of the Max - MDC

Structure of the Group
Group Leader
Prof. Dr. Claus Scheidereit
Dr. Ruth Schmidt-Ullrich
Dr. Buket Yilmaz*
Philip Tomann*
Elmar Wegener*
Secretariat
Daniela Keyner
Scientists
Dr. Annette Ahlers
Dr. Norbert Henke*
Dr. Michael Hinz
Dr. Eva Kärgel
Dr. Giulietta Roel*
Graduate Students
Seda Cöl Arslan
Jan Ebert
Andrea Oeckinghaus
Michael Stilmann
Yoshiaki Sunami*
Technical Assistants
Rudolf Dettmer*
Karin Ganzel*
Sabine Jungmann
Inge Krahn*
Sarah Ugowski
* part of the period reported
Figure 2. Requirement of NF-κB for early hair follicle development. NF-κB activation in developing hair follicles was visualized by X-Gal staining of E14.5 embryos
from NF-κB reporter mice carrying the β-galactosidase gene under the control of NF-κB DNA binding sites (Igκ-conA-lacZ). Epidermal NF-κB activation is completely
lost, when reporter mice are mated with NF-κB repressor mice (IκBα∆N). Likewise, placodal NF-κB activity is lost, when reporter mice were crossed with mice
lacking functional Eda A1(tabby) or EdaR (downless) expression, although NF-κB activity in blood vessel endothelial cells is maintained (left panels). Thus,
IKK/NF-κB is under control of the EdaA1/EdaR cascade. Downstream targets include sonic hedgehog (Shh) and cyclin D1 (CycD1) (center panel). The expression
of Shh and CycD1 is lost in NF-κB repressor mice (IκBα∆N), as shown by in situ hybridization on E15.5 embryonic sagittal skin sections. NF-κB is not needed for
the initiation of hair follicle development, but for the subsequent proliferation of epidermal cells, mediated by Shh and CycD1, which causes the down-growth of
the developing hair follicle into the underlying mesenchyme.
ac hypertrophy. Likewise, a causal link between hypertrophy-induced
NF-κB activation in endothelium and renal
damage was demonstrated using mice with endothelial cellspecific
Cre-lox mediated NF-κB suppression. Surprisingly,
NF-κB inhibition exclusively in endothelial cells attenuates
hypertension-mediated inflammatory effects on neighboring
renal structures, indicating an interplay of NF-κB
signaling in vascular endothelial cells with that in macrophages
and the kidney.
Selected Publications
Oeckinghaus, A, Wegener, E, Welteke, V, Ferch, U, Çöl Arslan, S,
Ruland, J, Scheidereit, C, Krappmann, D. (2007). TRAF6 mediated
Malt1 ubiquitination triggers IKK/NF-κB signalling upon T
cell activation. EMBO J., in press
Hinz, M, Broemer, M, Çöl Arslan, S, Dettmer, R, Scheidereit, C.
(2007). Signal-responsiveness of IκB kinases is determined by
Cdc37-assisted transient interaction with Hsp90. J. Biol. Chem.
in press.
Henke, N, Schmidt-Ullrich, R, Dechend, R, Park, JK, Qadri, F,
Wellner, M, Obst, M, Gross, V, Dietz, R, Luft, FC, Scheidereit, C,
and Müller DN. (2007). Vascular endothelial-specific NF-κB suppression
attenuates hypertension-induced renal damage. Circ
Res 101, 268-276.
Schmidt-Ullrich, R, Tobin, DJ, Lenhard, D, Schneider, P, Paus, R,
Scheidereit, C. (2006). NF-κB transmits Eda A1/EdaR signalling
to activate Shh and cyclin D1 expression, and controls post-initiation
hair placode down-growth. Development 133, 1045-1057.
Mehrhof, FB, Schmidt-Ullrich, R, Dietz, R, Scheidereit, C. (2005).
Regulation of Vascular Smooth Muscle Cell Proliferation: Role of
NF-κB Revisited. Circ Res 96, 958-964
Cancer Research 97