Affinage

KRT5

Keratin, type II cytoskeletal 5 · UniProt P13647

Length
590 aa
Mass
62.4 kDa
Annotated
2026-04-28
61 papers in source corpus 22 papers cited in narrative 20 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KRT5 encodes keratin 5, a type II intermediate filament protein that obligately heterodimerizes with keratin 14 to form the 10-nm cytoskeletal filament network essential for mechanical integrity of basal epithelial cells; complete loss of KRT5 is perinatally lethal, and missense mutations in the conserved rod-domain helix boundary motifs cause epidermolysis bullosa simplex (EBS), with severity correlating to mutation position (PMID:9036937, PMID:16786515, PMID:31302245). Beyond its structural role, KRT5 marks tissue-regenerative stem/progenitor populations—p63+/KRT5+ distal airway stem cells regenerate alveolar epithelium after injury, KRT5+ foregut basal progenitors serve as cells of origin for gastric and bladder tumors, and aberrant TGF-β1/anti-BMP mesenchymal signaling drives alveolar-to-KRT5+ basal cell conversion in idiopathic pulmonary fibrosis (PMID:25383540, PMID:34969962, PMID:31110179, PMID:32339497). KRT5 transcription is activated by FoxM1 and p63 and repressed by retinoic acid signaling, while KRT5 protein stability is controlled by TRIM29-mediated ubiquitination; functionally, KRT5 in keratinocytes regulates paracrine Notch signaling to melanocytes, linking it to pigmentation and Dowling-Degos disease pathogenesis (PMID:32659254, PMID:27884045, PMID:37671092, PMID:36809573, PMID:20222933). KRT5 mutations also modulate MAPK-EGFR signaling and desmosomal protein expression, revealing signaling functions beyond cytoskeletal scaffolding (PMID:34912369).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 1992 High

    Identifying the chromosomal locus of KRT5 established it as the candidate gene for the EBS locus on 12q, enabling subsequent mutation hunting in mechanobullous disease.

    Evidence PCR analysis of somatic cell hybrids and multicolor FISH mapping KRT5 to chromosome 12q

    PMID:1377166

    Open questions at the time
    • No causative mutations yet identified
    • Functional consequence of KRT5 disruption not demonstrated
  2. 1997 High

    Direct sequencing of KRT5 in EBS patients demonstrated that single missense mutations in the rod domain (e.g., E477K in the KLLEGE helix-boundary motif) disrupt intermediate filament formation, establishing the molecular basis of EBS and the structural criticality of helix boundary motifs.

    Evidence Direct sequencing of KRT5 exons from patient genomic DNA with genotype–phenotype correlation across multiple cohorts

    PMID:9036937

    Open questions at the time
    • No in vitro reconstitution of mutant filament assembly
    • Mechanism of aggregate formation under stress not yet characterized
  3. 1999 Medium

    Identification of the P24L head-domain mutation as the cause of EBS with mottled pigmentation extended the KRT5 disease spectrum beyond purely mechanical fragility to include pigmentary phenotypes.

    Evidence KRT5 gene mutation analysis in affected families and sporadic patients

    PMID:10494094

    Open questions at the time
    • Mechanism linking a head-domain KRT5 mutation to pigmentation abnormality unknown
    • Only a single recurrent mutation identified
  4. 2006 High

    Systematic genotype–phenotype mapping across large EBS cohorts established that helix initiation and termination peptides of the KRT5 rod domain are the structural determinants of filament assembly, with mutations at these sites causing the most severe (Dowling-Meara) phenotype.

    Evidence Complete KRT5/KRT14 coding sequence analysis in EBS patient cohorts with phenotype stratification

    PMID:16786515 PMID:20199538 PMID:21375516

    Open questions at the time
    • No atomic-resolution structural model of the KRT5/KRT14 heterodimer
    • Mechanism by which specific mutations differentially weaken filaments not resolved
  5. 2010 Medium

    Functional cell-based assays demonstrated that different KRT5 missense mutations confer mutation-specific degrees of cytoskeletal vulnerability to heat stress, and that the chemical chaperone TMAO can partially rescue mutant filament aggregation, providing proof-of-concept for pharmacological intervention.

