An upstream regulatory element of human kapp gkne promoter binds a distinct protkin

Research output: Contribution to journalArticle

Abstract

Amylloi hei.i-protem (AU) is Ihe major proleineaceous component of the amyloid deposits that accumulate extracelluiarly in the brain of Al/heirncr's disease (AD). A is generated proieolyik-ally from a larger amyloid precursor proteins (BAPP). The apparent over expression of llie UAl'P gene in certain areas of AD brains indicate that abnormalities in gene regulation might he .in important I'arior in AD. Study of the structure and function of the IJAPi1 gene-promoter is an important urea ot" research. Here I report that an upstream regulatory element <URE) located between -22H t" -22fi5 of the human BAPP promoter may interact Mlh a novel proicm (s), U REP. as determined hy the eleclrophorelic mobility shift assay (EMSA). To determine if UREP is related to an already characleriJ.ed transcription fat-tor, EMSA wjs peitnimed iixiiig various -pecil'ic competitors. The labeled URE prohe could interact wiih a disinui mide.ii- factor which was no l cumpcMed hy l lie oligonncleolide.s specific for ditk-rem transcription tacu.rs. AI'l. M'2. Al'3. Ocl-l, NF-1, NF-kB. ORE. and alternatively Hie speeihc pmieiti h.nul M deeded wiili tilher the labeled NF-kB or NF-I probe could not he competed out with excess unlalvlcd URE. To cleleiniuie if such a UREP hand could he detected ID human brain li-siie samples, EMSA from Hie nuclear extracts of the human hrain was pcTloiiiK-d. A disiinu URE specific nuclear factor w.is detected in ditferen! regions of the brain .is well. To (leieiiiimc ilie si/e of ilK- proiem(s) that were specifically bound in Ihe DNApi.ilun uiniplexcs. Soiilhwestein blotting was peiformed. Using Ihe URE probe. Iwo protein bands ol - M kHa .nul l l f. kDa wvio detected m PC12 nuclear extracts. A pCATP/URE reeombin.ini pl.iMind w.is made hy svihcloiung URE in an enliancerless promoter vector pCATl'. I'Ci: cells ih.n were traiisfccted wiih pCATP/ URE displayed 34-fold mon- promoter .Ktivny Hum i-olls thai were iraiislVcR'd with pCATl1. These results suggest that the URE seiiueiifc displayed .in enhjiifer-like activity, lh.it the UREP factor interacting with the URE is no! related to the known transcription factors tested, and that Die protein is expressed in various .ell \\,vs ,iid ,1,Ik-rent rmnv of Ihe huin.m bum. Supported b> a N1H grant.

Original languageEnglish
JournalFASEB Journal
Volume11
Issue number9
StatePublished - 1997

Fingerprint

promoter regions
amyloid
Brain
Genes
central nervous system diseases
genes
Amyloid beta-Protein Precursor
Organized Financing
Amyloid Plaques
Brain Diseases
Amyloid
Gene expression
Urea
Deposits
urea
brain
Research
proteins
metsulfuron methyl

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

An upstream regulatory element of human kapp gkne promoter binds a distinct protkin. / Lahiri, Debomoy.

In: FASEB Journal, Vol. 11, No. 9, 1997.

Research output: Contribution to journalArticle

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title = "An upstream regulatory element of human kapp gkne promoter binds a distinct protkin",
abstract = "Amylloi hei.i-protem (AU) is Ihe major proleineaceous component of the amyloid deposits that accumulate extracelluiarly in the brain of Al/heirncr's disease (AD). A is generated proieolyik-ally from a larger amyloid precursor proteins (BAPP). The apparent over expression of llie UAl'P gene in certain areas of AD brains indicate that abnormalities in gene regulation might he .in important I'arior in AD. Study of the structure and function of the IJAPi1 gene-promoter is an important urea ot{"} research. Here I report that an upstream regulatory element <URE) located between -22H t{"} -22fi5 of the human BAPP promoter may interact Mlh a novel proicm (s), U REP. as determined hy the eleclrophorelic mobility shift assay (EMSA). To determine if UREP is related to an already characleriJ.ed transcription fat-tor, EMSA wjs peitnimed iixiiig various -pecil'ic competitors. The labeled URE prohe could interact wiih a disinui mide.ii- factor which was no l cumpcMed hy l lie oligonncleolide.s specific for ditk-rem transcription tacu.rs. AI'l. M'2. Al'3. Ocl-l, NF-1, NF-kB. ORE. and alternatively Hie speeihc pmieiti h.nul M deeded wiili tilher the labeled NF-kB or NF-I probe could not he competed out with excess unlalvlcd URE. To cleleiniuie if such a UREP hand could he detected ID human brain li-siie samples, EMSA from Hie nuclear extracts of the human hrain was pcTloiiiK-d. A disiinu URE specific nuclear factor w.is detected in ditferen! regions of the brain .is well. To (leieiiiimc ilie si/e of ilK- proiem(s) that were specifically bound in Ihe DNApi.ilun uiniplexcs. Soiilhwestein blotting was peiformed. Using Ihe URE probe. Iwo protein bands ol - M kHa .nul l l f. kDa wvio detected m PC12 nuclear extracts. A pCATP/URE reeombin.ini pl.iMind w.is made hy svihcloiung URE in an enliancerless promoter vector pCATl'. I'Ci: cells ih.n were traiisfccted wiih pCATP/ URE displayed 34-fold mon- promoter .Ktivny Hum i-olls thai were iraiislVcR'd with pCATl1. These results suggest that the URE seiiueiifc displayed .in enhjiifer-like activity, lh.it the UREP factor interacting with the URE is no! related to the known transcription factors tested, and that Die protein is expressed in various .ell \\,vs ,iid ,1,Ik-rent rmnv of Ihe huin.m bum. Supported b> a N1H grant.",
author = "Debomoy Lahiri",
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AU - Lahiri, Debomoy

