Affinage

Showing ZDHHC17 — HIP14 is a alias.

ZDHHC17

Palmitoyltransferase ZDHHC17 · UniProt Q8IUH5

Length
632 aa
Mass
72.6 kDa
Annotated
2026-06-11
25 papers in source corpus 21 papers cited in narrative 21 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ZDHHC17 (HIP14) is a Golgi- and vesicle-localized DHHC palmitoyl acyltransferase that S-acylates a broad set of neuronal and non-neuronal substrates, coupling protein palmitoylation to intracellular trafficking, synaptic function, and signaling (PMID:15603740, PMID:12393793). It recognizes many substrates through its N-terminal ankyrin repeat (AR) domain, which binds a conserved zDHHC AR-binding motif (zDABM, consensus [VIAP][VIT]XXQP) present in SNAP25, cysteine string protein, huntingtin, MAP6, and dozens of other predicted interactors, recruiting them prior to S-acylation by the DHHC catalytic domain (PMID:26198635, PMID:28882895); for the Sprouty/SPRED family it engages substrates through their cysteine-rich SPR domain in a zDABM- and AR-independent manner (PMID:36442513). Validated substrates include SNAP-25, PSD-95, GAD65, synaptotagmin I, and huntingtin (palmitoylated at Cys214) (PMID:15603740, PMID:16699508), as well as GPM6A, SPRED1/SPRED3, the axonal regulators DLK and NMNAT2, HSP90α, Smad7, and CDK4 (PMID:24705354, PMID:33207199, PMID:37769867, PMID:38876303, PMID:42133178). Its enzymatic output is reciprocally tuned by huntingtin: wild-type HTT is both a substrate and a potentiator of HIP14-mediated palmitoylation, and polyglutamine-expanded HTT reduces HTT–HIP14 interaction and impairs HIP14 activity in vivo (PMID:16699508, PMID:21636527, PMID:21775500, PMID:24651384). Loss of HIP14 function—by constitutive knockout, adult-specific deletion, or mutant-HTT impairment—reduces substrate palmitoylation and causes progressive synaptic dysfunction, neurodegeneration, paralysis, and lethality, establishing this single PAT as non-redundant for synaptic plasticity and adult neuronal maintenance (PMID:21775500, PMID:24277827, PMID:27927242). Beyond the nervous system, ZDHHC17 supports diverse cellular programs through substrate palmitoylation, including MAPK signaling in glioma, HSP90α/aromatase-dependent estrogen synthesis, TGF-β regulation via Smad7, CDK4-driven cell cycle progression, and SADS-CoV RNA replication (PMID:31938047, PMID:33207199, PMID:37769867, PMID:38876303, PMID:42133178, PMID:34700373).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2002 High

    Established HIP14 as a huntingtin-interacting protein with a defined subcellular home and a conserved trafficking function, anchoring later mechanistic work.

    Evidence Yeast two-hybrid, Golgi co-localization, and rescue of akr1Δ yeast trafficking/endocytosis defects

    PMID:12393793

    Open questions at the time
    • Enzymatic activity not yet demonstrated at this stage
    • Molecular basis of polyglutamine-sensitive interaction unresolved
  2. 2004 High

    Defined HIP14 as a substrate-selective neuronal palmitoyl acyltransferase, answering whether it is an enzyme and which proteins it modifies.

    Evidence In vitro palmitoylation assays with multiple substrates plus siRNA knockdown showing reduced PSD-95/GAD65 clustering in neurons

    PMID:15603740

    Open questions at the time
    • Substrate recognition mechanism not yet defined
    • Catalytic residue requirements not mapped
  3. 2006 High

    Identified huntingtin Cys214 as a specific HIP14 palmitoylation site whose modification controls htt trafficking and toxicity, linking enzyme activity to disease.

    Evidence Metabolic labeling, Cys214 mutagenesis, knockdown/overexpression, and inclusion quantification in mouse neurons

    PMID:16699508

    Open questions at the time
    • Whether reduced htt palmitoylation is causal in vivo not yet tested
    • Effect on broader substrate pool unaddressed
  4. 2008 Medium

    Proposed an unexpected Mg2+ transport function regulated by autopalmitoylation, raising the possibility of activity beyond classical PAT chemistry.