    Evidence Heat-shock assays in primary and immortalized EBS keratinocytes with TMAO dose-response quantification of keratin aggregate formation

    PMID:19157792 PMID:20128788

    Open questions at the time
    • TMAO mechanism of action on keratin folding not defined
    • No in vivo therapeutic validation
    • Applicability across all mutation classes untested
  6. 2010 Medium

    KRT5 loss-of-function frameshift mutations were shown to cause Dowling-Degos/Galli-Galli disease, unifying these as a single disorder and extending KRT5's disease repertoire to reticular pigmentation syndromes.

    Evidence Systematic KRT5 sequencing with histopathological re-evaluation

    PMID:20222933

    Open questions at the time
    • Mechanism linking KRT5 haploinsufficiency to aberrant pigmentation not identified
    • Cell-type-specific consequences of KRT5 loss in melanocyte–keratinocyte interaction unknown
  7. 2014 High

    Lineage tracing and selective ablation in vivo established that p63+/KRT5+ distal airway stem cells are the regenerative progenitors that reconstitute alveolar epithelium after influenza injury, repositioning KRT5 as a marker and functional component of adult lung stem cells.

    Evidence Lineage tracing, in vivo ablation, single-cell transplantation, and organoid culture in H1N1 mouse model

    PMID:25383540

    Open questions at the time
    • Whether KRT5 protein is functionally required for progenitor behavior or is merely a marker
    • Origin of KRT5+ progenitors in distal airways not fully resolved
  8. 2014 High

    Single-cell profiling revealed that KRT5 expression in basal-like breast epithelial cells is controlled by an anticorrelated TGFBR3–JUND regulatory circuit modulated by ECM attachment, revealing upstream signaling logic governing KRT5 in epithelial identity.

    Evidence Single-cell gene expression profiling, 3D culture, siRNA knockdown, circuit modeling, and in vivo intraductal transplantation

    PMID:24658685

    Open questions at the time
    • Whether this circuit operates in non-mammary KRT5+ epithelia untested
    • Direct transcription factor binding at KRT5 locus not demonstrated in this study
  9. 2017 Medium

    Retinoic acid signaling was shown to directly repress KRT5 transcription in epithelial explants independently of stem cell markers, identifying RA as a negative regulator of the KRT5 basal cell program.

    Evidence Mouse embryonic salivary gland epithelial explant culture with RA signaling inhibition and qPCR

    PMID:27884045

    Open questions at the time
    • Direct RA receptor binding at KRT5 regulatory elements not demonstrated
    • Generalizability to other epithelial tissues not tested
  10. 2019 High

    A human homozygous KRT5 null mutation resulting in complete absence of protein was shown to be perinatally lethal, definitively establishing KRT5 as essential for basal keratinocyte survival, while biallelic missense variants cause autosomal recessive EBS.

    Evidence Whole exome sequencing, NGS panel, immunofluorescence, and ultrastructural analysis in human patients

    PMID:31302245

    Open questions at the time
    • Molecular mechanism of lethality (pure structural failure vs. signaling disruption) not dissected
    • No rescue experiment performed
  11. 2019 Medium

    ChIP-seq demonstrated that FoxM1 directly binds KRT5 regulatory regions to activate transcription, and KRT5 knockdown inhibited cancer cell migration without affecting proliferation, placing KRT5 as a FoxM1-driven effector of cell motility.

    Evidence ChIP-seq, RNA-seq, qPCR, Western blot, KRT5 knockdown, and wound healing assay in SK-OV-3 cells

    PMID:32659254

    Open questions at the time
    • Mechanism by which KRT5 promotes migration not defined
    • Tested in a single ovarian cancer cell line
  12. 2020 Medium

    In vivo lineage tracing established that Krt5+ basal urothelial cells are a preferred cell of origin for basal-squamous bladder cancer, with Trp53 loss in these cells driving more efficient muscle-invasive tumorigenesis than in luminal cells.

