Affinage

KRT14

Keratin, type I cytoskeletal 14 · UniProt P02533

Length
472 aa
Mass
51.6 kDa
Annotated
2026-06-10
46 papers in source corpus 17 papers cited in narrative 17 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

KRT14 encodes a type I intermediate filament keratin that heterodimerizes with KRT5 to form the structural cytoskeleton of basal epithelial cells, and it marks self-renewing basal progenitor populations that regenerate epithelia and serve as cells of origin for cancer (PMID:27320313). Filament assembly depends on conserved rod-domain motifs: mutations in the helix initiation/termination motifs produce the most severe epidermolysis bullosa simplex phenotype (PMID:21375516), and pathogenicity is determined by the specific substitution, with C-terminal 2B-helix residues stabilizing the KRT14:KRT5 heterodimer (PMID:21593775). Mutant KRT14 acts in a dominant-negative manner by forming cytoplasmic aggregates that disrupt intermediate filament polymerization, as shown by gene correction restoring normal filament organization and skin architecture (PMID:20571545, PMID:28888469). Distinct truncating mutations in the nonhelical N-terminal head domain cause Naegeli-Franceschetti-Jadassohn syndrome and dermatopathia pigmentosa reticularis through haploinsufficiency, with reduced K14 increasing susceptibility to TNF-alpha-induced apoptosis in basal keratinocytes (PMID:16960809, PMID:18049449). Beyond its cytoskeletal role, KRT14 functions as a signaling scaffold: it binds stratifin to control airway basal cell differentiation (PMID:36512409), drives cisplatin resistance in bladder cancer by interacting with eIF4H through its head domain to selectively promote ACOX2 mRNA translation (PMID:41444318), and promotes invasive bladder cancer by stabilizing IGF2BP1 via a defined nuclear-export-signal interaction (PMID:42261838). Its expression is set by chromatin and RNA-level regulators including EZH2/SP1 in triple-negative breast cancer (PMID:36446780) and a destabilizing lncRNA upstream of mTOR/AKT signaling in pulmonary fibrosis (PMID:40111939).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2006 High

    Established that head-domain truncating mutations define a disease class distinct from rod-domain EBS and revealed an anti-apoptotic function for the KRT14 N-terminus.

    Evidence Linkage and sequencing across 5 NFJS/DPR families with ultrastructural analysis of basal keratinocytes

    PMID:16960809

    Open questions at the time
    • Did not define the molecular mechanism linking head-domain loss to apoptosis
    • No direct biochemical readout of the protective activity
  2. 2007 Medium

    Showed NFJS mutations act through haploinsufficiency and mechanistically tied K14 loss to enhanced pro-apoptotic signaling.

    Evidence siRNA knockdown in HaCaT keratinocytes with TNF-alpha apoptosis assay and doxycycline rescue

    PMID:18049449

    Open questions at the time
    • Single cell line, single lab
    • Apoptotic effector pathway downstream of TNF-alpha not resolved
  3. 2010 Medium

    Demonstrated that mutant KRT14 exerts dominant-negative activity by correcting the mutant allele and restoring normal skin.

    Evidence AAV gene targeting in EBS patient keratinocytes and grafting onto athymic mice

    PMID:20571545

    Open questions at the time
    • Single lab
    • Correction efficiency and durability in vivo not fully characterized
  4. 2011 High

    Defined a genotype-phenotype correlation in which helix boundary motif mutations produce the most severe EBS, and showed substitution identity—not just position—dictates pathogenicity.

    Evidence Sequencing of 76 EBS probands and transfection-based filament assays distinguishing p.Ala413Pro from benign p.Ala413Thr

    PMID:21375516 PMID:21593775

    Open questions at the time
    • Quantitative assembly defects not measured biochemically
    • Mechanism by which proline distorts the helix not directly visualized
  5. 2014 Low

    Proposed an atomistic basis for heterodimer stability via π-stacking between KRT14 and KRT5 tyrosines.

    Evidence Sanger sequencing and molecular dynamics simulations of the KRT14:KRT5 2B helix

    PMID:24981776

    Open questions at the time
    • Computational prediction only, no in vitro validation of the interaction
    • Functional consequence on filament assembly not tested experimentally
  6. 2016 High

    Identified KRT14 as a marker of self-renewing basal progenitors that regenerate urothelium and seed urothelial cancer, extending KRT14 from structural marker to functional stem-cell lineage label.