    Evidence Xenopus oocyte electrophysiology with DHHC deletion and 2-bromopalmitate inhibition

    PMID:18794299

    Open questions at the time
    • Palmitoylation not directly measured
    • Single lab, not independently confirmed
    • Physiological relevance of Mg2+ transport unestablished
  5. 2011 High

    Showed bidirectional regulation between HTT and HIP14 and demonstrated in vivo that reduced or mutant HTT lowers HIP14 activity, framing palmitoylation deficits as a Huntington disease mechanism.

    Evidence In vitro palmitoylation assays, HTT-ASO knockdown and hdh+/- brain biochemistry, plus Hip14 gene-trap knockout and YAC128 comparison with behavioral/neuropathological endpoints

    PMID:21636527 PMID:21775500

    Open questions at the time
    • Mechanism by which mutant HTT impairs HIP14 catalysis not resolved
    • Relative contribution of individual substrates to phenotype unclear
  6. 2013 High

    Demonstrated that a single PAT has non-redundant roles in synaptic plasticity and memory, ruling out full compensation by other DHHC enzymes.

    Evidence Hip14 knockout mouse electrophysiology (LTP) and hippocampus-dependent memory tasks

    PMID:24277827

    Open questions at the time
    • Causal substrates underlying plasticity deficit not identified
    • Developmental vs ongoing requirement not separated here
  7. 2014 Medium

    Mapped the AR domain as the huntingtin-binding region and expanded the substrate/interactor set, beginning to define recognition rules.

    Evidence Co-IP deletion mapping of HTT, plus Y2H screen with acyl-RAC validation of GPM6A, SPRED1, SPRED3

    PMID:24651384 PMID:24705354

    Open questions at the time
    • Exact binding motif not yet defined
    • Distinction between binding and palmitoylation (e.g. optineurin) mechanistically unexplained
  8. 2015 High

    Defined the zDABM linear motif recognized by the AR domain, providing a generalizable substrate-recruitment code, and uncovered a PAT-independent role in TrkA signaling and axon outgrowth.

    Evidence Peptide arrays, mutagenesis, and in vitro S-acylation across multiple substrates; zebrafish/PC12 knockdown with TrkA-tubulin Co-IP and ERK1/2 readouts

    PMID:26198635 PMID:26232532

    Open questions at the time
    • zDABM-independent recognition modes not yet defined
    • PAT-independence of ERK signaling not fully confirmed by catalytic-dead mutagenesis
  9. 2016 High

    Separated developmental from adult function, showing HIP14 is continuously required for neuronal integrity and survival in the adult brain.

    Evidence Inducible conditional knockout (iHip14Δ/Δ) mice with striatal electrophysiology, behavior, and histology

    PMID:27927242

    Open questions at the time
    • Molecular pathway from substrate hypopalmitoylation to degeneration not delineated
    • Specific lethal substrate(s) unidentified
  10. 2017 Medium

    Built a predictive PSSM for AR binding, scaling substrate identification to ~90 candidate human interactors and generalizing the recruitment model.

    Evidence Peptide arrays (400 peptides), PSSM construction, and in vitro binding validation of a predicted subset

    PMID:28882895

    Open questions at the time
    • Most predicted interactors not validated as palmitoylation substrates
    • Binding does not guarantee acylation
  11. 2020 Medium

    Extended ZDHHC17 function to non-neuronal disease (glioma) signaling and to coordinated control of distinct axon degeneration pathways via substrate palmitoylation.

    Evidence Co-IP/GST pulldown of MAP2K4 with JNK/p38 readouts in GBM; conditional KO optic nerve crush with DLK and NMNAT2 zDABM mutagenesis

    PMID:31938047 PMID:33207199

    Open questions at the time
    • MAP2K4 module placement relies partly on pharmacological disruption
    • Whether DLK/NMNAT2 effects generalize beyond optic nerve unaddressed
  12. 2022 High

    Revealed a second, AR-independent substrate-recognition mode through the SPR domain of Sprouty/SPRED proteins, broadening the enzyme's engagement repertoire.