    Evidence Lineage tracing in genetically engineered mouse model with BBN chemical carcinogenesis

    PMID:32339497

    Open questions at the time
    • Whether KRT5 functionally contributes to tumorigenesis or marks the susceptible population
    • Applicability to human bladder cancer subtypes not directly tested
  13. 2021 High

    Human alveolar type 2 cells were shown to undergo TGF-β1/anti-BMP-driven transdifferentiation into KRT5+ basal cells through alveolar-basal intermediates, establishing a disease-relevant lineage conversion mechanism in idiopathic pulmonary fibrosis.

    Evidence Organoid co-cultures, single-cell RNA-seq trajectory analysis, TGF-β/BMP manipulation, in vivo xenograft, and IPF tissue analysis

    PMID:34969962

    Open questions at the time
    • Whether preventing KRT5+ conversion would ameliorate fibrosis not tested
    • Signals directing KRT5+ cells to pathological vs. regenerative fates not distinguished
  14. 2021 Medium

    A homozygous KRT5 missense mutation was shown to collapse keratin filaments and inhibit MAPK signaling, leading to DSG1 upregulation, revealing that KRT5 structural integrity feeds into MAPK-EGFR signaling and desmosomal protein expression.

    Evidence Biochemical structural analysis, immunofluorescence, Western blot, in vitro EGFR inhibitor treatment, and patient skin biopsy analysis

    PMID:34912369

    Open questions at the time
    • Mechanism linking filament collapse to MAPK inhibition not determined
    • Single mutation studied; generalizability uncertain
  15. 2023 Medium

    TRIM29 was identified as a direct E3 ubiquitin ligase for KRT5, controlling its protein stability via ubiquitination; TRIM29 knockdown stabilized KRT5 and inhibited colon cancer cell proliferation in a KRT5-dependent manner.

    Evidence Co-immunoprecipitation, cycloheximide chase, ubiquitination assays, and proliferation rescue experiments

    PMID:37671092

    Open questions at the time
    • Ubiquitination sites on KRT5 not mapped
    • No reciprocal IP or structural evidence for direct binding
    • In vivo relevance not tested
  16. 2023 Medium

    KRT5 in keratinocytes was shown to regulate melanocyte melanogenesis through paracrine Notch signaling: KRT5 loss reduced Notch ligand expression in keratinocytes and Notch activation in co-cultured melanocytes, mechanistically explaining the pigmentation defects in Dowling-Degos disease.

    Evidence CRISPR/Cas9 and shRNA KRT5 knockdown in keratinocytes, melanocyte co-culture, Notch pathway inhibitor/activator treatment, and DDD patient lesion immunohistochemistry

    PMID:36809573

    Open questions at the time
    • Specific Notch ligand(s) regulated by KRT5 not identified
    • How a cytoskeletal protein controls Notch ligand transcription is mechanistically unresolved
  17. 2023 Medium

    ECM composition was shown to modulate KRT5+ basal cell migration in the IPF lung context, with fibroblast-secreted SPARC restricting KRT5+ cell motility, revealing extracellular control of KRT5+ progenitor behavior in fibrotic disease.

    Evidence In vitro migration assays on defined ECM substrates, mass spectrometry-based proteomics, and SPARC overexpression in primary human KRT5+ cells

    PMID:37758700

    Open questions at the time
    • Whether SPARC acts directly on KRT5+ cells or through indirect signaling not resolved
    • In vivo validation of SPARC–KRT5+ cell interaction not performed

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: how KRT5 structural integrity is mechanistically linked to MAPK and Notch signaling outputs; whether KRT5 protein has a functional role in stem/progenitor cell behavior beyond serving as a marker; and the atomic-resolution structural basis for genotype–severity correlations in EBS.
  • No high-resolution structure of KRT5/KRT14 heterodimer available
  • Whether KRT5 protein is functionally required in lung/bladder progenitor biology is untested by conditional knockout
  • Mechanism coupling keratin filament integrity to transcriptional or signaling output remains undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 5
Localization
GO:0005856 cytoskeleton 5 GO:0005829 cytosol 2
Pathway
R-HSA-1643685 Disease 5 R-HSA-1266738 Developmental Biology 3 R-HSA-162582 Signal Transduction 3
Partners
FOXM1KRT14SPARCTP63TRIM29
Complex memberships
KRT5/KRT14 heterodimer

