Affinage

KRT5

Keratin, type II cytoskeletal 5 · UniProt P13647

Length
590 aa
Mass
62.4 kDa
Annotated
2026-06-10
61 papers in source corpus 18 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KRT5 encodes keratin 5, the major type II keratin of basal cells in epidermis and stratified epithelia, which pairs with its type I partner keratin 14 to form the primary 10-nm intermediate filament cytoskeleton of mitotic basal keratinocytes (PMID:1377166, PMID:9036937). Filament assembly depends on highly conserved helix boundary motifs of the central rod domain; missense mutations in these motifs (e.g., the KLLEGE motif, E477K) collapse the keratin filament network and cause epidermolysis bullosa simplex (EBS), with helix boundary lesions producing the most severe Dowling-Meara phenotype (PMID:9036937, PMID:16786515, PMID:21375516). Mutant KRT5 destabilizes the cytoskeleton under mechanical and thermal stress, driving formation of cytoplasmic keratin aggregates through protein misfolding that chemical chaperones such as TMAO can mitigate (PMID:19157792, PMID:20128788). Complete biallelic KRT5 loss abolishes keratin 5 expression and causes perinatally lethal EBS, establishing KRT5 as essential for basal keratinocyte survival (PMID:31302245). Beyond its structural role, KRT5 functions in signaling: it maintains the desmosomal protein DSG1 through MAPK/EGFR signaling (PMID:34912369) and, via keratinocyte Notch ligand expression, regulates melanogenesis in adjacent melanocytes (PMID:36809573). KRT5 expression is controlled transcriptionally by FoxM1 acting through an AP-2 cis element in the promoter (PMID:32659254) and post-translationally by TRIM29-mediated ubiquitination and degradation (PMID:37671092). Distinct from its epidermal role, KRT5 marks p63+ basal stem/progenitor cells that act as injury-responsive progenitors regenerating lung epithelium after damage (PMID:25383540), that arise by TGF-β/anti-BMP-driven transdifferentiation of alveolar type 2 cells in fibrosis (PMID:34969962), and that serve as a cell of origin for squamous and basal tumors (PMID:31110179, PMID:32339497).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 1992 Medium

    Establishing where KRT5 sits in the genome and what it does at the protein level defined keratin 5 as the major type II keratin of basal epithelial cells partnering with keratin 14.

    Evidence PCR of somatic cell hybrids and FISH mapping to chromosome 12q with protein identification

    PMID:1377166

    Open questions at the time
    • Did not establish the structural requirements for filament assembly
    • No functional perturbation of KRT5
  2. 1997 Medium

    Linking specific rod-domain mutations to disease showed that conserved helix boundary motifs are essential for keratin filament integrity and that their disruption causes EBS skin fragility.

    Evidence Direct sequencing of KRT5 exons from EBS patient genomic DNA identifying recurrent missense mutations

    PMID:9036937

    Open questions at the time
    • Functional consequence inferred from conservation rather than measured directly
    • Cellular mechanism of filament collapse not yet shown
  3. 2006 Medium

    Correlating mutation position with phenotype severity established structure-function rules, with helix boundary motif lesions producing the most severe Dowling-Meara EBS.

    Evidence Full coding sequence analysis of KRT5 and KRT14 in EBS patients with structural inference

    PMID:16786515

    Open questions at the time
    • Did not directly test filament assembly biochemically
    • Genotype-phenotype mechanism inferred from sequence
  4. 2011 Medium

    A large cohort with immunofluorescence validation reinforced that helix boundary motifs underlie the severest EBS, anchoring the structure-function model.

    Evidence Genomic and cDNA sequencing of 76 EBS probands plus K5/K14 immunofluorescence on skin biopsies

    PMID:21375516

    Open questions at the time
    • Correlative; no in vitro assembly reconstitution
    • Modifier contributions not addressed
  5. 2010 Medium

    Testing patient keratinocytes under stress showed that mutant KRT5 causes allele-specific cellular fragility via protein misfolding, and that chemical chaperones can stabilize the cytoskeleton.

    Evidence Heat stress and TMAO treatment of primary and immortalized EBS keratinocytes carrying defined KRT5 mutations

    PMID:19157792 PMID:20128788

    Open questions at the time
    • TMAO efficacy shown in vitro only
    • Misfolding pathway not structurally resolved
  6. 2014 High

    Identifying KRT5+/p63+ distal airway stem cells as injury-responsive progenitors extended KRT5 biology beyond skin into regenerative lung epithelium.

    Evidence In vivo ablation of Krt5+ cells and single-cell pedigree transplantation in a mouse influenza model

    PMID:25383540

    Open questions at the time
    • Role of KRT5 protein itself versus the cell population not separated
    • Signals initiating expansion not defined in this study
  7. 2019 High

    Generating complete human KRT5 knockouts showed that total loss is perinatally lethal, establishing KRT5 as essential for basal keratinocyte survival rather than merely modulatory.