    Evidence zDABM and SPR domain mutagenesis, Co-IP, and in vitro S-acylation with ANK-deletion constructs

    PMID:36442513

    Open questions at the time
    • Structural basis of SPR-domain recognition unknown
    • Generality of this mode across other substrates untested
  13. 2024 High

    Demonstrated regulatory palmitoylation of a signaling effector (Smad7), showing site-specific acylation controls localization, stability, and pathway output.

    Evidence RAC/metabolic labeling, Smad7 cysteine mutagenesis, subcellular fractionation, and TGF-β/Smad reporter assays in mammary epithelial cells

    PMID:38876303

    Open questions at the time
    • In vivo relevance to TGF-β biology not shown
    • Whether AR/zDABM or SPR recognition mediates Smad7 binding unclear
  14. 2023 Medium

    Connected ZDHHC17 to endocrine function via HSP90α palmitoylation and aromatase-dependent estrogen synthesis.

    Evidence siRNA knockdown in granulosa cells, RAC palmitoylation assay, CYP19A1/hormone measurement, and in vivo PCOS model

    PMID:37769867

    Open questions at the time
    • Direct HSP90α palmitoylation site not mapped
    • Mechanistic link from HSP90α acylation to CYP19A1 expression incomplete
  15. 2026 Medium

    Linked ZDHHC17 to cell cycle control by palmitoylating CDK4 in coordination with TRAF6-mediated ubiquitination to promote cyclin D1 binding and kinase activity.

    Evidence 2-BP inhibition, depletion, CDK4-cyclin D1 Co-IP, K11-ubiquitination and kinase assays, and a high-fat-diet mouse model

    PMID:42133178

    Open questions at the time
    • CDK4 palmitoylation site not defined
    • Crosstalk mechanism between palmitoylation and K11 ubiquitination unresolved
    • Single lab
  16. 2025 Medium

    Extended a conserved role to lysosome biogenesis and secretory granule-lysosome fusion, placing Hip14 upstream of Rab2-dependent membrane trafficking.

    Evidence Drosophila Hip14/patsas mutants and RNAi with lysosomal imaging, hydrolase trafficking assays, and Rab2 genetic epistasis (preprint)

    PMID:bio_10.1101_2025.02.06.636816

    Open questions at the time
    • Not yet peer-reviewed
    • Mammalian conservation of the lysosomal role untested
    • Direct palmitoylation substrate driving Rab2 effect unidentified

Open questions

Synthesis pass · forward-looking unresolved questions
  • How ZDHHC17 substrate selection, catalytic turnover, and HTT-dependent activity modulation are structurally integrated—and which specific substrate hypopalmitoylation events drive neurodegeneration—remains unresolved.
  • No structure of the AR-DHHC enzyme with substrate
  • Causal substrate(s) for lethality/neurodegeneration not pinpointed
  • Mechanism of mutant-HTT impairment of catalysis unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 9 GO:0016740 transferase activity 3 GO:0060090 molecular adaptor activity 3
Localization
GO:0005794 Golgi apparatus 2 GO:0031410 cytoplasmic vesicle 2
Pathway
R-HSA-112316 Neuronal System 4 R-HSA-162582 Signal Transduction 3 R-HSA-392499 Metabolism of proteins 3
Partners
CDK4DLKHSP90AA1HTTMAP2K4SNAP25SPRED1SPRED3