    Evidence Genetic lineage tracing with KRT14-Cre in mouse homeostasis, injury, and tumor initiation models

    PMID:27320313

    Open questions at the time
    • Whether KRT14 protein actively drives stemness versus merely marking it is unresolved
  7. 2016 Medium

    Linked KRT14 to osteoblast matrix mineralization via the AMPK/mTOR pathway.

    Evidence siRNA knockdown in rat primary osteoblasts with pathway inhibitors and AFM ultrastructure

    PMID:26956522

    Open questions at the time
    • Single lab
    • Direct molecular connection between KRT14 and AMPK/mTOR not defined
  8. 2017 Medium

    Placed basal keratin expression under retinoic acid control during salivary epithelial development.

    Evidence Isolated embryonic mouse salivary epithelium explants treated with RA signaling inhibitors

    PMID:27884045

    Open questions at the time
    • Transcriptional mediators between RA signaling and the Krt5/Krt14 promoters not identified
  9. 2019 Medium

    Defined an invasion-specific role for KRT14+ leader cells distinct from proliferation in ovarian cancer.

    Evidence In vitro mesothelial clearance/invasion model with KRT14 loss-of-function and viability/proliferation controls

    PMID:31443478

    Open questions at the time
    • Molecular effectors of invasion downstream of KRT14 not identified
    • In vivo metastasis not tested in this study
  10. 2022 High

    Resolved transcriptional and protein-interaction control of KRT14 across tissues: EZH2/SP1 chromatin regulation drives KRT14 in TNBC metastasis, and KRT14-stratifin binding governs airway basal cell differentiation.

    Evidence EZH2 knockdown, H3K27me3 inhibition and SP1 ChIP in TNBC; CRISPR KO and Co-IP in primary airway basal cells

    PMID:36446780 PMID:36512409

    Open questions at the time
    • Whether stratifin binding is direct or filament-mediated not fully dissected
    • How KRT14 loss elevates ΔNp63α mechanistically unresolved
  11. 2022 Medium

    Used KRT14+ cells to define a progenitor compartment whose autophagy restrains gasdermin D-mediated pyroptosis in salivary gland homeostasis.

    Evidence Atg5 conditional knockout under Krt14-Cre with pyroptosis markers and pharmacological rescue

    PMID:36342387

    Open questions at the time
    • KRT14 protein function not directly implicated; KRT14-Cre used as a cell-type driver
    • Mechanism linking ATG5 loss to gasdermin D activation not defined
  12. 2025 Medium

    Established KRT14 as a signaling scaffold in bladder cancer through two defined direct interactions: head-domain binding to eIF4H driving ACOX2 translation and cisplatin resistance, and a nuclear-export-signal interaction with IGF2BP1 driving invasion.

    Evidence Co-IP with domain and residue-level mapping, translation and mRNA stability assays, xenograft/BMIBC mouse models and patient tissue

    PMID:41444318 PMID:42261838

    Open questions at the time
    • Both interactions from single labs without reciprocal independent confirmation
    • How a cytoskeletal keratin engages translation machinery structurally remains unclear
  13. 2025 Medium

    Positioned KRT14 downstream of a destabilizing lncRNA and upstream of mTOR/AKT signaling in pulmonary fibrosis.

    Evidence RNA pulldown-MS and RIP for lncRNA ABCE1-5 binding to KRT14 mRNA, with KRT14 knockdown epistasis and AAV6 in vivo bleomycin model

    PMID:40111939

    Open questions at the time
    • Single lab
    • Mechanism by which KRT14 activates mTOR/AKT phosphorylation not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How a single keratin reconciles its cytoskeletal scaffolding function with diverse signaling roles—translation control, RNA-binding-protein stabilization, and apoptosis regulation—remains mechanistically unintegrated.
  • No unifying structural model linking filament assembly to non-structural partner binding
  • Independent confirmation of the eIF4H and IGF2BP1 interactions outside originating labs is lacking
  • Whether signaling functions require assembled filaments or soluble KRT14 is unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 4 GO:0008092 cytoskeletal protein binding 3 GO:0060090 molecular adaptor activity 3
Localization
GO:0005829 cytosol 2 GO:0005856 cytoskeleton 2
Pathway
R-HSA-1643685 Disease 4 R-HSA-1266738 Developmental Biology 3 R-HSA-5357801 Programmed Cell Death 2
Partners
EIF4HIGF2BP1KRT5SFN

