SPINK5

(redirected from LEKTI)

SPINK5

A gene on chromosome 5q32 that encodes a multidomain serine protease inhibitor with 15 potential inhibitory domains, which may play a role in skin and hair morphogenesis and anti-inflammatory and/or antimicrobial protection of mucous epithelia.

Molecular pathology
SPINK5 mutations cause Netherton syndrome.
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References in periodicals archive ?
On the contrary, IL-4/13 significantly decreased, while IFN-a increased the expression of LEKTI and caspase-14.
LEKTI inhibits FLG degradation processing through suppressing the proteases mentioned above.
Here, we examined the expression of FLG and related serine proteases (KLK5, KLK7, matriptase, and CAP1), cysteine protease caspase-14, and LEKTI by immunohistochemical staining in acute and chronic lesions of AD.
Expression of FLG, LEKTI, caspase14, KLK7, KLK5, matriptase, and CAP1 proteins was evaluated by Western blotting.
As shown in [Figure 1], FLG, LEKTI, and caspase14 expressions were significantly decreased, whereas matriptase, CAP1, KLK5, and KLK7 expressions were increased in acute AD lesions, as compared to normal controls.
As shown in [Figure 4]a, IL-4/13 significantly reduced LEKTI mRNA in both NHK and HaCaT cells.
The protein expression levels of LEKTI by Western blotting analysis were consistent with respective mRNA changes in HC and LC culture conditions, as shown in [Figure 4]b.
LEKTI can globally inhibit FLG degradation processing through suppressing the proteases mentioned above.
LEKTI is expressed in the most differentiated epidermis.
The SPs expression (such as KLK5, 7, matriptase, and CAP1) was higher in acute lesions than chronic lesions, while caspase14, LEKTI expression was lower than in chronic lesions.
In the absence of LEKTI, serine proteases increase markedly and attack structures in the stratum corneum and the underlying epidermis.
Serine protease activity and residual LEKTI expression determine phenotype in Netherton syndrome.