Biomedical Engineering Reference
In-Depth Information
which are often misconstrued as passive barriers, rely on NF-
B in their responses
to physiological and nonphysiological stress. Likewise, the development and periph-
eral homeostasis of leukocytes is critically linked to NF-
κ
κ
B as a regulator of apop-
tosis. Research has tended to focus on NF-
B signaling in the effector functions of
these hematopoietic components of the immune system and its role has thus been
well established in innate responses to all classes of pathogen. In addition, there is
now increasing evidence to support a broader model in which NF-
κ
B also supports
the resolution of inflammatory responses and, in situations that require it, initiation
and coordination of the adaptive immune response.
κ
REFERENCES
[1]
Beg, A.A., Sha, W.C., Bronson, R.T. et al., Constitutive NF-kappaB activation,
enhanced granulopoiesis, and neonatal lethality in I kappaB alpha-deficient mice,
Genes Dev., 9, 2736, 1995.
[2]
Seitz, C.S., Lin, Q., Deng, H. et al., Alterations in NF-kappaB function in transgenic
epithelial tissue demonstrate a growth inhibitory role for NF-kappaB, Proc. Natl.
Acad. Sci. USA, 95, 2307, 1998.
[3]
Banno, T., Gazel, A., and Blumenberg, M., Pathway-specific profiling identifies the
NF-kappaB-dependent tumor necrosis factor alpha-regulated genes in epidermal kera-
tinocytes, J. Biol. Chem., 280, 18973, 2005.
[4]
Pasparakis, M., Courtois, G., Hafner, M. et al., TNF-mediated inflammatory skin
disease in mice with epidermis-specific deletion of IKK2, Nature, 417, 861, 2002.
[5]
Nenci, A., Huth, M., Funteh, A. et al., Skin lesion development in a mouse model of
incontinentia pigmenti is triggered by NEMO deficiency in epidermal keratinocytes
and requires TNF signaling, Hum. Mol. Genet., 15, 531, 2006.
[6]
Li, Q., Lu, Q., Hwang, J.Y. et al., IKK1-deficient mice exhibit abnormal development
of skin and skeleton, Genes Dev., 13, 1322, 1999.
[7]
Takeda, K., Takeuchi, O., Tsujimura, T. et al., Limb and skin abnormalities in mice
lacking IKKα, Science, 284, 313, 1999.
[8]
Hu, Y., Baud, V., Delhase, M. et al., Abnormal morphogenesis but intact IKK acti-
vation in mice lacking the IKKα subunit of IkappaB kinase, Science, 284, 316, 1999.
[9]
Hu, Y., Baud, V., Oga, T. et al., IKKalpha controls formation of the epidermis
independently of NF-kappaB, Nature, 410, 710, 2001.
[10]
Zandi, E., Chen, Y., and Karin, M., Direct phosphorylation of IkappaB by IKKalpha
and IKKbeta: Discrimination between free and NF-kappaB-bound substrate, Science,
281, 1360, 1998.
[11]
Sil, A.K., Maeda, S., Sano, Y. et al., IkappaB kinase-α acts in the epidermis to control
skeletal and craniofacial morphogenesis, Nature, 428, 660, 2004.
[12]
Egan, L.J., de Lecea, A., Lehrman, E.D. et al., Nuclear factor-kappaB activation
promotes restitution of wounded intestinal epithelial monolayers, Am. J. Physiol. Cell
Physiol., 285, C1028, 2003.
[13]
Egan, L.J., Eckmann, L., Greten, F.R. et al., IkappaB-kinaseβ-dependent NF-kappaB
activation provides radioprotection to the intestinal epithelium, Proc. Natl. Acad. Sci.
USA, 101, 2452, 2004.
[14]
Jiang, D., Liang, J., Fan, J. et al., Regulation of lung injury and repair by Toll-like
receptors and hyaluronan, Nat. Med., 11, 1173, 2005.
 
Search WWH ::




Custom Search