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Showing ZDHHC9 — DHHC9 is a alias.

ZDHHC9

Palmitoyltransferase ZDHHC9 · UniProt Q9Y397

Length
364 aa
Mass
40.9 kDa
Annotated
2026-06-11
36 papers in source corpus 23 papers cited in narrative 23 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ZDHHC9 is an integral-membrane DHHC-family protein S-palmitoyltransferase that catalyzes lipid modification of substrate cysteines through a two-step mechanism requiring formation of an autopalmitoyl-enzyme intermediate, and it acts in obligate partnership with GCP16 (PMID:16000296, PMID:24811172). GCP16 stabilizes ZDHHC9 by preventing its aggregation, and only the properly folded ZDHHC9–GCP16 complex is enzymatically active; complex formation depends on a conserved C-terminal cysteine motif, and the complex localizes to the Golgi apparatus (PMID:16000296, PMID:37035671). The enzyme palmitoylates a broad substrate repertoire to control substrate membrane targeting, stability, or activity: it palmitoylates H-Ras and N-Ras to direct their membrane localization (PMID:16000296, PMID:24127608), GLUT1 (Cys207) to maintain its plasma-membrane localization and support glycolysis (PMID:34620861), LAMTOR1 (Cys3/4) to promote mTORC1 recruitment to the lysosome (PMID:41856969), and numerous other targets including β-catenin, STRN4, ACSL4, PCBP1, KLF5, STAT1, CD38, hnRNPU, and CD36, frequently regulating their stability or downstream signaling output across cancer and fibrosis contexts (PMID:37865665, PMID:40903842, PMID:42085610, PMID:40121269). In the nervous system, ZDHHC9 is required for palmitoylation of Ras and TC10, shaping dendritic arborization, inhibitory synapse number, and excitatory/inhibitory balance (PMID:31747610), and it is the dominant palmitoyltransferase in myelinating oligodendrocytes where it palmitoylates Myelin Basic Protein to support normal myelin structure (PMID:41031565). Loss-of-function mutations in ZDHHC9 impair the autopalmitoylation step and ZDHHC9–GCP16 complex formation and cause X-linked intellectual disability with Marfanoid habitus (PMID:17436253, PMID:24811172, PMID:37035671).

Mechanistic history

Synthesis pass · year-by-year structured walk · 9 steps
  1. 2005 High

    Establishing that ZDHHC9 is a bona fide palmitoyltransferase answered whether it had intrinsic enzymatic activity and revealed that this activity requires a partner subunit.

    Evidence Co-IP and in vitro palmitoylation with purified DHHC9·GCP16 complex showing H-Ras/N-Ras specificity and Golgi co-distribution

    PMID:16000296

    Open questions at the time
    • Substrate range beyond Ras isoforms not defined
    • Structural basis of GCP16 dependence not resolved
    • Catalytic mechanism not yet dissected
  2. 2007 Medium

    Identifying loss-of-function ZDHHC9 mutations in XLID families connected a palmitoyltransferase deficiency to a human neurodevelopmental disease for the first time.

    Evidence DNA sequencing of 250 XLID families identifying four independent mutations; mechanism inferred from Ras palmitoylation

    PMID:17436253

    Open questions at the time
    • No direct cellular rescue in this study
    • Neuronal substrate consequences not measured directly
    • Marfanoid habitus mechanism unexplained
  3. 2013 Medium

    Demonstrating miR-134 control of DHHC9 mRNA defined how ZDHHC9 expression is dynamically tuned to neuronal activity to set H-Ras membrane targeting.

    Evidence CLASH miRNA-mRNA trapping, miRNA sensor, and H-Ras membrane localization reporter after bicuculline stimulation in somatostatin interneurons

    PMID:24127608

    Open questions at the time
    • Single lab
    • In vivo relevance of the miR-134 axis not established
    • Effect on other substrates not tested
  4. 2014 High

    Showing that XLID variants R148W and P150S reduce the palmitoyl-enzyme intermediate located the disease defect at the autopalmitoylation step of the two-step catalytic cycle.

    Evidence In vitro autopalmitoylation assays with purified mutant ZDHHC9

    PMID:24811172

    Open questions at the time
    • Does not show downstream substrate consequences in neurons
    • Other XLID mutations not all tested
    • Step-two transfer kinetics not quantified
  5. 2019 High

    Linking Zdhhc9 loss to dendritic and inhibitory-synapse phenotypes through specific substrates explained the neuronal basis of the XLID/epilepsy phenotype.