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1992 KRT5 (keratin 5) was mapped to human chromosome 12q near D12S14 by PCR analysis of somatic cell hybrids and multicolor fluorescence in situ hybridization, establishing it as the candidate gene for epidermolysis bullosa simplex linked to that locus. PCR analysis of somatic cell hybrids; multicolor fluorescence in situ hybridization (FISH) Genomics High 1377166
1997 KRT5 encodes a type II keratin that, together with KRT14, constitutes the primary structural component of 10-nm intermediate filaments in mitotic epidermal basal cells; single missense mutations in the rod domain (e.g., E477K in the conserved KLLEGE motif at the helix boundary) disrupt the keratin intermediate filament cytoskeleton, causing epidermolysis bullosa simplex. Direct sequencing of KRT5 exons amplified from leukocyte genomic DNA; genotype-phenotype correlation The Journal of investigative dermatology High 9036937
1999 The P24L (P25L) substitution in the KRT5 gene (71C→T transition in the non-helical head domain) is the causative mutation for epidermolysis bullosa simplex with mottled pigmentation (EBS-MP), confirmed by mutation analysis in affected family members and sporadic patients. KRT5 gene mutation analysis; clinical correlation in families American journal of medical genetics Medium 10494094
2006 Mutations affecting the highly conserved helix boundary motifs (helix initiation and termination peptides) of the rod domain of KRT5 (and KRT14) cause the most severe EBS phenotype (Dowling-Meara), while mutations elsewhere produce milder forms, demonstrating that the rod domain helix boundaries are structurally critical for keratin intermediate filament assembly. Sequence analysis of entire coding sequences of KRT5 and KRT14 in EBS patients; genotype-phenotype correlation Human mutation High 16786515 20199538 21375516
2009 Immortalized keratinocytes carrying a KRT5 V186L mutation form cytoplasmic keratin filament aggregates upon heat-shock stress, and this aggregation (a measure of cytoskeletal disruption) is significantly reduced by pretreatment with the chemical chaperone trimethylamine N-oxide (TMAO), demonstrating that TMAO stabilizes the mutant KRT5 protein against thermal stress. Immortalized cell lines from EBS patients (HPV16 E6E7 transduction); heat-shock assay; assessment of keratin aggregate formation with and without TMAO Journal of dermatological science Medium 19157792
2010 Different KRT5 missense mutations (I183M, E475G, V186L) confer mutation-specific degrees of cellular fragility in primary keratinocytes upon heat stress, and TMAO dose-dependently reduces keratin aggregate formation and cell loss in all three mutant lines, establishing a genotype-dependent cytoskeletal vulnerability mechanism. Primary EBS keratinocyte cultures; heat-stress assay; TMAO treatment; keratin aggregate quantification The British journal of dermatology Medium 20128788
2010 KRT5 frameshift/insertion mutations (c.418dupA) in the Dowling-Degos disease/Galli-Galli disease spectrum demonstrate that loss-of-function mutations in KRT5 cause reticular hyperpigmentation phenotypes, and that Galli-Galli disease (with acantholysis) shares identical KRT5 mutations with Dowling-Degos disease, establishing them as variants of the same disorder. Systematic KRT5 sequencing; histopathological re-evaluation; genotype-phenotype correlation The British journal of dermatology Medium 20222933