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2004 HIP14 (ZDHHC17) is a neuronal palmitoyl acyltransferase (PAT) that palmitoylates SNAP-25, PSD-95, GAD65, synaptotagmin I, and huntingtin, but not paralemmin or synaptotagmin VII, demonstrating substrate specificity. Exogenous HIP14 enhances palmitoylation-dependent vesicular trafficking, and knockdown of endogenous HIP14 reduces clustering of PSD-95 and GAD65 in neurons. Biochemical palmitoylation assays, overexpression and siRNA knockdown in heterologous cells and neurons, vesicular trafficking assays Neuron High 15603740
2002 HIP14 (ZDHHC17) localizes to the Golgi and cytoplasmic vesicles, and functionally rescues temperature-sensitive lethality and endocytosis defects in akr1Δ yeast, establishing a role for HIP14 in intracellular trafficking and endocytosis. Its interaction with huntingtin is inversely correlated with polyglutamine tract length. Yeast two-hybrid, subcellular localization (co-localization with Golgi markers), yeast complementation assay (rescue of akr1Δ phenotype) Human molecular genetics High 12393793
2006 Huntingtin (htt) is palmitoylated at cysteine 214 by HIP14 (ZDHHC17), which is essential for htt trafficking and function. Polyglutamine expansion reduces htt-HIP14 interaction and htt palmitoylation. Palmitoylation-resistant htt (C214 mutant) accelerates inclusion formation and increases neuronal toxicity. HIP14 overexpression reduces inclusions, while HIP14 downregulation increases them. Metabolic palmitoylation labeling, site-directed mutagenesis of htt Cys214, siRNA knockdown, overexpression in mouse neurons, inclusion body quantification Nature neuroscience High 16699508
2008 HIP14 (ZDHHC17) mediates electrogenic, voltage-dependent, saturable Mg2+ uptake when expressed in Xenopus oocytes (Km ~0.87 mM). Inhibition of palmitoylation (2-bromopalmitate) or deletion of the DHHC motif reduces HIP14-mediated Mg2+ transport by ~50%, suggesting autopalmitoylation regulates its Mg2+ transport function. HIP14 localizes to Golgi and sub-plasma membrane vesicles, with redistribution under low-Mg2+ conditions. Xenopus oocyte electrophysiology (Mg2+ uptake assays), DHHC deletion mutagenesis, GFP-fusion localization in transfected epithelial cells, 2-bromopalmitate pharmacological inhibition The Journal of biological chemistry Medium 18794299
2011 Wild-type HTT modulates HIP14 (ZDHHC17) enzymatic activity: HTT itself is palmitoylated by HIP14, and wild-type HTT in turn potentiates HIP14-mediated palmitoylation of SNAP25 in vitro. In mice with reduced HTT (hdh+/- or HTT-ASO knockdown), HIP14 palmitoylation and the palmitoylation of its substrates SNAP25 and GluR1 are reduced in vivo. Among 23 DHHC PATs, HIP14 and HIP14L (DHHC13) are the two major PATs that palmitoylate HTT. In vitro palmitoylation assay, HTT antisense oligonucleotide knockdown in cortical neurons, brain biochemistry from hdh+/- mice, acyl-RAC/ABE palmitoylation assay Human molecular genetics High 21636527
2011 Hip14 (ZDHHC17) knockout mice exhibit behavioral, biochemical, and neuropathological defects reminiscent of Huntington disease. Palmitoylation of HIP14 substrates (other than HTT itself) is reduced in Hip14−/− brains. HIP14 is dysfunctional in YAC128 (mutant HTT) mice, indicating mutant HTT impairs HIP14 palmitoyl transferase activity in vivo. Hip14 gene-trap knockout mouse generation, palmitoylation assays in brain tissue, behavioral testing, neuropathological analysis, YAC128 mouse model comparison Human molecular genetics High 21775500
2013 Constitutive loss of Hip14 (ZDHHC17) in mice produces marked alterations in synaptic function across multiple brain regions, and significantly impairs hippocampal long-term plasticity and memory, demonstrating that a single PAT has non-redundant roles in synaptic physiology. Hip14 knockout mouse, electrophysiology (LTP recordings), behavioral memory tests (hippocampus-dependent tasks) Proceedings of the National Academy of Sciences of the United States of America High 24277827