    Evidence Zdhhc9 KO mouse hippocampal neurons with morphology, electrophysiology, and Ras/TC10 palmitoylation assays

    PMID:31747610

    Open questions at the time
    • Circuit-level mechanism of seizures incomplete
    • Relative contribution of Ras vs TC10 not quantified
    • Human variant correspondence not modeled
  6. 2023 High

    Defining GCP16 as an anti-aggregation chaperone and identifying the C-terminal cysteine motif clarified why ZDHHC9 needs a partner and why XLID mutations destabilize it.

    Evidence Size-exclusion chromatography, in vitro PAT assay, and CCM mutagenesis of the reconstituted complex

    PMID:37035671

    Open questions at the time
    • High-resolution structure of the complex not determined
    • Mechanism by which CCM mediates assembly not resolved
    • Single lab
  7. 2023 High

    A series of substrate-mapping studies expanded ZDHHC9 from a Ras enzyme to a broad regulator of substrate stability, localization, and signaling across diverse tissues.

    Evidence ABE/Co-IP palmitoylation assays with site mutagenesis defining β-catenin, GLUT1 (Cys207), Rab3gap1, and Bip/GRP78 (Cys420) substrates in fibrosis, glioblastoma, cardiomyocyte, and ER-stress models

    PMID:34620861 PMID:37325411 PMID:37865665 PMID:39002690

    Open questions at the time
    • Substrate selectivity determinants not defined
    • How one enzyme accesses such varied substrates unclear
    • Tissue-specific cofactors not identified
  8. 2025 Medium

    Identifying ZDHHC9 as the dominant oligodendrocyte palmitoyltransferase that modifies MBP added a myelination arm to the XLID mechanism.

    Evidence Cell-type expression analysis, Golgi-outpost imaging, OL fate tracing, and MBP palmitoylation assays in heterologous cells and Zdhhc9 KO brain

    PMID:41031565

    Open questions at the time
    • MBP palmitoylation site not pinpointed
    • Functional myelin consequence at behavioral level not connected
    • Single lab
  9. 2026 Medium

    An accumulating set of cancer studies showed ZDHHC9 palmitoylation rewires multiple signaling and metabolic pathways via stabilization or relocalization of effectors.

    Evidence ABE/Co-IP with cysteine-specific mutagenesis defining STRN4 (Cys701)–YAP, LAMTOR1–mTORC1, ACSL4 (Cys595)–ferroptosis, PCBP1 (Cys109)–SLC7A11, KLF5 (Cys438)–cAMP, STAT1 (Cys577), CD38 (Cys16), hnRNPU, CD36, and KRAS, with in vivo tumor models

    PMID:40121269 PMID:40903842 PMID:41087383 PMID:41087856 PMID:41419885 PMID:41535416 PMID:41711908 PMID:41856969 PMID:41882103 PMID:42085610

    Open questions at the time
    • Most defined in single labs without reconstitution
    • Physiological vs pathological substrate prioritization unclear
    • Reversal by depalmitoylases mapped only for some substrates (APT1)

Open questions

Synthesis pass · forward-looking unresolved questions
  • How ZDHHC9 achieves such broad substrate recognition, and which substrates dominate in each physiological versus disease context, remains the central open question.
  • No structure of substrate-bound ZDHHC9–GCP16
  • No defined substrate-selectivity code
  • Quantitative substrate hierarchy across tissues unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 7 GO:0016740 transferase activity 3
Localization
GO:0005794 Golgi apparatus 2
Pathway
R-HSA-162582 Signal Transduction 7 R-HSA-392499 Metabolism of proteins 4 R-HSA-112316 Neuronal System 2
Partners
CTNNB1GLUT1GOLGA7HRASKRASLAMTOR1NRASSTRN4
Complex memberships
ZDHHC9-GCP16 palmitoyltransferase complex