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2006 Heterozygous nonsense or frameshift mutations in the E1/V1-encoding region (nonhelical head domain) of KRT14 cause Naegeli-Franceschetti-Jadassohn syndrome (NFJS) and dermatopathia pigmentosa reticularis (DPR), distinct from rod-domain mutations that cause EBS. Ultrastructural examination showed increased apoptotic activity in the basal cell layer, suggesting the N-terminal domain of KRT14 protects against apoptosis. Linkage analysis (LOD score 8.3), direct sequencing of KRT14 in 5 families, ultrastructural examination of patient skin biopsies, immunofluorescence American journal of human genetics High 16960809
2007 NFJS-causing KRT14 mutations result in haploinsufficiency for K14 protein. Decreased KRT14 expression in HaCaT keratinocytes increases susceptibility to TNF-alpha-induced apoptosis, establishing a mechanistic link between K14 loss and enhanced pro-apoptotic signaling in basal keratinocytes. siRNA knockdown of KRT14 in HaCaT cells, apoptosis assay with TNF-alpha stimulation, doxycycline rescue experiment The Journal of investigative dermatology Medium 18049449
2011 Mutations in the helix boundary motifs (helix initiation and termination motifs) of the KRT14 rod domain are associated with the most severe EBS phenotype (Dowling-Meara), establishing a genotype-phenotype correlation based on structural disruption of keratin intermediate filament assembly. Direct sequencing of KRT14 coding sequence and cDNA in 76 EBS probands; immunofluorescence microscopy with anti-K14/K5 antibodies on skin biopsies The British journal of dermatology High 21375516
2011 Two different amino acid substitutions at KRT14 position Ala413 produce different clinical outcomes: p.Ala413Pro (proline) causes pathogenic structural distortion of the keratin filament and keratin clumping in transfected cells, while p.Ala413Thr (threonine) does not disrupt filament structure and is a benign polymorphism. This demonstrates that the nature of the amino acid change, not just its position, determines pathogenicity. In silico structural modeling, in vitro transfection of HaCaT cells with mutant KRT14 cDNA constructs, quantification of keratin-clumped cells The Journal of investigative dermatology Medium 21593775
2014 The EIATYR/KLLEGE motif at the C-terminal end of KRT14's 2B helix (around residues 413-418) is critical for maintaining structural stability of the KRT14:KRT5 heterodimer. Molecular dynamics simulations show that p.Leu418Gln disrupts intermolecular π-stacking between KRT14:Tyr415 and KRT5:Tyr470. Sanger sequencing, molecular dynamics simulations of KRT14:KRT5 heterodimer structure Experimental dermatology Low 24981776
2016 KRT14 expression marks a minor subpopulation of bladder basal cells that possesses self-renewal capacity and gives rise to all cell types of the urothelium during natural and injury-induced regeneration. These KRT14+ cells also represent cells of origin of urothelial cancer. Genetic lineage tracing in mice using KRT14-Cre, injury-induced regeneration assays, urothelial cancer initiation experiments Nature communications High 27320313
2016 KRT14 regulates osteoblast matrix mineralization. siRNA knockdown of Krt14 in rat primary osteoblasts reduces ColI and osteocalcin gene expression, decreases soluble osteocalcin and collagen levels, and attenuates mineralization induced by kaempferol via the AMPK/mTOR pathway. siRNA knockdown of Krt14, gene expression analysis, AMPK/mTOR inhibitor experiments, AFM ultrastructural analysis Life sciences Medium 26956522
2017 Inhibition of retinoic acid (RA) signaling upregulates Krt5 and Krt14 expression in isolated salivary gland epithelium explants independently of stem cell markers, demonstrating that RA signaling directly represses basal keratin expression in developing salivary epithelium. Isolated embryonic mouse salivary gland epithelium explant culture with RA signaling inhibitors, gene expression analysis Developmental dynamics Medium 27884045
2019 A sub-population of ovarian cancer spheroid cells expressing KRT14 functions as 'leader cells' that mediate mesothelial clearance and invasion. Loss of KRT14 completely abrogates invasive capacity without affecting cell viability or proliferation, indicating an invasion-specific role. In vitro invasion model with imaging mass spectrometry, KRT14 siRNA/knockout loss-of-function, viability and proliferation assays Cancers Medium 31443478