2014 Pre-existing p63+/KRT5+ distal airway stem cells (DASCp63/Krt5) undergo proliferative expansion after influenza-induced lung damage, assemble into nascent alveoli, and differentiate into type I and type II pneumocytes as well as bronchiolar secretory cells after transplantation; selective in vivo ablation of these cells prevents lung regeneration and leads to pre-fibrotic lesions. Lineage tracing; in vivo selective ablation; single-cell pedigree transplantation; live imaging; organoid culture; H1N1 mouse model Nature High 25383540
2014 In basal-like breast epithelial cells, KRT5 expression is regulated by an anticorrelated TGFBR3-JUND circuit: TGFBR3 and JUND are connected through four negative-feedback loops, and their dynamic toggling controls KRT5 expression in ECM-attached cells during 3D culture; ECM detachment rewires the circuit via RPS6 dephosphorylation and juxtacrine tenascin C. Single-cell gene expression profiling; 3D organotypic culture; siRNA knockdown; circuit modelling; in vivo intraductal transplantation Nature cell biology High 24658685
2019 Biallelic homozygous missense variants of KRT5 in human patients cause autosomal recessive EBS with generalized phenotype; a homozygous null (KRT5 'knock-out') mutation results in complete absence of KRT5 RNA and protein and is perinatally lethal, demonstrating that KRT5 is essential for basal keratinocyte integrity and survival. Whole exome sequencing; NGS panel; immunofluorescence microscopy; expression profiling; ultrastructural analysis Matrix biology High 31302245
2019 FoxM1 transcription factor directly binds a consensus AP-2 cis element in KRT5 (and KRT7) regulatory regions and activates their transcription; KRT5 and KRT7 loss-of-function inhibits migration but not proliferation of SK-OV-3 ovarian cancer cells, placing KRT5 downstream of FoxM1 in a migration-promoting pathway. ChIP-seq; RNA-seq; qPCR; Western blot; KRT5 knockdown; wound healing/migration assay Gene Medium 32659254
2019 Krt5+/Krt15+ foregut basal progenitor cells are the cell of origin for gastric acid stress-induced tumors, and tumor formation from these cells is dependent on Cyclooxygenase-2 (COX-2) activity, as demonstrated in genetically engineered mouse models. Genetically engineered mouse models; lineage tracing; COX-2-dependent tumor formation assay Nature communications Medium 31110179
2021 Human alveolar type 2 cells (hAEC2s), but not murine AEC2s, transdifferentiate into KRT5+ basal cells in response to fibrotic mesenchymal signaling (TGF-β1 and anti-BMP signaling) through alveolar-basal intermediates, demonstrating that aberrant mesenchymal signals drive hAEC2-to-KRT5+ basal cell lineage conversion in IPF. Organoid co-cultures; single-cell RNA-seq trajectory analysis; TGF-β1/BMP pathway manipulation; in vivo xenograft; histologic analysis of IPF tissue Nature cell biology High 34969962
2021 A KRT5 homozygous missense mutation (c.1474T>C) causes structural alteration of keratin 5 and collapse of keratin intermediate filaments without a quantitative change in protein level; the KRT5 mutation inhibits MAPK signaling, leading to upregulation of the desmosomal protein DSG1 (desmoglein 1), and EGFR phosphorylation inhibition in vitro similarly upregulates DSG1, placing KRT5 upstream of MAPK-EGFR-DSG1 signaling. Biochemical experiments (structural analysis); immunofluorescence; Western blot; in vitro EGFR inhibitor treatment; patient skin biopsy analysis Frontiers in genetics Medium 34912369