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2005 ZDHHC9 (DHHC9) forms a protein complex with GCP16 and together they function as a human protein palmitoyltransferase with specificity for H-Ras and N-Ras, but not myristoylated Gαi1 or GAP-43. DHHC9 is an integral membrane protein with a DHHC cysteine-rich domain; GCP16 is required for DHHC9 enzymatic activity and protein stability. The complex co-distributes in the Golgi apparatus. Co-immunoprecipitation, purified DHHC9·GCP16 in vitro palmitoylation assay, subcellular fractionation/co-distribution studies The Journal of biological chemistry High 16000296
2007 Loss-of-function mutations in ZDHHC9 (frameshift, splice-site, and missense) cause X-linked intellectual disability associated with Marfanoid habitus, establishing ZDHHC9 as the first palmitoyltransferase whose disruption causes intellectual disability. The mechanism involves altered palmitoylation of NRAS and HRAS, affecting their subcellular localization. DNA sequencing of 250 XLID families identifying four independent mutations in ZDHHC9; functional interpretation based on known palmitoyltransferase activity American journal of human genetics Medium 17436253
2014 Two XLID-associated missense variants of ZDHHC9, R148W and P150S, reduce the steady-state level of the palmitoyl-ZDHHC9 intermediate, demonstrating that these mutations impair the autopalmitoylation step (step 1) of the two-step palmitoyltransferase reaction mechanism. In vitro autopalmitoylation assay with purified mutant ZDHHC9 proteins; biochemical characterization of enzyme-palmitoyl intermediate The Journal of biological chemistry High 24811172
2013 miR-134 directly interacts with DHHC9 mRNA in somatostatin interneurons. Activity-dependent stimulation (bicuculline treatment) decreases DHHC9 expression in a miR-134-dependent manner, reducing membrane localization of H-Ras, establishing a miR-134 → DHHC9 → H-Ras membrane targeting axis. miRNA-mRNA complex trapping assay (CLASH), ratiometric miRNA sensor, DHHC9 expression measurement after bicuculline treatment, H-Ras membrane localization reporter assay Proceedings of the National Academy of Sciences of the United States of America Medium 24127608
2019 Loss of Zdhhc9 in hippocampal neurons causes shorter dendritic arbors (via impaired Ras palmitoylation) and fewer inhibitory synapses (via impaired TC10 palmitoylation), altering the excitatory-to-inhibitory balance. Zdhhc9 knockout mice exhibit seizure-like activity and altered synaptic currents. Hippocampal neuron cultures from Zdhhc9 KO mice; dendritic morphology quantification; inhibitory synapse immunostaining; electrophysiology (mEPSC/mIPSC recording); palmitoylation assay for Ras and TC10 substrates Cell reports High 31747610
2021 ZDHHC9 palmitoylates GLUT1 at Cys207, and this S-palmitoylation is required to maintain GLUT1 plasma membrane localization. Knockout of ZDHHC9 or C207S mutation abrogates palmitoylation, causes GLUT1 mislocalization, impairs glycolysis, cell proliferation, and glioblastoma tumorigenesis in vivo. Acyl-biotin exchange (ABE) assay, ZDHHC9 knockout, site-directed mutagenesis (C207S), immunofluorescence for GLUT1 localization, glycolysis assay, xenograft tumor model Nature communications High 34620861
2023 GCP16 stabilizes DHHC9 by preventing its aggregation through protein complex formation. Only properly folded DHHC9-GCP16 complex is enzymatically active in vitro. The C-terminal cysteine motif (CCM) conserved in the DHHC9 subfamily is required for DHHC9-GCP16 complex formation and activity. XLID mutations in ZDHHC9 reduce protein stability and complex formation with GCP16. Size-exclusion chromatography, in vitro palmitoyl acyltransferase assay, mutagenesis of CCM, co-expression stability assays Frontiers in physiology High 37035671