    Evidence Whole exome/NGS sequencing with expression, immunofluorescence and ultrastructural validation in EBS patients

    PMID:31302245

    Open questions at the time
    • Cause of cell death downstream of KRT5 loss not dissected
    • Compensation by other keratins not characterized
  8. 2020 Medium

    Defining FoxM1-driven transcription and KRT5+ cell-of-origin roles in cancer connected KRT5 to migration programs and tumorigenesis.

    Evidence ChIP-seq/RNA-seq with KRT5 knockdown migration assays in ovarian cancer cells; lineage-specific Trp53 mutation in Krt5+ bladder cells

    PMID:32339497 PMID:32659254

    Open questions at the time
    • Mechanism linking KRT5 to migration not resolved
    • Whether KRT5 is driver or marker in these tumors unclear
  9. 2021 High

    Mapping AEC2-to-KRT5+ basal transdifferentiation defined a causal fibrotic lineage trajectory driven by TGF-β and anti-BMP signaling from mesenchyme.

    Evidence hAEC2-mesenchyme organoid co-culture, scRNA-seq trajectory analysis, pathway perturbation and IPF tissue validation

    PMID:34969962

    Open questions at the time
    • Reversibility of the metaplastic state not established
    • Role of KRT5 protein in the transition itself unknown
  10. 2023 Medium

    Demonstrating KRT5 signaling outputs showed that beyond structure it maintains DSG1 via MAPK/EGFR, regulates melanogenesis via Notch in neighboring melanocytes, and is degraded by TRIM29 ubiquitination.

    Evidence Patient keratinocyte biochemistry with Co-IP and EGFR inhibition; CRISPR/shRNA KRT5 knockdown with Notch modulation; TRIM29 Co-IP and CHX chase in colon cancer cells

    PMID:34912369 PMID:36809573 PMID:37671092

    Open questions at the time
    • Each signaling link rests on single-lab assays
    • Direct versus indirect coupling of KRT5 to MAPK/Notch not resolved
  11. 2023 Medium

    Identifying SPARC as an ECM regulator of KRT5+ cell migration linked the fibrotic matrix microenvironment to aberrant basal cell behavior.

    Evidence Mass spectrometry of IPF versus control fibroblast ECM with SPARC gain-of-function migration assays

    PMID:37758700

    Open questions at the time
    • SPARC receptor on KRT5+ cells unidentified
    • In vivo relevance shown only in vitro

Open questions

Synthesis pass · forward-looking unresolved questions
  • How mechanical stress and chromatin regulation toggle KRT5 expression to generate transitional basal cell states remains incompletely defined.
  • Preprint findings lack direct KRT5 functional perturbation
  • Causal role of KRT5 level in transitional state not tested
  • Mechanotransduction pathway to KRT5 promoter unmapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 4 GO:0005856 cytoskeleton 3
Localization
GO:0005856 cytoskeleton 2 GO:0005829 cytosol 1
Pathway
R-HSA-1266738 Developmental Biology 2
Partners
DSG1KRT14TRIM29