2023 TRIM29 E3 ubiquitin ligase directly interacts with KRT5 (confirmed by co-immunoprecipitation) and promotes its ubiquitination, reducing KRT5 protein stability; TRIM29 knockdown decreases KRT5 ubiquitination, enhances KRT5 protein stability and expression, and inhibits colon cancer cell proliferation, which is reversed by KRT5 knockdown. Co-immunoprecipitation; cycloheximide chase (protein stability assay); Western blot; qRT-PCR; CCK-8/colony formation/EDU proliferation assays Open life sciences Medium 37671092
2023 Downregulation of KRT5 in keratinocytes (via CRISPR/Cas9 or shRNA) decreases expression of Notch ligands in keratinocytes and Notch1 intracellular domain in melanocytes, reducing melanogenesis markers TYR and Fascin1; activation of Notch signaling reverses these effects, establishing that KRT5 in keratinocytes regulates melanocyte melanogenesis through paracrine Notch signaling. CRISPR/Cas9 site-directed mutation; lentivirus-mediated shRNA; co-culture system; Western blot; Notch inhibitor/activator treatment; immunohistochemistry of DDD patient lesions Experimental dermatology Medium 36809573
2023 KRT5+ basal cell migratory behavior and expression of extracellular matrix remodeling genes are modulated by ECM composition and organization; SPARC (secreted by IPF lung fibroblasts and identified by mass spectrometry-based proteomics) restricts KRT5+ cell migration in vitro, revealing a mechanism by which altered ECM in IPF directly controls KRT5+ cell activity. In vitro migration assays on defined ECM substrates; mass spectrometry-based proteomics of fibroblast-secreted ECM; SPARC overexpression; primary human KRT5+ cell culture Nature communications Medium 37758700
2017 Retinoic acid (RA) signaling directly in salivary gland epithelium represses Krt5 and Krt14 expression; inhibition of RA signaling upregulates Krt5/Krt14 independently of stem cell markers (Kit), demonstrated by isolating epithelial explants from other tissues. Mouse embryonic salivary gland epithelial explant culture; RA signaling inhibition; qPCR for Krt5/Krt14 expression; Kit expression analysis Developmental dynamics Medium 27884045
2020 Trp53 mutation specifically in Krt5-expressing basal urothelial cells facilitates more efficient tumorigenesis of muscle-invasive bladder cancer with squamous differentiation compared to Trp53 mutation in Upk2-expressing cells, establishing that Krt5+ basal cells are a preferred cell of origin for the basal-squamous subtype of bladder cancer. Lineage tracing in genetically engineered mouse model; BBN chemical carcinogenesis; morphological and genetic characterization of tumors The American journal of pathology Medium 32339497
2025 p63 regulates the Krt8-to-Krt5 transition during ameloblast (AmG) cell differentiation in the enamel organ, paralleling its function in skin; this regulation involves chromatin landscape remodeling at Krt5 loci, with shared transcription factor usage (p63 and AP-2 family members) between skin and enamel organ development. Single-cell RNA sequencing; trajectory reconstruction; comparative transcriptome analysis; chromatin accessibility (ATAC-seq); comparative motif discovery; p63 knockout mouse model bioRxivpreprint Medium 39990386