2014 The ankyrin repeat (AR) domain of HIP14 (ZDHHC17) mediates its interaction with HTT. HTT amino acids 1–548 are sufficient for full interaction; partial interaction occurs with HTT 1–427 and HTT 224–548. Deletion of residues 257–315 reduces but does not abolish binding, suggesting two potential binding domains near residues 224 and 427. Co-immunoprecipitation with N- and C-terminal HTT deletion constructs, HIP14-GFP pulldown assays PloS one Medium 24651384
2014 Yeast two-hybrid screening identified a large overlap between HIP14 (ZDHHC17) interactors and published HTT interactors. Three novel HIP14 substrates were confirmed: GPM6A, SPRED1, and SPRED3, each palmitoylated by HIP14. Optineurin co-immunoprecipitates with HIP14 but is not palmitoylated by it. Yeast two-hybrid screen, co-immunoprecipitation, palmitoylation assay (acyl-RAC) for substrate confirmation Human molecular genetics Medium 24705354
2015 The ankyrin repeat (AR) domain of zDHHC17 (HIP14) and zDHHC13 recognizes a conserved short linear motif with consensus [VIAP][VIT]XXQP in substrates including SNAP25, SNAP23, cysteine string protein, huntingtin, CLIP-3, and MAP6, mediating substrate recruitment prior to S-acylation. Peptide array binding assays, mutational analysis, in vitro S-acylation assays, sequence motif analysis across substrate proteins The Journal of biological chemistry High 26198635
2015 ZDHHC17 is required for proper TrkA-tubulin complex formation in PC12 cells, promoting ERK1/2 phosphorylation and axon outgrowth. Knockdown of ZDHHC17 in zebrafish results in motor dysfunction due to defective axon outgrowth in spinal motor neurons. The promotion of ERK1/2 phosphorylation by ZDHHC17 overexpression was independent of its palmitoyl transferase activity. ZDHHC17 siRNA knockdown in zebrafish (motor behavior, immunolabeling of axons), siRNA in NSCs and PC12 cells, co-immunoprecipitation of TrkA-tubulin, ERK1/2 phosphorylation western blot, overexpression experiments Molecular and cellular neurosciences Medium 26232532
2016 Adult-specific deletion of Hip14 (ZDHHC17) in mice leads to rapid progressive paralysis and death within 10 weeks, accompanied by striatal synaptic deficits (reduced transmitter release probability, altered spontaneous postsynaptic currents), behavioral deficits, and cortical microgliosis/astrogliosis, demonstrating that HIP14 is essential for maintenance of neuronal integrity and life in the adult. Inducible conditional knockout (iHip14Δ/Δ) mice, electrophysiology (striatal synaptic recordings), behavioral tests, brain histology/immunohistochemistry BMC biology High 27927242
2017 Using peptide arrays based on SNAP25 and CSPα zDHHC AR-binding motifs (zDABM), a position-specific scoring matrix was derived for zDHHC17 AR binding, predicting and validating 90 human proteins as putative zDHHC17 interactors via their zDABM sequences, including all SNAP25, sprouty, cornifelin, ankyrin, and SLAIN-motif family members. Peptide array binding assays (400 peptides), PSSM construction, in vitro binding validation of predicted interactors The Journal of biological chemistry Medium 28882895
2020 ZDHHC17 interacts with MAP2K4 and p38/JNK to form a signaling module that activates JNK and p38 MAPK pathways, promoting GBM cell tumorigenicity and glioma stem cell self-renewal. Co-immunoprecipitation and GST pulldown confirmed the ZDHHC17-MAP2K4 interaction. A small molecule genistein disrupts ZDHHC17-MAP2K4 complex formation. Co-immunoprecipitation, GST pulldown, pharmacological inhibition (genistein), in vitro and in vivo tumor models, flow cytometry, transwell migration assay Theranostics Medium 31938047
