Cur面culumVitae
ClauSSCheidereit
Contactlnfbrmation
Max‑Delbmck‑CenterfbrMolecularMedicmeWC
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13125Belim,Germany Tel"hone
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+49‑30‑9406‑3816 +49‑30‑9406‑3866
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PaFsonallnfbnnation C u n ℃ n t p l i v a t e a d d r e s s DateofBirth23.07.1954DIoysalstr.16 City/CountIySchleswig,Gennany 10629Berim, CitizenshipGennan Germany
Education
Date
Degee
1992
Habilitation
( V e n i a L e g e n d i )
1984
1982
1976‑1982
Ph.D.
(summacumlaude) Diploma
( G r a d e l . 0 )
A p p o i n t m e n t s I A f f i l i a t i o n s
Date
T i t l e
1994‑Present
1992‑PIesent
1989‑1994
1986‑1989 1984‑1985
ResearchGroupLeader, HeadofLaboratoly AmliateProfessor
( P r i v a t d o z e n t ) I n d e p e n d e n t R e s e a r c h GroupLeader
PostdoctoralFellow ResearchAssistant
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Instinmon
FIeeUmversity ofBeIim
P h i l i p p s U m v e r s i t y ofMarburg P h i l i p p s U m v e r s i t y
ofMarburg P h i l i p p s U m v e r s i t y ofMarburg
Instimtion
Max‑Delbmck‑Center
fMMolecularMedicme FI℃eUmversity
Max‑Planck‑Instimte
fbrMolecularGenetics
nleRockefenerUmversity P h i l i p p s ‑ U m v e r s i t y
S u b j e c t
MoleularBiology
B i o c h e m i s t I y
C h e m i s t r y
ChemitIy
C i t y
Bedm
Bedm
Bedm
NewYmk
Marburg
NF‑KB/IKKandAP‑1pathwaysasmOleculartargetsmhumanlymphomas
ClausScheidereit
Max‑Delbruck‑CemerfbrMolecularMedicine,Bellin,Germany
TransientlyactivatedlKBkinaseS(KK)andNF‑KBtranscriptionfactorsarecentral regulatorsofimmuneresponsesanddifferentiation.Howeverlundervariouspathological conditions,aberrampersistemactivation,refiactorytononnalhomeostaticcontrols, contributestodiseaseprogression.NF‑KBproteinsprovideabroadpathogeneticpotential, basedonthediverseprocessescontrolled.Subgroupsoflymphoma,suchasHodgkin's lymphoma(II)andotherneoplasticdiseasesrevealconstimtiveactivationofNF‑KBandof thelKBkinase(KK)Complex.Activationinvolvestheclassicalp65‑p50heteromer,aswell
a s t h e p l O O N F ‑ K B ‑ p r e c u r s o r p a t h w a y . C o n s t i m t i v e l y a c t i v a t e d N F ‑ K B r e s u l t s i n r e s i s t a n c e t o
apoptosis,enhancedGl‑Sphaseprogressionandmmorigenicity,Agenome‑wide idemificationofNF‑KBregulatedgenesinlymphomacellswithconstimtiveactivationandin lipopolysaccharidestimulatedcellsbyhighdensitymicroalTayshasbeenundertakentodissectKKandNF‑KBdependentpro‑oncogenicandinnateimmuneresponsegenenetworks.
InadditiontoKK/NF‑KB,HLmmorcellsbearaMAPkinaseindependemsuperactivationof
transcriptionfactorAP‑1(c‑Jun/JUnB),whichdistinguishesclassicalHodgkin'sdiseasefiPomo t h e r B o r T c e l l m a l i g n a n c i e s . A P ‑ l s u p p o r t s c e l l c y c l e p r o g r e s s i o n a n d c o o p e r a t e s w i t h N F ‑ KBtoco‑stimulateexpressionofcyclinD2andthelymphocytehomingreceptorCCR7.
ThesedatasuggestanimportantrolefbracooperationbetweenKK/NF‑KBandAP‑lin Hodgkinlymphomapathogenesis.
ConstimtiveactivationoflKK/NF‑KB,butnotofAP‑linHLcellsisabrogatedbydrugs
whichinhibitHsp90.ThischaperoneHsp90isgenerallyreqUiredfbrbothconstitutiveandi n d u c i b l e l K K a n d N F ‑ K B a c t i v i t y a n d c o m r o l s K K s a t t w o l e v e l s , i n d u c i b i l i t y o f e n z y m a t i c a c t i v i t y a n d b i o g e n e s i s . F u l t h e r m o d e s o f p h a n n a c o l o g i c a l i n t e r f e r e n C e w i l l b e d i s c u s s e d .
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