2023 ZDHHC9 palmitoylates β-catenin, promoting its ubiquitination and degradation, thereby suppressing Wnt/β-catenin signaling. Acyl protein thioesterase 1 (APT1) depalmitoylates β-catenin and opposes this effect. DHHC9 ablation in tubular cells aggravates renal fibrosis, while DHHC9 overexpression is protective. Co-immunoprecipitation, ABE palmitoylation assay, ubiquitination assay, genetic knockout and overexpression in mouse UUO and IRI fibrosis models Nature communications High 37865665
2023 ZDHHC9 palmitoylates Rab3gap1, which causes Rab3gap1 spatial segregation from Rab3a, elevates Rab3a-GTP levels, promotes formation of Rab3a-positive peripheral vesicles, and impairs exocytosis, thereby limiting atrial natriuretic peptide (ANP) release from cardiomyocytes. Palmitoylation assay, co-immunoprecipitation, subcellular localization imaging, Rab3a-GTP pull-down, ANP secretion assay in cardiomyocytes JACC. Basic to translational science Medium 37325411
2024 ZDHHC9 binds to and palmitoylates Bip/GRP78 at Cys420, enhancing Bip protein stability and preserving its ER localization, thereby inhibiting the unfolded protein response (UPR). SP1 transcriptionally activates ZDHHC9 expression. Co-immunoprecipitation, ABE palmitoylation assay, site-directed mutagenesis (C420), subcellular localization imaging (ER marker), UPR reporter assays, ZDHHC9 knockdown Cancer letters Medium 39002690
2025 ZDHHC9 localizes to Golgi outposts in oligodendrocyte (OL) processes and is the most highly expressed PAT in myelinating OLs. Zdhhc9 KO mice display myelin morphological and structural abnormalities and impaired MBP palmitoylation. ZDHHC9 palmitoylates Myelin Basic Protein (MBP) in heterologous cells, and MBP palmitoylation is reduced in Zdhhc9 KO brain. Cell-type-specific expression analysis, live imaging/immunofluorescence for Golgi outpost localization, OL fate tracing, sparse cell labeling morphology, MBP palmitoylation assay in heterologous cells and KO brain eLife Medium 41031565
2025 ZDHHC9 palmitoylates STRN4 (a STRIPAK complex component) at Cys701. This palmitoylation reduces YAP phosphorylation, promotes YAP nuclear translocation, and activates Hippo pathway transcriptional targets (CCN1, CCN2, ANKRD1), driving cancer cell migration. Proteomic analysis, co-immunoprecipitation, site-directed mutagenesis (C701), YAP phosphorylation and nuclear localization assays, ZDHHC9 knockdown migration assays in vitro and in vivo metastasis assay Journal of cellular and molecular medicine Medium 40903842
2025 ZDHHC9 palmitoylates LAMTOR1 at Cys3/4 residues, enhancing mTORC1 recruitment to the lysosomal surface and activating mTOR signaling in renal cell carcinoma. Co-immunoprecipitation, ABE palmitoylation assay, site-directed mutagenesis (Cys3/4), mTORC1 lysosomal recruitment assay, ZDHHC9 knockdown with mTOR signaling readouts Cell death & disease Medium 41856969
2025 ZDHHC9 palmitoylates hnRNPU at Cys497 and Cys607, increasing its protein stability. This stabilization promotes SAT1 transcription, enhancing spermine catabolism, and contributes to prostate cancer proliferation. Mass spectrometry, co-immunoprecipitation, site-directed mutagenesis (Cys497/607), palmitoylation assay, RNA sequencing, xenograft model Journal of translational medicine Medium 41419885
2025 ZDHHC9 palmitoylates ACSL4 at Cys595, enhancing ACSL4 enzymatic activity, promoting lipid peroxidation, and driving ferroptosis in corpus cavernosum fibroblasts. PI3K/AKT signaling is identified as an upstream regulator of ZDHHC9 expression in this context. ABE palmitoylation assay, site-directed mutagenesis (C595), ACSL4 enzymatic activity assay, lipid peroxidation measurement, ZDHHC9 knockdown with siRNA-LNPs in vivo mouse model Advanced science Medium 42085610
