KRT5

Last update 08 May 2025

Basic Info

Synonyms

58 kDa cytokeratin, CK-5, Cytokeratin-5

+ [8]

Introduction

Required for the formation of keratin intermediate filaments in the basal epidermis and maintenance of the skin barrier in response to mechanical stress (By similarity). Regulates the recruitment of Langerhans cells to the epidermis, potentially by modulation of the abundance of macrophage chemotactic cytokines, macrophage inflammatory cytokines and CTNND1 localization in keratinocytes (By similarity).

100 Clinical Results associated with KRT5

100 Translational Medicine associated with KRT5

0 Patents (Medical) associated with KRT5

2,520

Literatures (Medical) associated with KRT5

01 Jun 2025·Biochemistry and Biophysics Reports

Fibroblasts fluctuating between mesenchyme and epithelium are involved in hair follicle mesenchyme development

Article

Author: Shimbo, Takashi ; Omura, Souki ; Tanaka, Akio ; Fujimoto, Manabu ; Saga, Kotaro ; Ouchi, Yuya ; Tamai, Katsuto ; Hirose, Yoshikazu ; Kitayama, Tomomi ; Miura, Asaka

The transition between the mesenchyme and epithelium contributes to the development of various tissues. During skin development, epithelial-mesenchymal transition in the ectodermal epithelia is involved in the development of the dermal mesenchyme in early embryos. However, the precise roles and functions of epithelial-mesenchymal/mesenchymal-epithelial transition in cutaneous development have not been fully elucidated. In this study, we aimed to elucidate these roles and functions in the neonatal mouse skin. We conducted single-cell RNA sequencing and immunohistochemical analyses to search for Pdgfra-expressing (Pα ⁺) fibroblasts with transition activities to/from Krt5-expressing keratinocytes. We determined that the Pα ⁺/Krt5-lineage (K5 ^lin+) fibroblasts significantly contributed to developing hair follicle dermal stem cells to generate lower dermal papilla cells and lower dermal sheath cells. In the developing mouse skin, K5 ^lin ⁺ fibroblasts appeared concurrently with hair follicle development and formed outer edge cells in the early dermal papilla on embryonic day 16.5. K5 ^lin ⁺ hair follicle mesenchymal cells were also maintained in aged mouse skin. These results provide insights into the role and function of the transition between the mesenchyme and epithelium in hair follicle development and maintenance.

01 May 2025·Journal of Gastroenterology

Aldh2 and the tumor suppressor Trp53 play important roles in alcohol-induced squamous field cancerization

Article

Author: Shimonosono, Masataka ; Hirohashi, Kenshiro ; Tamaoki, Masashi ; Oryu, Kohei ; Kondo, Yuki ; Yamada, Atsushi ; Nakai, Yukie ; Uneno, Yu ; Vu, Trang H Nguyen ; Nakagawa, Hiroshi ; Kikuchi, Osamu ; Matsubara, Junichi ; Mitani, Yosuke ; Matsuda, Tomonari ; Naganuma, Seiji ; Flashner, Samuel ; Saito, Tomoki ; Yamamoto, Yoshihiro ; Sunami, Tomohiko ; Ohashi, Shinya ; Kataoka, Shigeki ; Muto, Manabu ; Katada, Chikatoshi ; Kondo, Tomohiro ; Yokoyama, Akira