2020 ZDHHC17-dependent palmitoylation of DLK enables DLK-dependent somal degeneration after optic nerve crush (ONC), while ZDHHC17-dependent palmitoylation of NMNAT2 maintains distal axon integrity in healthy optic nerves. Conserved zDABM motifs in both DLK and NMNAT2 govern their ZDHHC17-dependent regulation. ZDHHC17 thus couples two previously considered independent pathways of somal and distal axon degeneration. Optic nerve crush in conditional ZDHHC17 knockout mice/RGCs, palmitoylation assays, motif mutagenesis, DRG neuron loss-of-function experiments Cell reports High 33207199
2021 ZDHHC17 is required as a host factor for SADS-CoV genomic RNA replication. The DHHC domain (palmitoylation-active domain) of ZDHHC17 is specifically required for this function, as truncation mutagenesis removing the DHHC domain abolished virus-supporting activity. The palmitoylation inhibitor 2-bromopalmitate suppresses SADS-CoV infection. Genome-wide CRISPR knockout screen (HeLa cells), truncation mutagenesis of ZDHHC17, viral replication assays, 2-bromopalmitate pharmacological inhibition mBio Medium 34700373
2022 zDHHC17 can S-acylate Sprouty-2 (Spry2) and SPRED3 via zDABM-independent mechanisms in addition to zDABM-dependent binding. The cysteine-rich SPR domain of SPRED3 (and Spry2) interacts with zDHHC17 independently of the ankyrin repeat domain, revealing a novel mode of enzyme-substrate recognition. Mutational analysis of zDABM and SPR domains, Co-IP, in vitro S-acylation assays, zDHHC17 ANK-deletion mutant binding experiments The Journal of biological chemistry High 36442513
2023 ZDHHC17 is the major palmitoyl acyltransferase responsible for HSP90α palmitoylation in granulosa cells. ZDHHC17-mediated palmitoylation of HSP90α is required for CYP19A1 (aromatase) expression and androgen-to-estrogen conversion. Loss of ZDHHC17 reduces HSP90α palmitoylation, decreases CYP19A1 levels, and impairs estrogen production. siRNA knockdown of ZDHHC17 in granulosa cells, resin-assisted capture palmitoylation assay, CYP19A1 expression analysis, hormone measurement, in vivo PCOS model Molecular and cellular endocrinology Medium 37769867
2024 zDHHC17 S-palmitoylates Smad7 at Cys202, Cys225, Cys415, and Cys417 in mammary epithelial cells. Palmitoylation at Cys415 and Cys417 promotes nuclear-to-cytoplasmic translocation of Smad7, enhances Smad7 protein stability, and enforces its inhibitory effect on TGF-β-induced Smad transcriptional responses. Resin-assisted capture (RAC) and metabolic palmitoylation labeling, site-directed mutagenesis of Smad7 cysteine residues, subcellular fractionation, TGF-β/Smad transcriptional reporter assays The Journal of biological chemistry High 38876303
2026 ZDHHC17 palmitoylates CDK4, and this palmitoylation facilitates CDK4 interaction with cyclin D1. CDK4 palmitoylation depends on TRAF6-mediated K11-linked ubiquitination of CDK4. Blockade of either CDK4 palmitoylation or ubiquitination markedly reduces CDK4 kinase activity and causes cell cycle arrest. ZDHHC17 depletion reduces cell cycle progression and immune response in a high-fat-diet mouse model. 2-BP palmitoylation inhibition, ZDHHC17 siRNA/depletion, Co-IP (CDK4-cyclin D1), ubiquitination assays (K11-linkage specificity), CDK4 kinase activity assay, in vivo mouse model Advanced science Medium 42133178
2025 Drosophila Hip14 (ortholog of ZDHHC17) acts as a rate-limiting factor for lysosome formation and secretory granule-lysosome fusion, lysosomal acidification, and biosynthetic transport of lysosomal hydrolases in larval salivary glands and neurons. Hip14 overexpression accelerates these processes, and Hip14 loss in adult neurons impairs lysosome formation and neuromuscular function. Rab2 GTPase hyperactivation rescues lysosomal and neuronal defects caused by Hip14 or Patsas (HIP14L ortholog) loss. Drosophila Hip14 and patsas mutants/RNAi, larval salivary gland and neuron imaging, lysosomal acidification assays, hydrolase trafficking assays, genetic epistasis with constitutively active Rab2 bioRxivpreprint Medium bio_10.1101_2025.02.06.636816

