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German Medical Science
Conference object . 2019
License: CC BY
Data sources: German Medical Science
https://dx.doi.org/10.3205/19d...
Conference object . 2019
License: CC BY
Data sources: Datacite
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Claim

Study of the DNA promoter methylation of CCM genes in human cerebral cavernous malformation

Studie des Methylierungsstatus der Promotoren der CCMGene bei kavernösen Hämangiomen
descriptionPublicationkeyboard_double_arrow_right Conference object 08 May 2019 English Publisher:German Medical Science GMS Publishing House
Authors: Saban, DV; Larisch, J; Nickel, AC; Dammann, P; Sure, U; Zhu, Y;

doi: 10.3205/19dgnc473

Study of the DNA promoter methylation of CCM genes in human cerebral cavernous malformation

Abstract

Objective: CCM is the second most common cerebrovascular disease and is classified as familial (20%) and sporadic (80%) forms. Loss of function mutation of three CCM genes can cause the familial CCM. However, the mechanism causing sporadic CCM remains unclear. Considering the DNA promoter [for full text, please go to the a.m. URL]

70. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Skandinavischen Gesellschaft für Neurochirurgie

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Keywords

ddc: 610, 610 Medical sciences; Medicine

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
0
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