KRT10

SECTIONS

1 - Function
2 - Involvement in disease
3 - Sequence similarities
4 - Tissue specificity
5 - Cellular localization
6 - Alternative names
7 - Database links
8 - Target type
9 - Primary research area
10 - Molecular weight

Function

Plays a role in the establishment of the epidermal barrier on plantar skin (By similarity). Involved in the maintenance of cell layer development and keratin filament bundles in suprabasal cells of the epithelium (By similarity).

(Microbial infection) Acts as a mediator of S.aureus adherence to desquamated nasal epithelial cells via clfB, and hence may play a role in nasal colonization.

(Microbial infection) Binds S.pneumoniae PsrP, mediating adherence of the bacteria to lung cell lines. Reduction of levels of KRT10 keratin decrease adherence, overexpression increases adherence. Neither protein has to be glycosylated for the interaction to occur.

Involvement in disease

Epidermolytic hyperkeratosis 2A

EHK2A

An autosomal dominant form of epidermolytic hyperkeratosis, a skin disorder characterized by widespread blistering and an ichthyotic erythroderma at birth that persist into adulthood. Histologically there is a diffuse epidermolytic degeneration in the lower spinous layer of the epidermis. Within a few weeks from birth, erythroderma and blister formation diminish and hyperkeratoses develop. EHK2 inheritance is autosomal dominant or autosomal recessive.

None

The disease is caused by variants affecting the gene represented in this entry.

Epidermolytic hyperkeratosis 2B, autosomal recessive

EHK2B

An autosomal recessive form of epidermolytic hyperkeratosis, a skin disorder characterized by widespread blistering and an ichthyotic erythroderma at birth that persist into adulthood. Histologically there is a diffuse epidermolytic degeneration in the lower spinous layer of the epidermis. Within a few weeks from birth, erythroderma and blister formation diminish and hyperkeratoses develop.

None

The disease is caused by variants affecting the gene represented in this entry.

Ichthyosis, annular epidermolytic, 1

AEI1

A form of annular epidermolytic ichthyosis, an autosomal dominant skin disorder characterized by polycyclic, migratory erythematous and scaly plaques. AEI1 is characterized by the development of widespread erythematous blistering in the neonatal period or early childhood that subsides over time.

None

The disease is caused by variants affecting the gene represented in this entry.

Ichthyosis with confetti

IWC

An autosomal dominant, rare skin condition characterized by slowly enlarging islands of normal skin surrounded by erythematous ichthyotic patches in a reticulated pattern. The condition starts in infancy as a lamellar ichthyosis, with small islands of normal skin resembling confetti appearing in late childhood and at puberty. Histopathologic findings include band-like parakeratosis, psoriasiform acanthosis, and vacuolization of keratinocytes with binucleated cells in the upper epidermis, sometimes associated with amyloid deposition in the dermis. Ultrastructural abnormalities include perinuclear shells formed from a network of fine filaments in the upper epidermis.

None

The disease is caused by variants affecting the gene represented in this entry.

Ichthyosis histrix, Lambert type

IHL

An autosomal dominant form of ichthyosis, a disorder of keratinization with abnormal differentiation and desquamation of the epidermis, resulting in abnormal skin scaling. IHL is characterized by normal skin at birth that develops striking spiny hyperkeratotic lesions within a few months. There is sparing of the face, palms, and soles, and affected individuals do not experience blistering.

None

The disease may be caused by variants affecting the gene represented in this entry.

Sequence similarities

Belongs to the intermediate filament family.

Tissue specificity

Seen in all suprabasal cell layers including stratum corneum. Expressed on the surface of lung cell lines (PubMed:19627498). Localized on the surface of desquamated nasal epithelial cells (at protein level) (PubMed:12427098).