Source papers

Stage 0 corpus · 61 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 p63(+)Krt5(+) distal airway stem cells are essential for lung regeneration. Nature 428 25383540
2021 Human alveolar type 2 epithelium transdifferentiates into metaplastic KRT5+ basal cells. Nature cell biology 196 34969962
2007 The diagnostic value of TTF-1, CK 5/6, and p63 immunostaining in classification of lung carcinomas. Applied immunohistochemistry & molecular morphology : AIMM 132 18091384
2011 Mutations in KRT5 and KRT14 cause epidermolysis bullosa simplex in 75% of the patients. The British journal of dermatology 85 21375516
1997 Primers for exon-specific amplification of the KRT5 gene: identification of novel and recurrent mutations in epidermolysis bullosa simplex patients. The Journal of investigative dermatology 70 9036937
2014 A time- and matrix-dependent TGFBR3-JUND-KRT5 regulatory circuit in single breast epithelial cells and basal-like premalignancies. Nature cell biology 65 24658685
2017 In stage pT1 non-muscle-invasive bladder cancer (NMIBC), high KRT20 and low KRT5 mRNA expression identify the luminal subtype and predict recurrence and survival. Virchows Archiv : an international journal of pathology 59 28074276
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
2018 Depletion of Airway Submucosal Glands and TP63+KRT5+ Basal Cells in Obliterative Bronchiolitis. American journal of respiratory and critical care medicine 47 29236513
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
2023 Lung extracellular matrix modulates KRT5+ basal cell activity in pulmonary fibrosis. Nature communications 43 37758700
2020 FoxM1 promotes the migration of ovarian cancer cell through KRT5 and KRT7. Gene 43 32659254
2010 Systematic mutation screening of KRT5 supports the hypothesis that Galli-Galli disease is a variant of Dowling-Degos disease. The British journal of dermatology 41 20222933
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
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
2009 Characterization of immortalized human epidermolysis bullosa simplex (KRT5) cell lines: trimethylamine N-oxide protects the keratin cytoskeleton against disruptive stress condition. Journal of dermatological science 34 19157792
2019 miR-601 inhibits proliferation, migration and invasion of prostate cancer stem cells by targeting KRT5 to inactivate the Wnt signaling pathway. International journal of clinical and experimental pathology 23 31933840
2019 Krt5+/Krt15+ foregut basal progenitors give rise to cyclooxygenase-2-dependent tumours in response to gastric acid stress. Nature communications 22 31110179
1999 Epidermolysis bullosa simplex with mottled pigmentation: clinical aspects and confirmation of the P24L mutation in the KRT5 gene in further patients. American journal of medical genetics 22 10494094
2010 Epidermolysis bullosa simplex due to KRT5 mutations: mutation-related differences in cellular fragility and the protective effects of trimethylamine N-oxide in cultured primary keratinocytes. The British journal of dermatology 20 20128788
2017 A Review of 52 Pedigrees with Epidermolysis Bullosa Simplex Identifying Ten Novel Mutations in KRT5 and KRT14 in Australia. Acta dermato-venereologica 18 28561874
2008 Immunohistochemical analysis of ER, PR, HER-2, CK 5/6, p63 and EGFR antigen expression in medullary breast cancer. Tumori 18 19267102
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
2020 p63+Krt5+ basal cells are increased in the squamous metaplastic epithelium of patients with radiation-induced chronic Rhinosinusitis. Radiation oncology (London, England) 13 32977822
1992 Regional assignment of the human keratin 5 (KRT5) gene to chromosome 12q near D12S14 by PCR analysis of somatic cell hybrids and multicolor in situ hybridization. Genomics 13 1377166
2021 KRT20, KRT5, ESR1 and ERBB2 Expression Can Predict Pathologic Outcome in Patients Undergoing Neoadjuvant Chemotherapy and Radical Cystectomy for Muscle-Invasive Bladder Cancer. Journal of personalized medicine 12 34073233
2019 Biallelic KRT5 mutations in autosomal recessive epidermolysis bullosa simplex, including a complete human keratin 5 "knock-out". Matrix biology : journal of the International Society for Matrix Biology 12 31302245
2020 Trp53 Mutation in Keratin 5 (Krt5)-Expressing Basal Cells Facilitates the Development of Basal Squamous-Like Invasive Bladder Cancer in the Chemical Carcinogenesis of Mouse Bladder. The American journal of pathology 11 32339497
2022 Hsa_circRNA_0017620 regulated cell progression of non-small-cell lung cancer via miR-520a-5p/KRT5 axis. Journal of clinical laboratory analysis 10 35302673
2022 Novel variants in LAMA3 and COL7A1 and recurrent variant in KRT5 underlying epidermolysis bullosa in five Chinese families. Frontiers of medicine 8 35314946