Source papers

Stage 0 corpus · 25 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2004 Huntingtin-interacting protein HIP14 is a palmitoyl transferase involved in palmitoylation and trafficking of multiple neuronal proteins. Neuron 253 15603740
2006 Palmitoylation of huntingtin by HIP14 is essential for its trafficking and function. Nature neuroscience 247 16699508
2002 HIP14, a novel ankyrin domain-containing protein, links huntingtin to intracellular trafficking and endocytosis. Human molecular genetics 175 12393793
2011 Altered palmitoylation and neuropathological deficits in mice lacking HIP14. Human molecular genetics 95 21775500
2015 Identification of a Novel Sequence Motif Recognized by the Ankyrin Repeat Domain of zDHHC17/13 S-Acyltransferases. The Journal of biological chemistry 81 26198635
2011 Wild-type HTT modulates the enzymatic activity of the neuronal palmitoyl transferase HIP14. Human molecular genetics 78 21636527
2008 Huntingtin-interacting proteins, HIP14 and HIP14L, mediate dual functions, palmitoyl acyltransferase and Mg2+ transport. The Journal of biological chemistry 63 18794299
2020 Activation of JNK and p38 MAPK Mediated by ZDHHC17 Drives Glioblastoma Multiforme Development and Malignant Progression. Theranostics 60 31938047
2014 The palmitoyl acyltransferase HIP14 shares a high proportion of interactors with huntingtin: implications for a role in the pathogenesis of Huntington's disease. Human molecular genetics 58 24705354
2013 Memory and synaptic deficits in Hip14/DHHC17 knockout mice. Proceedings of the National Academy of Sciences of the United States of America 46 24277827
2017 Peptide array-based screening reveals a large number of proteins interacting with the ankyrin-repeat domain of the zDHHC17 S-acyltransferase. The Journal of biological chemistry 32 28882895
2020 Coupled Control of Distal Axon Integrity and Somal Responses to Axonal Damage by the Palmitoyl Acyltransferase ZDHHC17. Cell reports 30 33207199
2016 Sudden death due to paralysis and synaptic and behavioral deficits when Hip14/Zdhhc17 is deleted in adult mice. BMC biology 25 27927242
2014 Identification of binding sites in Huntingtin for the Huntingtin Interacting Proteins HIP14 and HIP14L. PloS one 25 24651384
2021 Identification of ZDHHC17 as a Potential Drug Target for Swine Acute Diarrhea Syndrome Coronavirus Infection. mBio 21 34700373
2018 Potentially critical roles of TNPO1, RAP1B, ZDHHC17, and PPM1B in the progression of coronary atherosclerosis through microarray data analysis. Journal of cellular biochemistry 20 30269354
2015 ZDHHC17 promotes axon outgrowth by regulating TrkA-tubulin complex formation. Molecular and cellular neurosciences 15 26232532
2022 S-acylation of Sprouty and SPRED proteins by the S-acyltransferase zDHHC17 involves a novel mode of enzyme-substrate interaction. The Journal of biological chemistry 12 36442513
2012 Low levels of human HIP14 are sufficient to rescue neuropathological, behavioural, and enzymatic defects due to loss of murine HIP14 in Hip14-/- mice. PloS one 12 22649491
2024 Smad7 palmitoylation by the S-acyltransferase zDHHC17 enhances its inhibitory effect on TGF-β/Smad signaling. The Journal of biological chemistry 11 38876303
2013 Dysregulated striatal neuronal processing and impaired motor behavior in mice lacking huntingtin interacting protein 14 (HIP14). PloS one 9 24376823
2013 Altered Neuronal Dynamics in the Striatum on the Behavior of Huntingtin Interacting Protein 14 (HIP14) Knockout Mice. Brain sciences 5 24961622
2023 ZDHHC17 participates in the pathogenesis of polycystic ovary syndrome by affecting androgen conversion to estrogen in granulosa cells. Molecular and cellular endocrinology 3 37769867
2026 ZDHHC17-Mediated CDK4 Palmitoylation Drives Cell Cycle Progression and Orchestrates Cancer Immune Surveillance. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 0 42133178
2025 DNA Methylation-Regulated ZDHHC17 Promotes the Risk of Facial Skin Aging. Clinical, cosmetic and investigational dermatology 0 41445853

Missed literature

Know a paper Affinage missed for ZDHHC17? Flag it for the maintainers and the community.

No submissions yet.