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1992 KRT5 gene was mapped to chromosome 12q near D12S14, and keratin 5 protein was identified as the major type II keratin of basal cells of epidermis and stratified epithelia, forming the primary structural cytoskeletal component together with its type I partner keratin 14. PCR analysis of somatic cell hybrids and multicolor fluorescence in situ hybridization Genomics Medium 1377166
1997 KRT5 encodes the primary structural component of 10-nm intermediate filaments in mitotic epidermal basal cells; single missense mutations in the highly conserved KLLEGE motif at the end of the central rod domain (e.g., E477K) disrupt the keratin intermediate filament cytoskeleton, causing EBS skin fragility and blistering. Direct sequencing of KRT5 exons amplified from leukocyte genomic DNA; identification of recurrent missense mutations The Journal of investigative dermatology Medium 9036937
2006 Mutations in KRT5 affecting helix boundary motifs of the rod domain disrupt keratin intermediate filament (KIF) formation; mutations at the helix initiation motif of KRT14 and helix boundary motifs of KRT5 are associated with the most severe EBS phenotype (Dowling-Meara), establishing structure-function correlation for keratin filament assembly. Sequence analysis of entire coding sequences of KRT5 and KRT14 in EBS patients; analysis of implications for protein structure and KIF formation Human mutation Medium 16786515
2009 EBS keratinocytes carrying a KRT5 mutation (V186L) form cytoplasmic keratin filament aggregates in response to heat stress, demonstrating that mutant KRT5 causes keratin cytoskeleton instability under mechanical/thermal stress; the chemical chaperone TMAO reduces aggregate formation, indicating that protein misfolding underlies the cytoskeletal disruption. Immortalized cell lines from EBS patients (KRT5 V186L mutation); heat stress experiments; assessment of keratin aggregate formation; TMAO treatment Journal of dermatological science Medium 19157792
2010 Different KRT5 missense mutations (I183M, E475G, V186L) produce distinct degrees of cellular fragility under heat stress in primary keratinocytes, establishing genotype-phenotype relationships at the cellular level; TMAO pretreatment dose-dependently reduces keratin aggregate formation and cell loss in all three mutant backgrounds, suggesting protein stabilization as a therapeutic mechanism. Primary EBS keratinocyte cultures from patients with identified KRT5 mutations; heat stress assays; TMAO treatment; quantification of aggregate-containing cells and cell loss The British journal of dermatology Medium 20128788
2011 Mutations in KRT5 and KRT14 affecting highly conserved helix boundary motifs of the rod domains, and the KRT14 helix initiation motif in particular, are associated with the severest EBS (Dowling-Meara) phenotype, reinforcing that these structural motifs are critical for keratin filament assembly and mechanical integrity of basal keratinocytes. Genomic DNA and cDNA sequencing of KRT5 and KRT14 in 76 EBS probands; immunofluorescence microscopy with K5 and K14 antibodies on skin biopsies The British journal of dermatology Medium 21375516
2014 Pre-existing p63+/Krt5+ distal airway stem cells (DASCp63/Krt5) undergo proliferative expansion in response to influenza-induced lung damage and assemble into nascent alveoli; selective ablation of DASCp63/Krt5 in vivo prevents lung regeneration, leading to pre-fibrotic lesions and deficient oxygen exchange; single DASCp63/Krt5-derived pedigrees differentiate to type I and II pneumocytes as well as bronchiolar secretory cells after transplantation. In vivo selective ablation of Krt5+ cells; transplantation of single-cell-derived pedigrees into infected lung; lineage tracing in mouse influenza model Nature High 25383540
2014 TGFBR3 and JUND form a negative-feedback circuit that regulates KRT5 expression in single basal-like breast epithelial cells during 3D organotypic culture; the circuit depends on ECM engagement, as cell detachment causes rewiring triggered by RPS6 dephosphorylation and maintained by juxtacrine tenascin C, establishing KRT5 as part of a dynamic ECM-dependent gene expression program. Single-cell gene expression analysis; 3D organotypic culture; genetic perturbation of TGFBR3 and JUND; detachment assays; in vivo intraductal colonization assay Nature cell biology Medium 24658685
2019 Biallelic (homozygous) KRT5 null mutations cause complete absence of KRT5 RNA and protein expression (human KRT5 knockout), resulting in perinatal lethal EBS, demonstrating that KRT5 is essential for basal keratinocyte survival; two homozygous KRT5 missense variants disrupt keratin 5 expression detected by immunofluorescence, causing generalized EBS with recessive inheritance. Whole exome sequencing and NGS panel; expression profiling; immunofluorescence microscopy on skin tissue; ultrastructural analysis Matrix biology High 31302245
2019 Krt5+/Krt15+ foregut basal progenitor cells give rise to tumors in response to gastric acid stress in a Cyclooxygenase-2 (COX-2)-dependent manner, establishing that KRT5+ basal progenitors are the cell of origin for these tumors and that COX-2 is required downstream of Krt5+ cell activation. Genetically engineered mouse models; lineage tracing of Krt5+ cells; COX-2 genetic/pharmacological manipulation; tumor formation assays Nature communications Medium 31110179
2020 FoxM1 directly binds to a consensus AP-2 cis element in the KRT5 promoter to regulate KRT5 gene expression; KRT5 knockdown prevents migration (but not proliferation) of ovarian cancer cells, establishing KRT5 as a downstream transcriptional target of FoxM1 required for cell migration. ChIP-seq; RNA-seq; qPCR; Western blot; wound healing and migration assays in KRT5-knockdown SK-OV-3 cells Gene Medium 32659254
