NF-κB and inflammation in genetic disease

[1]  P. Chambon,et al.  Localized inflammatory skin disease following inducible ablation of I kappa B kinase 2 in murine epidermis. , 2006, The Journal of investigative dermatology.

[2]  P. Chambon,et al.  Skin lesion development in a mouse model of incontinentia pigmenti is triggered by NEMO deficiency in epidermal keratinocytes and requires TNF signaling. , 2006, Human molecular genetics.

[3]  P. Proost,et al.  Synergy in cytokine and chemokine networks amplifies the inflammatory response. , 2005, Cytokine & growth factor reviews.

[4]  A. Smahi,et al.  A new mutation in exon 7 of NEMO gene: late skewed X-chromosome inactivation in an incontinentia pigmenti female patient with immunodeficiency , 2005, Human Genetics.

[5]  Michael Karin,et al.  NF-κB: linking inflammation and immunity to cancer development and progression , 2005, Nature Reviews Immunology.

[6]  Zhijian J. Chen.  Ubiquitin signalling in the NF-κB pathway , 2005, Nature Cell Biology.

[7]  M. Karin,et al.  NOD2 and Crohn's disease: loss or gain of function? , 2005, Immunity.

[8]  Sankar Ghosh,et al.  Signaling to NF-kappaB. , 2004, Genes & development.

[9]  M. D'urso,et al.  Molecular analysis of the genetic defect in a large cohort of IP patients and identification of novel NEMO mutations interfering with NF-kappaB activation. , 2004, Human molecular genetics.

[10]  K. Wilkinson.  Signal transduction: Aspirin, ubiquitin and cancer , 2003, Nature.

[11]  C. Bodemer,et al.  Late recurrence of inflammatory first-stage lesions in incontinentia pigmenti: an unusual phenomenon and a fascinating pathologic mechanism. , 2003, Archives of dermatology.

[12]  Carl Nathan,et al.  Points of control in inflammation , 2002, Nature.

[13]  E. García-Ramallo,et al.  Resident Cell Chemokine Expression Serves as the Major Mechanism for Leukocyte Recruitment During Local Inflammation , 2002, The Journal of Immunology.

[14]  A. Paller,et al.  Incontinentia pigmenti: a review and update on the molecular basis of pathophysiology. , 2002, Journal of the American Academy of Dermatology.

[15]  G. Courtois,et al.  TNF-mediated inflammatory skin disease in mice with epidermis-specific deletion of IKK2 , 2002, Nature.

[16]  D. Golan,et al.  CFTR is a pattern recognition molecule that extracts Pseudomonas aeruginosa LPS from the outer membrane into epithelial cells and activates NF-κB translocation , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[17]  W. Colledge,et al.  ΔF508-CFTR Causes Constitutive NF-κB Activation through an ER-Overload Response in Cystic Fibrosis Lungs , 2002 .

[18]  T. Lawrence,et al.  Possible new role for NF-κB in the resolution of inflammation , 2001, Nature Medicine.

[19]  C. Shaw,et al.  A recurrent deletion in the ubiquitously expressed NEMO (IKK-gamma) gene accounts for the vast majority of incontinentia pigmenti mutations. , 2001, Human molecular genetics.

[20]  Chi A. Ma,et al.  Specific missense mutations in NEMO result in hyper-IgM syndrome with hypohydrotic ectodermal dysplasia , 2001, Nature Immunology.

[21]  G. Courtois,et al.  Atypical forms of incontinentia pigmenti in male individuals result from mutations of a cytosine tract in exon 10 of NEMO (IKK-gamma). , 2001, American journal of human genetics.

[22]  M. Karin,et al.  IKKβ Is Essential for Protecting T Cells from TNFα-Induced Apoptosis , 2001 .

[23]  A. Fischer,et al.  X-linked anhidrotic ectodermal dysplasia with immunodeficiency is caused by impaired NF-κB signaling , 2001, Nature Genetics.

[24]  S. Orlow,et al.  A novel X-linked disorder of immune deficiency and hypohidrotic ectodermal dysplasia is allelic to incontinentia pigmenti and due to mutations in IKK-gamma (NEMO). , 2000, American journal of human genetics.

[25]  S. Makarov.  NF-κB as a therapeutic target in chronic inflammation: recent advances , 2000 .

[26]  Klaus Rajewsky,et al.  NEMO/IKKγ-Deficient Mice Model Incontinentia Pigmenti , 2000 .

[27]  V. Godfrey,et al.  Female mice heterozygous for IKK gamma/NEMO deficiencies develop a dermatopathy similar to the human X-linked disorder incontinentia pigmenti. , 2000, Molecular cell.

[28]  S. Klauck,et al.  Genomic rearrangement in NEMO impairs NF-κB activation and is a cause of incontinentia pigmenti , 2000, Nature.

[29]  A. Israël.  The IKK complex: an integrator of all signals that activate NF-κB? , 2000 .

[30]  T. Mak,et al.  Severe liver degeneration and lack of NF-kappaB activation in NEMO/IKKgamma-deficient mice. , 2000, Genes & development.

[31]  R. V. van Leeuwen,et al.  Incontinentia Pigmenti: An Extensive Second Episode of a “First‐Stage” Vesicobullous Eruption , 2000, Pediatric dermatology.

[32]  Inder M. Verma,et al.  Severe Liver Degeneration in Mice Lacking the IκB Kinase 2 Gene , 1999 .

[33]  L. Old,et al.  Absence of tumor necrosis factor rescues RelA-deficient mice from embryonic lethality. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[34]  David Baltimore,et al.  Embryonic lethality and liver degeneration in mice lacking the RelA component of NF-κB , 1995, Nature.

[35]  D. Donnai,et al.  Incontinentia pigmenti (Bloch-Sulzberger syndrome). , 1993, Journal of medical genetics.

[36]  C. Xiao,et al.  NF-κB, an Evolutionarily Conserved Mediator of Immune and Inflammatory Responses , 2005 .

[37]  P. Tak,et al.  NF-κB: a key role in inflammatory diseases , 2001 .

[38]  M. Karin,et al.  Phosphorylation meets ubiquitination: the control of NF-[kappa]B activity. , 2000, Annual review of immunology.