IKKbeta leads to an inflammatory skin disease resembling interface dermatitis. (Q42468137)

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19 January 2020

title

IKKbeta leads to an inflammatory skin disease resembling interface dermatitis (English)

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19 January 2020

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1

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19 January 2020

Manuel Navarro

2

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19 January 2020

Marina Garín

3

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19 January 2020

Paloma Pérez

4

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19 January 2020

M. Llanos Casanova

5

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19 January 2020

Angel Ramirez

10

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19 January 2020

author name string

Rodolfo Moreno

6

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19 January 2020

José L Jorcano

7

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19 January 2020

José L Cascallana

8

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19 January 2020

Ana Bravo

9

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19 January 2020

language of work or name

English

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publication date

4 March 2010

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Journal of Investigative Dermatology

19 January 2020

published in

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19 January 2020

volume

130

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19 January 2020

issue

6

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19 January 2020

page(s)

1598-1610

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Mice lacking the transcription factor RelB develop T cell-dependent skin lesions similar to human atopic dermatitis.

19 January 2020

cites work

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Constitutive IKK2 activation in acinar cells is sufficient to induce pancreatitis in vivo

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IkappaBalpha deficiency results in a sustained NF-kappaB response and severe widespread dermatitis in mice

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IKK beta suppression of TSC1 links inflammation and tumor angiogenesis via the mTOR pathway

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Severe liver degeneration in mice lacking the IkappaB kinase 2 gene

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IKKbeta couples hepatocyte death to cytokine-driven compensatory proliferation that promotes chemical hepatocarcinogenesis

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Female mice heterozygous for IKK gamma/NEMO deficiencies develop a dermatopathy similar to the human X-linked disorder incontinentia pigmenti

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Chemokines in the pathogenesis of lichenoid tissue reactions

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IKKalpha enhances human keratinocyte differentiation and determines the histological variant of epidermal squamous cell carcinomas

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Skin lesion development in a mouse model of incontinentia pigmenti is triggered by NEMO deficiency in epidermal keratinocytes and requires TNF signaling.

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Role of phosphorylated p50-NF-kappaB in the ultraviolet response of mouse skin

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Cellular and molecular pathophysiology of cutaneous drug reactions

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The nonobese diabetic scid mouse: model for spontaneous thymomagenesis associated with immunodeficiency

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A keratin K5Cre transgenic line appropriate for tissue-specific or generalized Cre-mediated recombination

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I{kappa}B kinase (IKK){beta}, but not IKK{alpha}, is a critical mediator of osteoclast survival and is required for inflammation-induced bone loss

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IkappaB kinases phosphorylate NF-kappaB p65 subunit on serine 536 in the transactivation domain

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NEMO/IKK gamma-deficient mice model incontinentia pigmenti.

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Tumour necrosis factor-alpha depletes histone deacetylase 1 protein through IKK2.

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7 January 2021

Phosphorylation of p53 by IkappaB kinase 2 promotes its degradation by beta-TrCP.

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