-
Je něco špatně v tomto záznamu ?
Brain lipid binding protein (FABP7) as modulator of astrocyte function
Kipp M, Clarner T, Gingele S, Pott F, Amor S, van der Valk P, Beyer C.
Jazyk angličtina Země Česko
Typ dokumentu přehledy
NLK
Directory of Open Access Journals
od 1991
Free Medical Journals
od 1998
ProQuest Central
od 2005-01-01
Medline Complete (EBSCOhost)
od 2006-01-01
Nursing & Allied Health Database (ProQuest)
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 1998
- MeSH
- astrocyty cytologie fyziologie chemie MeSH
- axony fyziologie patologie MeSH
- centrální nervový systém patofyziologie patologie MeSH
- demyelinizační nemoci diagnóza etiologie patologie MeSH
- fyziologie buňky fyziologie MeSH
- lidé MeSH
- metaanalýza jako téma MeSH
- myelinové proteiny chemie metabolismus MeSH
- myši MeSH
- nádorové supresorové proteiny fyziologie chemie MeSH
- oligodendroglie cytologie fyziologie patologie MeSH
- poranění mozku patofyziologie patologie MeSH
- regenerace fyziologie imunologie MeSH
- roztroušená skleróza etiologie patofyziologie patologie MeSH
- transportní proteiny fyziologie chemie MeSH
- Check Tag
- lidé MeSH
- myši MeSH
- Publikační typ
- přehledy MeSH
Over a century ago, hyperplasia and hypertrophy of astrocytes was noted as a histopathological hallmark of multiple sclerosis and was hypothesized to play an important role in the development and course of this disease. However until today, the factual contribution of astrocytes to multiple sclerosis is elusive. Astrocytes may play an active role during degeneration and demyelination by controlling local inflammation in the CNS, provoking damage of oligodendrocytes and axons, and glial scarring but might also be beneficial by creating a permissive environment for remyelination and oligodendrocyte precursor migration, proliferation, and differentiation. Recent findings from our lab suggest that brain lipid binding protein (FABP7) is implicated in the course of multiple sclerosis and the regulation of astrocyte function. The relevance of our findings and data from other groups are highlighted and discussed in this paper in the context of myelin repair.
Citace poskytuje Crossref.org
Lit.: 83
- 000
- 00000naa 2200000 a 4500
- 001
- bmc11042526
- 003
- CZ-PrNML
- 005
- 20151006142716.0
- 008
- 111201s2011 xr e eng||
- 009
- AR
- 024 7_
- $a 10.33549/physiolres.932168 $2 doi
- 035 __
- $a (PubMed)21777034
- 040 __
- $a ABA008 $b cze $c ABA008 $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xr
- 100 1_
- $a Kipp M,
- 245 10
- $a Brain lipid binding protein (FABP7) as modulator of astrocyte function / $c Kipp M, Clarner T, Gingele S, Pott F, Amor S, van der Valk P, Beyer C.
- 314 __
- $a Institute of Neuroanatomy, Faculty of Medicine, RWTH Aachen University, Aachen, Germany
- 504 __
- $a Lit.: 83
- 520 9_
- $a Over a century ago, hyperplasia and hypertrophy of astrocytes was noted as a histopathological hallmark of multiple sclerosis and was hypothesized to play an important role in the development and course of this disease. However until today, the factual contribution of astrocytes to multiple sclerosis is elusive. Astrocytes may play an active role during degeneration and demyelination by controlling local inflammation in the CNS, provoking damage of oligodendrocytes and axons, and glial scarring but might also be beneficial by creating a permissive environment for remyelination and oligodendrocyte precursor migration, proliferation, and differentiation. Recent findings from our lab suggest that brain lipid binding protein (FABP7) is implicated in the course of multiple sclerosis and the regulation of astrocyte function. The relevance of our findings and data from other groups are highlighted and discussed in this paper in the context of myelin repair.
- 650 _2
- $a roztroušená skleróza $x etiologie $x patofyziologie $x patologie $7 D009103
- 650 _2
- $a astrocyty $x cytologie $x fyziologie $x chemie $7 D001253
- 650 _2
- $a oligodendroglie $x cytologie $x fyziologie $x patologie $7 D009836
- 650 _2
- $a axony $x fyziologie $x patologie $7 D001369
- 650 _2
- $a demyelinizační nemoci $x diagnóza $x etiologie $x patologie $7 D003711
- 650 _2
- $a centrální nervový systém $x patofyziologie $x patologie $7 D002490
- 650 _2
- $a regenerace $x fyziologie $x imunologie $7 D012038
- 650 _2
- $a fyziologie buňky $x fyziologie $7 D002468
- 650 _2
- $a transportní proteiny $x fyziologie $x chemie $7 D002352
- 650 _2
- $a nádorové supresorové proteiny $x fyziologie $x chemie $7 D025521
- 650 _2
- $a myelinové proteiny $x chemie $x metabolismus $7 D009185
- 650 _2
- $a poranění mozku $x patofyziologie $x patologie $7 D001930
- 650 _2
- $a metaanalýza jako téma $7 D015201
- 650 _2
- $a lidé $7 D006801
- 650 _2
- $a myši $7 D051379
- 655 _2
- $a přehledy $7 D016454
- 700 1_
- $a Clarner T,
- 700 1_
- $a Gingele, S.
- 700 1_
- $a Pott, F.
- 700 1_
- $a Amor, S. $7 gn_A_00005705
- 700 1_
- $a Valk, P. van der
- 700 1_
- $a Beyer, C.
- 773 0_
- $w MED00003824 $t Physiological research $g Roč. 60,Suppl. 1 (2011), s. S49-S60 $x 0862-8408
- 773 0_
- $t One hundred years of Ivan Djaja's Belgrade school of physiology $g Roč. 60,Suppl. 1 (2011), s. S49-S60 $w MED00182207
- 856 41
- $u http://www.biomed.cas.cz/physiolres/pdf/60%20Suppl%201/60_S49.pdf $y plný text volně přístupný
- 910 __
- $a ABA008 $b A 4120 $c 266 $y 2 $z 0
- 990 __
- $a 20111201084518 $b ABA008
- 991 __
- $a 20151006142901 $b ABA008
- 999 __
- $a ok $b bmc $g 888786 $s 752994
- BAS __
- $a 3
- BMC __
- $a 2011 $b 60 $c Suppl. 1 $d S49-S60 $m Physiological research $x MED00003824
- BMC __
- $a 2011 $b 60 $c Suppl. 1 $d S49-S60 $m One hundred years of Ivan Djaja's Belgrade school of physiology $x MED00182207
- LZP __
- $a 2011-25/mkal