RIP, Co-IP, RNA-seq, mass spectrometry, METTL3 knockdown, m6A inhibitor, xenografts in glioblastoma

    PMID:35064112

    Open questions at the time
    • Generality beyond SLC7A11 transcript not established
    • Connection to the lymphocyte ferroptosis phenotype not tested
  14. 2023 High

    Established a genome-protection mechanism: the NKAP–HDAC3 complex maintains RNA Pol II pausing to prevent R-loop accumulation, with R-loops processed into double-strand breaks by XPF/XPG.

    Evidence Protein complex analysis, S9.6 R-loop detection, replication fork assays, XPF/XPG KO epistasis, RNA Pol II ChIP, HDAC3 stabilization assays

    PMID:37322264

    Open questions at the time
    • How NKAP enforces Pol II pausing mechanistically unresolved
    • Whether this complex equals the Notch-repressive HDAC3 complex unclear
  15. 2024 Medium

    Strengthened the disease link by showing a specific NKAP p.R330C mutation disrupts intranuclear distribution and HDAC3 binding, dysregulating cardiac morphogenesis genes.

    Evidence HEK293T transfection of mutant, immunofluorescence, Co-IP, RT-qPCR of DHRS3/DNAH11/JAG1

    PMID:38647244

    Open questions at the time
    • In vivo cardiac phenotype from this mutation not demonstrated
    • Heterologous-cell system only
  16. 2024 Low

    Proposed an upstream stabilizer of NKAP, with lncRNA GRAS1 binding NKAP and protecting it from proteasomal degradation to prevent DNA damage.

    Evidence RAP-MS, siRNA knockdown, proteasome inhibitor, overexpression rescue (preprint)

    PMID:38645172

    Open questions at the time
    • Preprint; direct GRAS1–NKAP binding lacks reciprocal validation
    • Mechanism of GRAS1-dependent stabilization undefined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How NKAP's distinct activities—Notch/HDAC3 repression, speckle-localized splicing, mitotic CENP-E anchoring, and R-loop suppression—are partitioned into separable complexes within a single cell, and which activity underlies each developmental phenotype, remains unresolved.
  • No structural model of NKAP or its complexes
  • No unified assignment of phenotype to specific molecular activity
  • Determinants of context-specific complex assembly unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 2 GO:0060090 molecular adaptor activity 2 GO:0140098 catalytic activity, acting on RNA 2 GO:0140110 transcription regulator activity 2
Localization
GO:0005634 nucleus 2 GO:0005654 nucleoplasm 2
Pathway
R-HSA-74160 Gene expression (Transcription) 2 R-HSA-8953854 Metabolism of RNA 2 R-HSA-1640170 Cell Cycle 1 R-HSA-73894 DNA Repair 1
Partners
BUB3BUBR1CENP-EFUSHDAC3MARCKSSFPQ
Complex memberships
NKAP–HDAC3 / Notch corepressor complexkinetochore (CENP-E anchoring)