AbstractBackgroundField cancerization defined by multiple development of squamous cell carcinomas (SCCs) in upper aerodigestive tract was explained by excessive alcohol intake. A dysfunctional mitochondrial aldehyde dehydrogenase 2 (Aldh2) delays the clearance of acetaldehyde, a genotoxic alcohol metabolite, and increases SCC risks. TP53 plays key roles in squamous carcinogenesis. However, the mechanism of alcohol-mediated squamous field cancerization has not been clearly elucidated.MethodsWe developed a novel genetically engineered mouse strain KTPA–/– (Krt5CreERT2; Trp53loxp/loxp; Aldh2–/–) featuring Aldh2-loss concurrent with epithelial-specific Trp53 deletion. These mice were given 10%-EtOH, and we evaluated the development of squamous cell carcinogenesis histologically and genetically.ResultsWidespread multifocal rete ridges (RRs), characterized by downward growth of proliferative preneoplastic cells, were found only in Aldh2+/– and Aldh2–/– mice with keratin5-specific Trp53 deletion (KTPA+/– and KTPA–/– mice, respectively), and alcohol drinking apparently increased RR formation rate. SCC occurred only in KTPA–/– (Aldh2 loss/TP53 loss) mice with alcohol drinking (15/18: 83%). Total alcohol consumption volume was significantly higher in KTPA–/– (Aldh2 loss/TP53 loss) mice with SCCs than those without SCCs. Further, target sequence revealed the occurrence of genetic abnormalities including Trp53 mutations in the esophageal epithelium of Aldh2–/– mice with alcohol drinking, suggesting direct mutagenic effects of alcohol drinking to the esophageal epithelium.ConclusionThis study provides for the first time the evidence that alcohol drinking, Aldh2 dysfunction and Trp53 loss cooperate in squamous field cancerization. Alcohol consumption volume affects the SCCs development, even in the same genotype.

15 Apr 2025·Journal of Virology

HSV-1 UL56 protein recruits cellular NEDD4-family ubiquitin ligases to suppress CD1d expression and NKT cell function

Article

Author: Lo, Jae Ho ; Yuan, Weiming ; Dong, Jonathan ; Gao, Xuedi ; Wang, Yi ; Rao, Samhita Divakar ; Chen, Siyang ; Yang, Rirong ; Qiu, Lingxi ; Pham, Thanh ; Xi, Jingwen ; Engel, Esteban A. ; Crump, Colin M. ; Hao, Jingting ; Shao, Xinyue

ABSTRACT Herpesviruses, including α-herpesvirus and herpes simplex virus (HSV-1), are masters of immune evasion. Previously we demonstrated that CD1d-restricted NKT cells are required for optimal anti-HSV-1 immune responses and HSV-1 efficiently downregulates CD1d to suppress NKT cell function. To delineate how the virus evades NKT cell function and establishes infection in vivo , we screened an HSV-1 expression library to identify the viral gene(s) downregulating CD1d and discovered that a leaky late gene, UL56, most efficiently suppresses CD1d expression by degrading the protein, apparently via both proteasome- and lysosome-dependent pathways. To investigate the molecular mechanism of UL56 suppression of CD1d expression, we purified and identified UL56-associated proteins by mass spectrometry. The most abundant associated proteins were members of NEDD4 E3 ubiquitin ligase family. Interestingly overexpression of one member, NEDD4L is sufficient to downregulate CD1d expression. However, different from the K5 protein from Kaposi sarcoma’s herpesvirus (KSHV), UL56 and NEDD4L did not directly ubiquitinate CD1d. CD1d protein lacking the key lysine residue in its cytoplasmic tail is similarly downregulated by UL56 and NEDD4L protein. Co-expression of UL56 and NEDD4L synergistically reduced the CD1d expression, suggesting that UL56 collaborates with NEDD4L to downregulate CD1d. During in vivo infection, UL56-deficient mutant virus showed significantly weaker virulence in NKT-sufficient mice but demonstrated higher virulence in mutant mice lacking NKT cells. All our results supported that at least one of the pathogenesis functions of UL56 is its suppression of NKT cell function during infection. IMPORTANCE In the large DNA genomes of herpeviruses, there are many genes encoding associate proteins. Most of these proteins are not essential for viral replication but play key roles in viral pathogenesis, in particular, modulating the host immune system to allow efficient viral replication in vivo and latency. The HSV-1 UL56 gene is one of such genes, and its exact pathogenic roles have remain elusive. After we demonstrated the essential roles of CD1d-restricted NKT cells in anti-HSV-1 immunity during HSV-1 ocular infection (P. Rao, X. Wen, J. H. Lo, S. Kim, X. Li, et al., J Virol 92:e01490-18, 2018, https://doi.org/10.1128/jvi.01490-18 ), we now screened the HSV-1 expression library and identified UL56 is a key factor downregulating CD1d and suppressing NKT cell function. In this manuscript, we are reporting our molecular mechanism study of how UL56 evades CD1d antigen presentation and NKT cell function.

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KRT5

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