2020 Trp53 mutation in Krt5-expressing basal cells results in more efficient tumorigenesis of muscle-invasive bladder cancer with squamous differentiation compared to Trp53 mutation in Upk2-expressing luminal cells, establishing Krt5+ basal cells as a cell of origin for basal squamous subtype bladder cancer. Lineage-specific Cre-mediated Trp53 mutation in Krt5+ vs. Upk2+ cells in mouse chemical carcinogenesis model; morphological and genetic tumor characterization The American journal of pathology Medium 32339497
2021 Human alveolar type 2 cells (hAEC2s) transdifferentiate into KRT5+ basal cells in response to TGF-β1 signaling and anti-BMP signaling from fibrotic mesenchyme; this transdifferentiation proceeds through alveolar-basal intermediate cell states, establishing a causal lineage trajectory from hAEC2 to metaplastic KRT5+ basal cells in human lung fibrosis. Organoid co-culture of hAEC2s with lung mesenchyme; single-cell RNA sequencing; TGF-β1 and BMP pathway perturbation; trajectory analysis; in vivo transplantation; histologic analysis of IPF lung Nature cell biology High 34969962
2021 KRT5 mutation causes collapsed keratin intermediate filaments and intraepidermal blisters without altering the interaction between keratin 5 and keratin 14 or the quantitative protein levels; additionally, KRT5 mutation inhibits MAPK signaling and upregulates desmosomal protein DSG1, and EGFR phosphorylation inhibition upregulates DSG1 in vitro, establishing that KRT5 maintains DSG1 expression through MAPK/EGFR signaling. Biochemical experiments in patient keratinocytes with homozygous KRT5 mutation; immunofluorescence; co-immunoprecipitation of K5 and K14; Western blot for MAPK and DSG1; EGFR inhibitor treatment in vitro Frontiers in genetics Medium 34912369
2023 TRIM29 physically interacts with KRT5 (confirmed by co-immunoprecipitation) and promotes ubiquitination-mediated degradation of KRT5; TRIM29 knockdown decreases KRT5 ubiquitination levels and enhances KRT5 protein stability and expression, and KRT5 knockdown neutralizes the anti-proliferative effect of TRIM29 knockdown in colon cancer cells. Co-immunoprecipitation; cycloheximide chase assay; Western blot; CCK-8, colony formation and EDU assays; KRT5 and TRIM29 knockdown in colon cancer cells Open life sciences Medium 37671092
2023 KRT5 downregulation in keratinocytes (via CRISPR/Cas9 or shRNA) decreases expression of Notch ligands in keratinocytes and Notch1 intracellular domain in melanocytes, leading to increased TYR and decreased Fascin1 expression in melanocytes; activation of Notch signaling reverses these effects on melanogenesis, establishing that KRT5 in keratinocytes regulates melanin metabolism in melanocytes through a Notch signaling pathway. CRISPR/Cas9 site-directed mutation and lentivirus-mediated shRNA KRT5 knockdown in keratinocytes; Notch inhibitor and activator treatment of melanocytes; Western blot; immunohistochemistry of DDD patient lesions with KRT5 mutations Experimental dermatology Medium 36809573
2023 KRT5+ basal cell migration within the fibrotic lung is modulated by ECM composition and organisation; SPARC overexpression in IPF fibroblast-derived ECM restricts KRT5+ cell migration in vitro, identifying SPARC as an ECM component that regulates KRT5+ cell behavior in pulmonary fibrosis. In vitro migration assays on defined ECM; mass spectrometry-based proteomics of ECM from IPF vs. control fibroblasts; SPARC overexpression in fibroblast-derived matrix; KRT5+ cell migratory assays on fibrotic lung collagen Nature communications Medium 37758700
2025 p63 regulates the Krt8-to-Krt5 transition during ameloblast cell differentiation in the enamel organ, paralleling its function in skin development; this regulation involves chromatin landscape remodeling by p63 at shared transcription factor binding sites (p63 and AP-2 family members). Single-cell RNA sequencing from mouse incisors; trajectory reconstruction; comparative transcriptome analysis; comparative motif discovery; chromatin accessibility analyses (ATAC-seq) bioRxivpreprint Low 39990386
2024 Epithelial detachment and cyclical mechanical stretch drive reduction of KRT5 expression in airway epithelial cells, providing a mechanism for the emergence of a KRT5low/KRT17+ transitional basal cell state in IPF fibrotic niches. Monolayer airway epithelial cell cultures subjected to detachment and cyclical mechanical stretch; keratin expression measurements; spatial transcriptomics and imaging mass cytometry of IPF lung tissue bioRxivpreprint Low

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 433 25383540
2021 Human alveolar type 2 epithelium transdifferentiates into metaplastic KRT5+ basal cells. Nature cell biology 209 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 86 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 66 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
2023 Lung extracellular matrix modulates KRT5+ basal cell activity in pulmonary fibrosis. Nature communications 48 37758700
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
2020 FoxM1 promotes the migration of ovarian cancer cell through KRT5 and KRT7. Gene 44 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 19 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) 15 32977822
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 13 31302245
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
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
2023 TRIM29 knockdown prevented the colon cancer progression through decreasing the ubiquitination levels of KRT5. Open life sciences 8 37671092
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
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
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 1 41341913
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 [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

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