2022 EZH2-mediated H3K27me3 promotes KRT14 transcription (not repression) in TNBC cells by attenuating binding of the transcriptional repressor SP1 to the KRT14 promoter. KRT14 loss significantly reduces TNBC migration, invasion, and peritoneal metastasis. EZH2 knockdown, H3K27me3 inhibitor (EPZ6438) treatment, SP1 chromatin immunoprecipitation at KRT14 promoter, KRT14 knockdown migration/invasion assays, in vivo peritoneal metastasis mouse model Nature communications High 36446780
2022 Krt14 binds the tumor suppressor stratifin (Sfn/14-3-3σ) in airway basal cells. Krt14 knockout reduces Sfn protein abundance and increases expression of ΔNp63α (an oncogene promoting basal cell identity), whereas Krt14 knockout basal cells fail to differentiate into club and ciliated cells but show enhanced clonogenicity. CRISPR knockout of Krt14 and Krt15 in primary mouse airway basal cells, co-immunoprecipitation/binding assay for Krt14-Sfn interaction, in vitro differentiation assays, in vivo label-retaining cell assay JCI insight Medium 36512409
2010 AAV-mediated gene targeting of KRT14 in human keratinocytes can precisely disrupt the mutant allele. EBS patient keratinocytes with corrected KRT14 mutations generate histologically normal skin grafts after transplantation to athymic mice, demonstrating that mutant KRT14 with dominant-negative activity is the cause of the weak epidermal phenotype. AAV gene targeting vector with promoter trap design, transplantation of corrected keratinocytes to athymic mice, histological analysis of skin grafts Molecular therapy Medium 20571545
2017 CRISPR/Cas9 double-nicking strategy targeting KRT14 intron 7 with HDR achieves >30% correction efficiency of the causative hotspot mutation in exon 6 in EBS keratinocytes. Corrected cells show absence of disease-associated K14 aggregates in the cytoplasm, confirming that the mutant KRT14 protein forms cytoplasmic aggregates that disrupt intermediate filament polymerization. CRISPR/Cas9 D10A nickase pair, homology-directed repair with minicircle donor, immunofluorescence for K14 aggregates, NGS off-target analysis Molecular therapy Medium 28888469
2025 KRT14 directly interacts with the translation initiation factor eIF4H through its N-terminal Head domain. This interaction modulates eIF4H association with the eIF4F complex and selectively promotes translation of ACOX2 mRNA via its 5' UTR, driving lipid metabolic reprogramming and cisplatin resistance in bladder cancer. Co-immunoprecipitation, molecular interaction assays, domain mapping (N-terminal Head domain), ACOX2 mRNA translation assays, xenograft mouse models, patient-derived tissue analysis Cell death & disease Medium 41444318
2025 KRT14 directly interacts with IGF2BP1 via residues D226/E227 within the nuclear export signal of KRT14, which are recognized by residues K294/E295 in the KH2 domain of IGF2BP1. This interaction facilitates IGF2BP1-mediated cytoplasmic trafficking and auto-stabilization of IGF2BP1 mRNA, amplifying pro-invasive gene expression in basal muscle-invasive bladder cancer. Co-immunoprecipitation, domain mapping, residue-level mutational analysis, mRNA stability assays, BMIBC mouse models, clinical cohort analysis Advanced science Medium 42261838
2025 lncRNA ABCE1-5 directly binds KRT14 mRNA sequences (demonstrated by RNA pulldown-mass spectrometry and RNA immunoprecipitation), destabilizing KRT14 mRNA. Decreased ABCE1-5 increases KRT14 expression, which activates mTOR/AKT phosphorylation; KRT14 knockdown reverses mTOR activation caused by ABCE1-5 silencing, placing KRT14 upstream of mTOR/AKT signaling in pulmonary fibrosis. RNA pulldown-mass spectrometry, RNA immunoprecipitation, loss- and gain-of-function experiments in vitro and in vivo (AAV6 intratracheal injection in bleomycin mouse model), KRT14 siRNA epistasis experiment American journal of physiology. Cell physiology Medium 40111939
2022 ATG5 deficiency specifically in KRT14+ salivary gland progenitor cells induces pyroptosis (cleaved gasdermin D elevation in KRT14+ cells), leading to functional impairment of salivary glands. Pyroptosis inhibitor treatment rescues the reduced saliva flow rate, placing KRT14+ cell autophagy upstream of gasdermin D-mediated pyroptosis in gland homeostasis. Conditional knockout (Atg5flox/flox; Krt14-Cre), immunofluorescence, TUNEL, western blot for cleaved gasdermin D and cleaved caspase 3, pyroptosis inhibitor rescue, saliva function measurement FASEB journal Medium 36342387