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2009 NKAP functions as a transcriptional repressor by associating with the histone deacetylase HDAC3 and the Notch corepressor complex, and is part of a DNA-binding complex as demonstrated by chromatin immunoprecipitation. Loss of NKAP in T cells blocks alphabeta T cell development and causes 8-20-fold upregulation of Notch target genes Hes1, Deltex1, and CD25. Genetic complementation screen, co-immunoprecipitation, chromatin immunoprecipitation, conditional knockout (Lck-cre) Immunity High 19409814
2011 NKAP is required for post-selection T cell maturation and acquisition of functional competency; loss of NKAP in CD4-cre conditional knockout mice causes a cell-intrinsic block in peripheral T cell maturation that is not rescued by a Bcl-2 transgene, indicating the defect is not simply in cell survival. Conditional knockout (CD4-cre), Bcl-2 transgene rescue experiment, flow cytometry The Journal of experimental medicine High 21624937
2013 NKAP is required for iNKT cell development; deletion of NKAP-associated protein HDAC3 causes a similar block, indicating NKAP and HDAC3 functionally interact to control iNKT cell development. The block is cell-intrinsic and not due to decreased survival or failure to rearrange the invariant TCR-alpha chain. Conditional knockout (CD4-cre), TCR transgene rescue, HDAC3 conditional knockout, flow cytometry Nature communications High 23481390
2013 NKAP localizes to nuclear speckles (with the basic domain required for this localization), binds RNA (both spliced mRNA and unspliced pre-mRNA), associates with RNA-binding proteins and splicing factors including FUS/TLS (through the RS domain of NKAP and RGG1/RGG3 domains of FUS/TLS), and associates with U1, U4, and U5 snRNAs. NKAP knockdown leads to increased pre-mRNA percentage, establishing a role in RNA splicing. Immunofluorescence, deletion analysis, pull-down assays, in vitro splicing assays, CLIP-seq, Co-IP Nucleic acids research High 24353314
2010 NKAP is required for adult hematopoietic stem cell (HSC) maintenance and survival; NKAP deletion leads to decreased HSC proliferation and increased apoptosis associated with increased expression of cyclin-dependent kinase inhibitors p21Cip1/Waf1 and p19Ink4d. This failure is cell-intrinsic as demonstrated by radiation chimera experiments. Conditional knockout (Mx1-cre), mixed radiation chimeras, flow cytometry, gene expression analysis Blood High 20610818
2016 NKAP is SUMOylated predominantly during mitosis, and this SUMOylation is required for NKAP to bind CENP-E. A SUMOylation-deficient NKAP mutant cannot support CENP-E localization to kinetochores or proper chromosome alignment. Bub3 recruits NKAP to stabilize the binding of CENP-E to BubR1 at kinetochores. NKAP knockdown causes chromosome misalignment, prometaphase arrest, and aneuploidy. Knockdown, SUMOylation-deficient mutant expression, co-immunoprecipitation, immunofluorescence, live imaging, kinetochore fractionation Nature communications High 27694884
2016 NKAP regulates iNKT cell proliferation and differentiation into NKT17 cells; NKAP-specific deletion in iNKT cells causes defective proliferation (not rescued by Bcl-xL overexpression) and failure of NKT17 differentiation; the NKT17 defect is rescued by promyelocytic leukemia zinc finger (PLZF) transgene, placing NKAP upstream of PLZF in NKT17 differentiation. Conditional knockout, Bcl-xL transgene rescue, PLZF transgene rescue, flow cytometry Journal of immunology Medium 27183586
2018 NKAP-deficient regulatory T cells are eliminated in the periphery after thymic egress through complement-mediated attack in a cell-intrinsic manner, similar to the mechanism by which NKAP-deficient conventional T cells fail maturation. Conditional knockout (Foxp3-YFP-cre), complement deposition assays, flow cytometry Journal of autoimmunity Medium 29366602
2019 The physical interaction between NKAP and HDAC3, mapped to NKAP residues Y352 and F347 (alanine substitution at Y352 abrogates binding), is critical for T cell maturation, Treg maturation, and iNKT cell development. NKAP(Y352A) recapitulates NKAP deficiency in these lineages but does not impair proliferation of murine embryonic fibroblasts, indicating NKAP functions in different complexes in different cell types. Serial truncation and alanine scanning, conditional deletion/re-expression transgenic system in vivo, Co-IP ImmunoHorizons / Journal of immunology High 30804042 31387873
