(Q28244416)

2

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Hiroshi Nagai

3

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Yuji Shirakata

4

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Xiuju Dai

5

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Satoshi Hirakawa

6

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Sho Tokumaru

7

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Mikiko Tohyama

8

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Lujun Yang

9

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Shintaro Sato

10

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Akira Shizuo

11

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Koji Hashimoto

Journal of Biological Chemistry

12

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language of work or name

English

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publication date

4 August 2006

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published in

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volume

281

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issue

31

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page(s)

22013-20

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cites work

Alterations in NF-kappaB function in transgenic epithelial tissue demonstrate a growth inhibitory role for NF-kappaB.

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Apoptosis signal-regulating kinase 1 (ASK1) is an intracellular inducer of keratinocyte differentiation

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NF-kappaB RelA opposes epidermal proliferation driven by TNFR1 and JNK.

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NF-kappaB blockade and oncogenic Ras trigger invasive human epidermal neoplasia.

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CDK4 regulation by TNFR1 and JNK is required for NF-kappaB-mediated epidermal growth control

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NF-kappaB determines localization and features of cell death in epidermis

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Identification of a member of the MAPKKK family as a potential mediator of TGF-beta signal transduction

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TAB2, a novel adaptor protein, mediates activation of TAK1 MAPKKK by linking TAK1 to TRAF6 in the IL-1 signal transduction pathway

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TAK1 is critical for IkappaB kinase-mediated activation of the NF-kappaB pathway

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Role of the TAB2-related protein TAB3 in IL-1 and TNF signaling

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TAB3, a new binding partner of the protein kinase TAK1

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Essential function for the kinase TAK1 in innate and adaptive immune responses.

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Conditional gene targeting and its application in the skin

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Role of TAK1 and TAB1 in BMP signaling in early Xenopus development

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Mutations in the Drosophila dTAK1 gene reveal a conserved function for MAPKKKs in the control of rel/NF-kappaB-dependent innate immune responses

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TAK1, but not TAB1 or TAB2, plays an essential role in multiple signaling pathways in vivo

21 January 2018

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Targeted disruption of the Tab1 gene causes embryonic lethality and defects in cardiovascular and lung morphogenesis

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TAB2 is essential for prevention of apoptosis in fetal liver but not for interleukin-1 signaling

21 January 2018

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Genomic rearrangement in NEMO impairs NF-kappaB activation and is a cause of incontinentia pigmenti. The International Incontinentia Pigmenti (IP) Consortium

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NEMO/IKK gamma-deficient mice model incontinentia pigmenti.

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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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Limb and skin abnormalities in mice lacking IKKalpha

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Abnormal morphogenesis but intact IKK activation in mice lacking the IKKalpha subunit of IkappaB kinase

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TNF-mediated inflammatory skin disease in mice with epidermis-specific deletion of IKK2

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Phosphatidylinositol 3-Kinase Is a Key Regulator of Early Phase Differentiation in Keratinocytes

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21 January 2018

Identifiers

DOI

10.1074/JBC.M601065200

1 reference

Consolidated OpenCitations Corpus – April 2017

1506850

1506850

1 reference

Consolidated OpenCitations Corpus – April 2017

Consolidated OpenCitations Corpus – April 2017

1 reference