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N2 - Amylloi hei.i-protem (AU) is Ihe major proleineaceous component of the amyloid deposits that accumulate extracelluiarly in the brain of Al/heirncr's disease (AD). A is generated proieolyik-ally from a larger amyloid precursor proteins (BAPP). The apparent over expression of llie UAl'P gene in certain areas of AD brains indicate that abnormalities in gene regulation might he .in important I'arior in AD. Study of the structure and function of the IJAPi1 gene-promoter is an important urea ot" research. Here I report that an upstream regulatory element <URE) located between -22H t" -22fi5 of the human BAPP promoter may interact Mlh a novel proicm (s), U REP. as determined hy the eleclrophorelic mobility shift assay (EMSA). To determine if UREP is related to an already characleriJ.ed transcription fat-tor, EMSA wjs peitnimed iixiiig various -pecil'ic competitors. The labeled URE prohe could interact wiih a disinui mide.ii- factor which was no l cumpcMed hy l lie oligonncleolide.s specific for ditk-rem transcription tacu.rs. AI'l. M'2. Al'3. Ocl-l, NF-1, NF-kB. ORE. and alternatively Hie speeihc pmieiti h.nul M deeded wiili tilher the labeled NF-kB or NF-I probe could not he competed out with excess unlalvlcd URE. To cleleiniuie if such a UREP hand could he detected ID human brain li-siie samples, EMSA from Hie nuclear extracts of the human hrain was pcTloiiiK-d. A disiinu URE specific nuclear factor w.is detected in ditferen! regions of the brain .is well. To (leieiiiimc ilie si/e of ilK- proiem(s) that were specifically bound in Ihe DNApi.ilun uiniplexcs. Soiilhwestein blotting was peiformed. Using Ihe URE probe. Iwo protein bands ol - M kHa .nul l l f. kDa wvio detected m PC12 nuclear extracts. A pCATP/URE reeombin.ini pl.iMind w.is made hy svihcloiung URE in an enliancerless promoter vector pCATl'. I'Ci: cells ih.n were traiisfccted wiih pCATP/ URE displayed 34-fold mon- promoter .Ktivny Hum i-olls thai were iraiislVcR'd with pCATl1. These results suggest that the URE seiiueiifc displayed .in enhjiifer-like activity, lh.it the UREP factor interacting with the URE is no! related to the known transcription factors tested, and that Die protein is expressed in various .ell \\,vs ,iid ,1,Ik-rent rmnv of Ihe huin.m bum. Supported b> a N1H grant.

AB - Amylloi hei.i-protem (AU) is Ihe major proleineaceous component of the amyloid deposits that accumulate extracelluiarly in the brain of Al/heirncr's disease (AD). A is generated proieolyik-ally from a larger amyloid precursor proteins (BAPP). The apparent over expression of llie UAl'P gene in certain areas of AD brains indicate that abnormalities in gene regulation might he .in important I'arior in AD. Study of the structure and function of the IJAPi1 gene-promoter is an important urea ot" research. Here I report that an upstream regulatory element <URE) located between -22H t" -22fi5 of the human BAPP promoter may interact Mlh a novel proicm (s), U REP. as determined hy the eleclrophorelic mobility shift assay (EMSA). To determine if UREP is related to an already characleriJ.ed transcription fat-tor, EMSA wjs peitnimed iixiiig various -pecil'ic competitors. The labeled URE prohe could interact wiih a disinui mide.ii- factor which was no l cumpcMed hy l lie oligonncleolide.s specific for ditk-rem transcription tacu.rs. AI'l. M'2. Al'3. Ocl-l, NF-1, NF-kB. ORE. and alternatively Hie speeihc pmieiti h.nul M deeded wiili tilher the labeled NF-kB or NF-I probe could not he competed out with excess unlalvlcd URE. To cleleiniuie if such a UREP hand could he detected ID human brain li-siie samples, EMSA from Hie nuclear extracts of the human hrain was pcTloiiiK-d. A disiinu URE specific nuclear factor w.is detected in ditferen! regions of the brain .is well. To (leieiiiimc ilie si/e of ilK- proiem(s) that were specifically bound in Ihe DNApi.ilun uiniplexcs. Soiilhwestein blotting was peiformed. Using Ihe URE probe. Iwo protein bands ol - M kHa .nul l l f. kDa wvio detected m PC12 nuclear extracts. A pCATP/URE reeombin.ini pl.iMind w.is made hy svihcloiung URE in an enliancerless promoter vector pCATl'. I'Ci: cells ih.n were traiisfccted wiih pCATP/ URE displayed 34-fold mon- promoter .Ktivny Hum i-olls thai were iraiislVcR'd with pCATl1. These results suggest that the URE seiiueiifc displayed .in enhjiifer-like activity, lh.it the UREP factor interacting with the URE is no! related to the known transcription factors tested, and that Die protein is expressed in various .ell \\,vs ,iid ,1,Ik-rent rmnv of Ihe huin.m bum. Supported b> a N1H grant.

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