2019 T cell maturation confers resistance to complement targeting by MBL2 (lectin pathway); NKAP-deficient T cells remain susceptible to complement (MBL2-dependent C3 deposition) but peripheral lymphopenia is not fully restored by genetic ablation of lectin and classical complement pathways, indicating complement is not the primary cause of T cell loss. Instead, accumulation of lipid peroxides (consistent with ferroptosis) was observed in NKAP-deficient T cells. Genetic ablation of complement pathways (MBL1, MBL2 KO, C4 KO), complement deposition assays, lipid peroxide measurement Journal of immunology Medium 31175160
2019 NKAP promotes glioma growth by directly binding to the Notch1 promoter and trans-activating Notch1 transcription, which in turn increases SDF-1 and M-CSF secretion to drive tumor-associated macrophage recruitment and polarization. ChIP assay, RNA sequencing, luciferase reporter assay, siRNA knockdown, xenograft models Journal of experimental & clinical cancer research Medium 31277684
2019 NKAP deficiency in hematopoietic progenitors leads to a senescent phenotype with altered expression of cell cycle regulators including p16INK4a; combined deficiency of p16INK4a and p21Cip1 does not reverse hematopoietic failure in vivo but shifts the consequence of NKAP deficiency from senescence to apoptosis in ex vivo cultures. Inducible conditional knockout (Mx1-cre), ex vivo cultures, double CDKI-deficient mice, senescence assays Frontiers in cell and developmental biology Medium 31632967
2021 MARCKS directly binds NKAP protein; upon cigarette smoke-induced phosphorylation of MARCKS at Ser159 and Ser163, the MARCKS-NKAP interaction is inhibited, leading to activation of NF-κB signaling in lung cancer cells. Functional proteomics (MARCKS interactome), co-immunoprecipitation, phosphomimetic mutants, NF-κB reporter assays Theranostics Medium 33754052
2022 NKAP acts as a ferroptosis suppressor in glioblastoma cells by binding to m6A-modified SLC7A11 transcript (via the RGAC/RGACH motif) in an METTL3-dependent manner, then recruiting splicing factor SFPQ to promote TTS splicing and retention of the last exon of SLC7A11 mRNA, resulting in SLC7A11 maturation and upregulation. RNA immunoprecipitation (RIP), Co-IP, RNA-seq, Mass Spectrometry, siRNA knockdown, m6A inhibitor treatment, METTL3 knockdown, xenograft models Cell death & disease Medium 35064112
2023 NKAP prevents R-loop accumulation and maintains genome integrity by forming a protein complex with HDAC3. NKAP depletion causes transcription-dependent R-loop accumulation, DNA damage, and replication fork defects. HDAC3 stabilizes NKAP protein independently of its deacetylase activity. R-loops induced by NKAP or HDAC3 depletion are processed into DNA double-strand breaks by XPF and XPG endonucleases. NKAP also maintains RNA polymerase II pausing to prevent R-loop formation. Protein complex analysis, siRNA knockdown, R-loop detection (S9.6 antibody), DNA damage assays, replication fork assays, XPF/XPG endonuclease knockout, RNA Pol II ChIP Cell death and differentiation High 37322264
2019 Missense mutations clustered in the C-terminal region of NKAP (where it interacts with HDAC3 and post-catalytic spliceosomal complex proteins) cause developmental defects; C-terminally truncated NKAP in zebrafish causes severe developmental defects, and affected human cases show downregulation of long genes with higher exon numbers as a transcriptome signature. Zebrafish nkap C-terminal truncation mutant, transcriptome analysis of patient samples, domain-interaction mapping American journal of human genetics Medium 31587868
2024 NKAP p.R330C mutation disrupts intra-nuclear distribution of NKAP protein and impairs its interaction with HDAC3, leading to dysregulation of cardiac morphogenesis gene transcription (DHRS3, DNAH11, JAG1) in HEK293T cells. Transfection of NKAP mutant in HEK293T, immunofluorescence (intra-nuclear distribution), Co-IP (NKAP-HDAC3 interaction), RT-qPCR (target gene transcription) Journal of cellular and molecular medicine Medium 38647244
2024 The lncRNA GRAS1 directly interacts with NKAP protein (identified by RAP-MS), and GRAS1 knockdown leads to proteasome-dependent degradation of NKAP protein, resulting in DNA damage and cell death that can be mitigated by NKAP overexpression. RNA antisense purification and mass spectrometry (RAP-MS), siRNA knockdown, proteasome inhibitor treatment, overexpression rescue bioRxivpreprint Low 38645172