2026 ZDHHC9 palmitoylates PCBP1 at Cys109, inhibiting PCBP1 ubiquitination and thereby stabilizing it. Stabilized PCBP1 promotes SLC7A11 RNA stability, suppressing ferroptosis and promoting gastric cancer liver metastasis. Co-immunoprecipitation, LC-MS, ABE palmitoylation assay, site-directed mutagenesis (C109), ubiquitination assay, RNA stability assay, in vivo metastasis model NPJ precision oncology Medium 41535416
2026 ZDHHC9 palmitoylates KLF5 at Cys438, enhancing ADCY4 activity and elevating intracellular cAMP levels, thereby activating the cAMP/PKA/CREB signaling pathway to promote colorectal cancer cell proliferation and migration. ABE palmitoylation assay, site-directed mutagenesis (C438), RNA sequencing, ADCY4 activity assay, cAMP measurement, ZDHHC9 knockdown in vitro and in vivo Oncogene Medium 41882103
2026 ZDHHC9 palmitoylates STAT1 at Cys577, and this palmitoylation competes with/converts to Tyr701 phosphorylation via the JAK1-STAT1 pathway, modulating STAT1 nuclear activity and downstream gene transcription to promote gastric cancer progression. ABE palmitoylation assay, co-immunoprecipitation, site-directed mutagenesis (Cys577), immunofluorescence, confocal imaging, Western blot for JAK1-STAT1 phosphorylation, ZDHHC9 knockdown Journal of gastroenterology Medium 41711908
2025 ZDHHC9 interacts with KRAS by co-immunoprecipitation and promotes osteosarcoma progression by palmitoylating KRAS to activate the RAS/MAPK signaling pathway (Raf1, ERK1/2 activation). Co-immunoprecipitation, molecular docking, proteomic sequencing, Western blot for MAPK pathway, xenograft model, KRAS overexpression rescue experiment Scientific reports Medium 41087383
2025 ZDHHC9 palmitoylates CD36 (binding confirmed by Co-IP), which promotes CD36 plasma membrane localization and formation of the CD36/Fyn/Lyn complex. This activates the JNK1 pathway and inhibits ERK1/2, impairing mammary epithelial cell proliferation under high-fat conditions. Co-immunoprecipitation, ABE palmitoylation assay, site-directed mutagenesis of CD36 cysteines, immunofluorescence for CD36 localization, DHHC9 knockdown, in vivo mouse HFD model Cellular & molecular biology letters Medium 41087856
2023 ZDHHC9 knockdown reduces PD-L1 palmitoylation and promotes PD-L1 protein degradation in lung adenocarcinoma cells, establishing ZDHHC9 as the palmitoyl transferase that stabilizes PD-L1 through palmitoylation. ZDHHC9 knockdown/overexpression, palmitoylation assay, PD-L1 protein stability measurement, proliferation and migration assays In vitro cellular & developmental biology. Animal Low 37002491
2025 ZDHHC9 palmitoylates CD38 at Cys16, which is required to maintain CD38 protein expression in tumor cells. APT1 acts as the opposing depalmitoylase. A competitive peptide blocking CD38 palmitoylation decreases CD38 expression and suppresses tumor progression in vivo. ABE palmitoylation assay, site-directed mutagenesis (Cys16), APT1 depalmitoylation assay, competitive peptide in vivo tumor model Communications biology Medium 40121269
2025 ZDHHC9 palmitoylates PKG1 in osteoblasts, and this palmitoylation alters the distance between the ER and mitochondria and changes MAMs-related protein expression, contributing to osteoblast dysfunction in T2DM. Co-immunoprecipitation, fluorescence co-localization, Zdhhc9 knockdown and Prkg1 silencing in MC3T3-E1 cells and T2DM mouse model, MAMs distance measurement Journal of dental research Low 40102769