Source papers

Stage 0 corpus · 46 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2016 KRT14 marks a subpopulation of bladder basal cells with pivotal role in regeneration and tumorigenesis. Nature communications 140 27320313
2022 EZH2-H3K27me3 mediated KRT14 upregulation promotes TNBC peritoneal metastasis. Nature communications 110 36446780
2011 Mutations in KRT5 and KRT14 cause epidermolysis bullosa simplex in 75% of the patients. The British journal of dermatology 86 21375516
2006 Naegeli-Franceschetti-Jadassohn syndrome and dermatopathia pigmentosa reticularis: two allelic ectodermal dysplasias caused by dominant mutations in KRT14. American journal of human genetics 83 16960809
2017 Cut and Paste: Efficient Homology-Directed Repair of a Dominant Negative KRT14 Mutation via CRISPR/Cas9 Nickases. Molecular therapy : the journal of the American Society of Gene Therapy 71 28888469
2019 Keratin-14 (KRT14) Positive Leader Cells Mediate Mesothelial Clearance and Invasion by Ovarian Cancer Cells. Cancers 49 31443478
2006 Novel and recurrent mutations in keratin KRT5 and KRT14 genes in epidermolysis bullosa simplex: implications for disease phenotype and keratin filament assembly. Human mutation 48 16786515
2010 Identification of novel and known KRT5 and KRT14 mutations in 53 patients with epidermolysis bullosa simplex: correlation between genotype and phenotype. The British journal of dermatology 46 20199538
2005 Epidermolysis bullosa simplex: recurrent and de novo mutations in the KRT5 and KRT14 genes, phenotype/genotype correlations, and implications for genetic counseling and prenatal diagnosis. The Journal of investigative dermatology 39 16098032
1998 Severe palmo-plantar hyperkeratosis in Dowling-Meara epidermolysis bullosa simplex caused by a mutation in the keratin 14 gene (KRT14). The Journal of investigative dermatology 37 9804355
2017 Retinoic acid signaling regulates Krt5 and Krt14 independently of stem cell markers in submandibular salivary gland epithelium. Developmental dynamics : an official publication of the American Association of Anatomists 35 27884045
2010 Efficient KRT14 targeting and functional characterization of transplanted human keratinocytes for the treatment of epidermolysis bullosa simplex. Molecular therapy : the journal of the American Society of Gene Therapy 34 20571545
2017 Epithelial Markers aSMA, Krt14, and Krt19 Unveil Elements of Murine Lacrimal Gland Morphogenesis and Maturation. Frontiers in physiology 31 29033846
2007 KRT14 haploinsufficiency results in increased susceptibility of keratinocytes to TNF-alpha-induced apoptosis and causes Naegeli-Franceschetti-Jadassohn syndrome. The Journal of investigative dermatology 31 18049449
2023 Krt14 and Krt15 differentially regulate regenerative properties and differentiation potential of airway basal cells. JCI insight 25 36512409
2008 Clinical heterogeneity in recessive epidermolysis bullosa due to mutations in the keratin 14 gene, KRT14. Clinical and experimental dermatology 23 18713255
2011 Two novel recessive mutations in KRT14 identified in a cohort of 21 Spanish families with epidermolysis bullosa simplex. The British journal of dermatology 21 21623745
2017 A Review of 52 Pedigrees with Epidermolysis Bullosa Simplex Identifying Ten Novel Mutations in KRT5 and KRT14 in Australia. Acta dermato-venereologica 19 28561874
2016 Kaempferol targets Krt-14 and induces cytoskeletal mineralization in osteoblasts: A mechanistic approach. Life sciences 18 26956522
2015 Novel sporadic and recurrent mutations in KRT5 and KRT14 genes in Polish epidermolysis bullosa simplex patients: further insights into epidemiology and genotype-phenotype correlation. Journal of applied genetics 16 26432462
2016 Influence of smoking on methylation and hydroxymethylation levels in global DNA and specific sites of KRT14, KRT19, MIR-9-3 and MIR-137 genes of oral mucosa. Archives of oral biology 14 27543926
2015 The influence of sun exposure on the DNA methylation status of MMP9, miR-137, KRT14 and KRT19 genes in human skin. European journal of dermatology : EJD 14 26424515