2021 The value of AGR2 and KRT5 as an immunomarker combination in distinguishing lung squamous cell carcinoma from adenocarcinoma. American journal of translational research 8 34150027
2014 The First Report of KRT5 Mutation Underlying Acantholytic Dowling-Degos Disease with Mottled Hypopigmentation in an Indian Family. Indian journal of dermatology 8 25284854
1990 Human nidogen gene: identification of multiple RFLP and exclusion as candidate gene in a family with epidermolysis bullosa (EBS2) with evidence for linkage to chromosome 1. The Journal of investigative dermatology 8 1977802
2023 KRT5 mutation regulate melanin metabolism through notch signalling pathway between keratinocytes and melanocytes. Experimental dermatology 7 36809573
2023 TRIM29 knockdown prevented the colon cancer progression through decreasing the ubiquitination levels of KRT5. Open life sciences 7 37671092
2021 Damaged Keratin Filament Network Caused by KRT5 Mutations in Localized Recessive Epidermolysis Bullosa Simplex. Frontiers in genetics 7 34912369
2014 Exome sequencing reveals a novel mutation, p.L325H, in the KRT5 gene associated with autosomal dominant Epidermolysis Bullosa Simplex Koebner type in a large family from western India. Human genome variation 6 27081501
2023 CAV1 and KRT5 are potential targets for prostate cancer. Medicine 5 38065913
2022 KRT5 missense variant in a Cardigan Welsh Corgi with epidermolysis bullosa simplex. Animal genetics 5 36004757
2020 Spontaneous KRT5 Gene Mutation in Rhesus Macaques (Macaca mulatta): A Novel Nonhuman Primate Model of Epidermolysis Bullosa Simplex. Veterinary pathology 5 32096448
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
2014 Cinical Significance of Androgen Receptor, CK-5/6, KI-67 and Molecular Subtypes in Breast Cancer. The journal of breast health 5 28331672
2024 Dual and triple gene combinations of KRT5, KRT17, and S100A2 identify basal-like subtype of pancreatic ductal adenocarcinoma and correlate with survival outcome. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 4 39101950
2023 KRT5+/p63+ Stem Cells Undergo Senescence in the Human Lung with Pathological Aging. Aging and disease 4 37191411
2020 A de novo mutation in KRT5 in a crossbred calf with epidermolysis bullosa simplex. Journal of veterinary internal medicine 4 33135329
2010 A transient epidermolysis bullosa simplex-like phenotype associated with bexarotene treatment in a G138E KRT5 heterozygote. Journal of cutaneous pathology 4 20849457
2021 A Familial Form of Epidermolysis Bullosa Simplex Associated with a Pathogenic Variant in KRT5. Genes 3 34680898
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
2020 A Novel Mutation p.L461P in KRT5 Causing Localized Epidermolysis Bullosa Simplex. Annals of dermatology 3 33911807
2019 A novel de novo mutation p.Ala428Asp in KRT5 gene as a cause of localized epidermolysis bullosa simplex. Experimental dermatology 3 30240119
2016 A Sporadic Neonatal Case of Epidermolysis Bullosa Simplex Generalized Intermediate with KRT5 and KRT14 Gene Mutations. AJP reports 3 26929861
2016 A novel KRT5 mutation associated with generalized severe epidermolysis bullosa simplex in a 2-year-old Chinese boy. Experimental and therapeutic medicine 3 27882080
2025 KRT5high TP63-expressing urothelial basal cells act as a driver to bladder urothelium regeneration in rabbit. Stem cell research & therapy 1 40483513
2024 KRT5 in-frame deletion in a family of German Shepherd dogs with split paw pad disease resembling localized epidermolysis bullosa simplex in human patients. Animal genetics 1 38742646
2025 p63 co-opts the skin Krt8-to-Krt5 transition for enamel organ development. bioRxiv : the preprint server for biology 0 39990386
2025 Clinical and genetic study of a family with epidermolysis bullosa simplex caused by a novel KRT5 gene mutation c.987C>G (p.Asn329Lys). Intractable & rare diseases research 0 41341913
2025 [Genetic analysis of a Chinese pedigree affected with Epidermolysis bullosa simplex due to a novel variant of KRT5 gene]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 0 41451495
2024 Identification of novel KRT5 gene variants in two Chinese patients with sporadic form of epidermolysis bullosa simplex: A case report. Experimental and therapeutic medicine 0 38414793
2023 Keratin 5 in Lung Cancer Specimens: Comparison of Four Antibody Clones and KRT5 mRNA-ISH. Applied immunohistochemistry & molecular morphology : AIMM 0 37212698
2022 Generation of three induced pluripotent stem cell lines (UQACi003-A, UQACi004-A, and UQACi006-A) from three patients with KRT5 epidermolysis bullosa simplex mutations. Stem cell research 0 35247839
2018 WITHDRAWN: KLF5 promoted symmetric cell division in KRT5 positive keratinocytes through suppression of Notch1 expression. Biochemical and biophysical research communications 0 29902455