Source papers

Stage 0 corpus · 36 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 DHHC9 and GCP16 constitute a human protein fatty acyltransferase with specificity for H- and N-Ras. The Journal of biological chemistry 290 16000296
2021 DHHC9-mediated GLUT1 S-palmitoylation promotes glioblastoma glycolysis and tumorigenesis. Nature communications 211 34620861
2007 Mutations in ZDHHC9, which encodes a palmitoyltransferase of NRAS and HRAS, cause X-linked mental retardation associated with a Marfanoid habitus. American journal of human genetics 140 17436253
2007 Differential expression of DHHC9 in microsatellite stable and instable human colorectal cancer subgroups. British journal of cancer 65 17519897
2023 Palmitoyltransferase DHHC9 and acyl protein thioesterase APT1 modulate renal fibrosis through regulating β-catenin palmitoylation. Nature communications 59 37865665
2023 Targeting ZDHHC9 potentiates anti-programmed death-ligand 1 immunotherapy of pancreatic cancer by modifying the tumor microenvironment. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 47 36963362
2014 Mutations in the X-linked intellectual disability gene, zDHHC9, alter autopalmitoylation activity by distinct mechanisms. The Journal of biological chemistry 47 24811172
2019 The X-Linked Intellectual Disability Gene Zdhhc9 Is Essential for Dendrite Outgrowth and Inhibitory Synapse Formation. Cell reports 44 31747610
2013 MicroRNA-134 activity in somatostatin interneurons regulates H-Ras localization by repressing the palmitoylation enzyme, DHHC9. Proceedings of the National Academy of Sciences of the United States of America 41 24127608
2024 ZDHHC9-mediated Bip/GRP78 S-palmitoylation inhibits unfolded protein response and promotes bladder cancer progression. Cancer letters 32 39002690
2015 Epilepsy, cognitive deficits and neuroanatomy in males with ZDHHC9 mutations. Annals of clinical and translational neurology 30 26000327
2013 Expanding the clinical phenotype of patients with a ZDHHC9 mutation. American journal of medical genetics. Part A 28 24357419
2023 Involvement of ZDHHC9 in lung adenocarcinoma: regulation of PD-L1 stability via palmitoylation. In vitro cellular & developmental biology. Animal 25 37002491
2023 zDHHC9 Regulates Cardiomyocyte Rab3a Activity and Atrial Natriuretic Peptide Secretion Through Palmitoylation of Rab3gap1. JACC. Basic to translational science 23 37325411
2018 Disruption of the Zdhhc9 intellectual disability gene leads to behavioural abnormalities in a mouse model. Experimental neurology 21 29944857
2022 ZDHHC9 promotes colon tumor growth by inhibiting effector T cells. Oncology letters 17 36419754
2023 GCP16 stabilizes the DHHC9 subfamily of protein acyltransferases through a conserved C-terminal cysteine motif. Frontiers in physiology 16 37035671
2017 The first patient with sporadic X-linked intellectual disability with de novo ZDHHC9 mutation identified by targeted next-generation sequencing. European journal of medical genetics 14 28687527
2025 ZDHHC9-mediated CD38 palmitoylation stabilizes CD38 expression and promotes pancreatic cancer growth. Communications biology 11 40121269
2009 Expression of microRNAs is not related to increased expression of ZDHHC9 in hind leg muscles of splay leg piglets. Molecular and cellular probes 10 19748569
2023 ZDHHC9: a promising therapeutic target for triple-negative breast cancer through immune modulation and immune checkpoint blockade resistance. Discover oncology 9 37875591
2018 Expanding the molecular basis and phenotypic spectrum of ZDHHC9-associated X-linked intellectual disability. American journal of medical genetics. Part A 9 29681091
2022 ZDHHC9 X-linked intellectual disability: Clinical and molecular characterization. American journal of medical genetics. Part A 5 36416207
2025 ZDHHC9-Mediated PKG1 Affects Osteogenesis by Regulating MAMs in T2DM. Journal of dental research 3 40102769
2025 Inhibition of DHHC9-mediated CD36 palmitoylation lessens high-fat diet (HFD)-induced impairment of pubertal mammary gland development through the JNK-ERK pathway. Cellular & molecular biology letters 3 41087856
2025 Micro-scale control of oligodendrocyte morphology and myelination by the intellectual disability-linked protein acyltransferase ZDHHC9. eLife 2 41031565
2026 ASF1B promotes gastric cancer liver metastasis through inhibiting ZDHHC9/PCBP1/ SLC7A11 signaling axis mediated ferroptosis. NPJ precision oncology 1 41535416
2025 The X-Linked Intellectual Disability Gene, ZDHHC9 , Is Important for Oligodendrocyte Subtype Determination and Myelination. Glia 1 40105030
2026 Targeting the ZDHHC9-mediated STAT1 palmitoylation-phosphorylation conversion inhibits gastric cancer progression. Journal of gastroenterology 0 41711908
2026 Anatid herpesvirus 1 UL51 protein is palmitoylated by DHHC9 and DHHC18 for viral replication and virulence. PLoS pathogens 0 41855189
2026 ZDHHC9 palmitoylates LAMTOR1 to promote renal cell carcinoma malignant progression. Cell death & disease 0 41856969
2026 ZDHHC9-mediated KLF5 palmitoylation enhances the cAMP/PKA/CREB axis to promote colorectal cancer progression. Oncogene 0 41882103
2026 ZDHHC9-Mediated Palmitoylation of ACSL4 Drives Ferroptosis in Diabetes Mellitus-Induced Erectile Dysfunction. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 0 42085610
2025 Pharmacological Targeting of DHHC9-Mediated STRN4 Palmitoylation to Suppress YAP-Driven Cancer Metastasis. Journal of cellular and molecular medicine 0 40903842
2025 ZDHHC9 promotes osteosarcoma progression via KRAS-associated enhancement of the RAS/MAPK signaling pathway. Scientific reports 0 41087383
2025 ZDHHC9 and spermine metabolism: a palmitoylation-driven pathway to prostate carcinogenesis. Journal of translational medicine 0 41419885

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