2002 Novel KRT14 mutation in a Taiwanese patient with epidermolysis bullosa simplex (Köbner type). Journal of the Formosan Medical Association = Taiwan yi zhi 14 12101866
2024 FBLN2 is associated with basal cell markers Krt14 and ITGB1 in mouse mammary epithelial cells and has a preferential expression in molecular subtypes of human breast cancer. Breast cancer research and treatment 13 39110274
2008 A case of dermatopathia pigmentosa reticularis with wiry scalp hair and digital fibromatosis resulting from a recurrent KRT14 mutation. Clinical and experimental dermatology 12 19040520
2011 Consequences of two different amino-acid substitutions at the same codon in KRT14 indicate definitive roles of structural distortion in epidermolysis bullosa simplex pathogenesis. The Journal of investigative dermatology 11 21593775
2023 Evaluation of IGF2, KRT14, and KRT20 as Urinary Biomarkers in Patients with Bladder Cancer. Reports of biochemistry & molecular biology 9 37131897
2022 Loss of ATG5 in KRT14+ cells leads to accumulated functional impairments of salivary glands via pyroptosis. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 7 36342387
2014 Novel KRT14 mutation causing epidermolysis bullosa simplex with variable phenotype. Experimental dermatology 7 24981776
2020 Severe Generalized Epidermolysis Bullosa Simplex in Two Hong Kong Children due to De Novo Variants in KRT14 and KRT5. Case reports in pediatrics 5 32351751
2022 Multiomic analysis revealed the regulatory role of the KRT14 gene in eggshell quality. Frontiers in genetics 4 36212119
2020 A nonsense variant in the KRT14 gene in a domestic shorthair cat with epidermolysis bullosa simplex. Animal genetics 4 32657488
2025 A novel lncRNA ABCE1-5 regulates pulmonary fibrosis by targeting KRT14. American journal of physiology. Cell physiology 3 40111939
2024 Exosomes derived from mucoperiosteum Krt14+Ctsk+ cells promote bone regeneration by coupling enhanced osteogenesis and angiogenesis. Biomaterials science 3 39392433
2020 Generation of a human induced pluripotent stem cell line (UQACi001-A) from a severe epidermolysis bullosa simplex patient with the heterozygous mutation p.R125S in the KRT14 gene. Stem cell research 3 32179493
2020 Analysis of KRT5 and KRT14 gene mutations and mode of inheritance in Iranian patients with clinical suspicion of Epidermolysis bullosa simplex. Medical journal of the Islamic Republic of Iran 3 32884918
2017 Rapid Decrease in KRT14 and TP53 mRNA Expression in the Buccal Mucosa of Patients Receiving Total-Body Irradiation for Allogeneic Stem Cell Transplantation. Radiation research 3 29232178
2016 A Sporadic Neonatal Case of Epidermolysis Bullosa Simplex Generalized Intermediate with KRT5 and KRT14 Gene Mutations. AJP reports 3 26929861
2024 EBS in Children with De Novo Pathogenic Variants Disturbing Krt14. International journal of molecular sciences 2 38474236
2022 The Role of SBI2/ALG12/EBS4 in the Regulation of Endoplasmic Reticulum-Associated Degradation (ERAD) Studied by a Null Allele. International journal of molecular sciences 2 35628619
2017 [Study of a family with epidermolysis bullosa simplex resulting from a novel mutation of KRT14 gene]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 2 28777847
2025 Cytoskeletal protein KRT14 governs cisplatin resistance by modulating eIF4H-dependent ACOX2 translation and lipid metabolism in bladder cancer. Cell death & disease 1 41444318
2021 Effects of Pulmonary Surfactant Combined with Noninvasive Positive Pressure Ventilation on KRT-14 and ET-1 Levels in Peripheral Blood and Therapeutic Effects in Neonates with Respiratory Distress Syndrome. BioMed research international 1 38617025
2026 KRT14 Drives Basal Muscle-Invasive Bladder Cancer Progression and Lung Metastasis by Directly Binding to and Stabilizing IGF2BP1. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 0 42261838
2024 Epidermolysis Bullosa: Two rare case reports of COL7A1 and EBS-GEN SEV KRT14 variants with review of literature. BMC pediatrics 0 38580989
2022 Generation of two induced pluripotent stem cell lines (UQACi002-A and UQACi005-A) from two patients with KRT14 epidermolysis bullosa simplex mutations. Stem cell research 0 35334406

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