Source papers

Stage 0 corpus · 32 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2022 RNA binding protein NKAP protects glioblastoma cells from ferroptosis by promoting SLC7A11 mRNA splicing in an m6A-dependent manner. Cell death & disease 105 35064112
2009 NKAP is a transcriptional repressor of notch signaling and is required for T cell development. Immunity 82 19409814
2011 NKAP is required for T cell maturation and acquisition of functional competency. The Journal of experimental medicine 48 21624937
2013 The transcriptional repressor NKAP is required for the development of iNKT cells. Nature communications 45 23481390
2013 NKAP is a novel RS-related protein that interacts with RNA and RNA binding proteins. Nucleic acids research 44 24353314
2016 SUMOylated NKAP is essential for chromosome alignment by anchoring CENP-E to kinetochores. Nature communications 38 27694884
2021 MARCKS cooperates with NKAP to activate NF-kB signaling in smoke-related lung cancer. Theranostics 36 33754052
2010 Adult hematopoietic stem cells require NKAP for maintenance and survival. Blood 35 20610818
2016 NKAP Regulates Invariant NKT Cell Proliferation and Differentiation into ROR-γt-Expressing NKT17 Cells. Journal of immunology (Baltimore, Md. : 1950) 28 27183586
2020 Silencing of lncRNA MIAT alleviates LPS-induced pneumonia via regulating miR-147a/NKAP/NF-κB axis. Aging 27 33318298
2019 NKAP alters tumor immune microenvironment and promotes glioma growth via Notch1 signaling. Journal of experimental & clinical cancer research : CR 27 31277684
2019 MiR-4766-5p Inhibits The Development And Progression Of Gastric Cancer By Targeting NKAP. OncoTargets and therapy 20 31802890
2019 Missense Mutations in NKAP Cause a Disorder of Transcriptional Regulation Characterized by Marfanoid Habitus and Cognitive Impairment. American journal of human genetics 16 31587868
2018 Treg-specific deletion of NKAP results in severe, systemic autoimmunity due to peripheral loss of Tregs. Journal of autoimmunity 14 29366602
2022 IL-1β promotes hypoxic vascular endothelial cell proliferation through the miR-24-3p/NKAP/NF-κB axis. Bioscience reports 10 35005769
2018 NKAP functions as an oncogene and its expression is induced by CoCl2 treatment in breast cancer via AKT/mTOR signaling pathway. Cancer management and research 10 30464609
2023 NKAP acts with HDAC3 to prevent R-loop associated genome instability. Cell death and differentiation 9 37322264
2020 NKAP promotes renal cell carcinoma growth via AKT/mTOR signalling pathway. Cell biochemistry and function 9 32032976
2019 NKAP plays an oncogenic function partly through AKT signaling pathway in hepatocellular carcinoma. Neoplasma 9 31305121
2019 NKAP Regulates Senescence and Cell Death Pathways in Hematopoietic Progenitors. Frontiers in cell and developmental biology 9 31632967
2014 The Notch co-repressor protein NKAP is highly expressed in adult mouse subventricular zone neural progenitor cells. Neuroscience 9 24583034
2019 The oncogenic role of NKAP in the growth and invasion of colon cancer cells. Oncology reports 8 31545474
2019 NKAP Must Associate with HDAC3 to Regulate Hematopoietic Stem Cell Maintenance and Survival. Journal of immunology (Baltimore, Md. : 1950) 6 30804042
2019 Murine T Cell Maturation Entails Protection from MBL2, but Complement Proteins Do Not Drive Clearance of Cells That Fail Maturation in the Absence of NKAP. Journal of immunology (Baltimore, Md. : 1950) 6 31175160
2019 The Interaction between NKAP and HDAC3 Is Critical for T Cell Maturation. ImmunoHorizons 6 31387873
2019 NKAP functions as an oncogene in Ewing sarcoma cells partly through the AKT signaling pathway. Experimental and therapeutic medicine 5 31555387
2024 From phenotype to mechanism: Prenatal spectrum of NKAP mutation-related disorder and its pathogenesis inducing congenital heart disease. Journal of cellular and molecular medicine 3 38647244
2022 LncRNA LINC00707 serves as a sponge of miR-382-5p to alleviate lipopolysaccharide (LPS)-induced WI-38 cell injury through upregulating NKAP in infantile pneumonia. Autoimmunity 3 35593504
2025 NKAP overexpression promotes gastric cancer immune escape by inducing IL-10 secretion from mature dendritic cells during anti-PD-L1 therapy. Journal of gastrointestinal oncology 1 40950333
2024 GRAS1 non-coding RNA protects against DNA damage and cell death by binding and stabilizing NKAP. bioRxiv : the preprint server for biology 1 38645172
2026 Deleterious NKAP Mutations Are Associated with Musculoskeletal Abnormalities in Hemizygous Males and Skewed X Chromosome Inactivation in Heterozygous Females. International journal of molecular sciences 0 41828556
2026 Marfanoid phenotype with intellectual disability associated with NKAP mutation: a case report. Journal of medical case reports 0 41917976

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