Phenotype of human epidermis with sIL-1ra deficiency

Skin is the largest organ in the body and it serves as a protective barrier. It is made up of an outermost epidermal layer and an underlying dermal layer (Fig 1). The formation and maintenance of the epidermis depend on the precise regulation of keratinocyte proliferation, differentiation and...

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Main Author: Ku, Chee Wai
Other Authors: Tan Nguan Soon
Format: Student Research Poster
Language:English
Published: 2013
Subjects:
Online Access:https://hdl.handle.net/10356/95257
http://hdl.handle.net/10220/8989
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Institution: Nanyang Technological University
Language: English
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spelling sg-ntu-dr.10356-952572020-09-27T20:29:14Z Phenotype of human epidermis with sIL-1ra deficiency Ku, Chee Wai Tan Nguan Soon School of Biological Sciences Interleukin-1 Interleukin-1 receptor antagonist Skin is the largest organ in the body and it serves as a protective barrier. It is made up of an outermost epidermal layer and an underlying dermal layer (Fig 1). The formation and maintenance of the epidermis depend on the precise regulation of keratinocyte proliferation, differentiation and apoptosis. This homeostasis relies on the network of cytokines and growth factors. Perturbation of this homeostasis leads to inflammatory skin diseases and cancer development. Interleukin-1 (IL-1) is a pro-inflammatory cytokine that is constitutively produced by keratinocytes. It is also involved in the proliferation and differentiation of keratinocytes. IL-1 binds to its cognate receptor and can trigger downstream pathways with different outcomes. sIL-1ra binds to IL-1 receptor and prevents the transmission of intracellular response. However, the phenotype of human epidermis when the underlying fibroblast cells is deficient of sIL-1ra remains unclear. [3rd Award] 2013-01-31T02:52:47Z 2019-12-06T19:11:26Z 2013-01-31T02:52:47Z 2019-12-06T19:11:26Z 2007 2007 Student Research Poster Ku, C. W. (2007, March). Phenotype of human epidermis with sIL-1ra deficiency. Presented at Discover URECA @ NTU poster exhibition and competition, Nanyang Technological University, Singapore. https://hdl.handle.net/10356/95257 http://hdl.handle.net/10220/8989 en © 2007 The Author(s). application/pdf
institution Nanyang Technological University
building NTU Library
country Singapore
collection DR-NTU
language English
topic Interleukin-1
Interleukin-1 receptor antagonist
spellingShingle Interleukin-1
Interleukin-1 receptor antagonist
Ku, Chee Wai
Phenotype of human epidermis with sIL-1ra deficiency
description Skin is the largest organ in the body and it serves as a protective barrier. It is made up of an outermost epidermal layer and an underlying dermal layer (Fig 1). The formation and maintenance of the epidermis depend on the precise regulation of keratinocyte proliferation, differentiation and apoptosis. This homeostasis relies on the network of cytokines and growth factors. Perturbation of this homeostasis leads to inflammatory skin diseases and cancer development. Interleukin-1 (IL-1) is a pro-inflammatory cytokine that is constitutively produced by keratinocytes. It is also involved in the proliferation and differentiation of keratinocytes. IL-1 binds to its cognate receptor and can trigger downstream pathways with different outcomes. sIL-1ra binds to IL-1 receptor and prevents the transmission of intracellular response. However, the phenotype of human epidermis when the underlying fibroblast cells is deficient of sIL-1ra remains unclear. [3rd Award]
author2 Tan Nguan Soon
author_facet Tan Nguan Soon
Ku, Chee Wai
format Student Research Poster
author Ku, Chee Wai
author_sort Ku, Chee Wai
title Phenotype of human epidermis with sIL-1ra deficiency
title_short Phenotype of human epidermis with sIL-1ra deficiency
title_full Phenotype of human epidermis with sIL-1ra deficiency
title_fullStr Phenotype of human epidermis with sIL-1ra deficiency
title_full_unstemmed Phenotype of human epidermis with sIL-1ra deficiency
title_sort phenotype of human epidermis with sil-1ra deficiency
publishDate 2013
url https://hdl.handle.net/10356/95257
http://hdl.handle.net/10220/8989
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