T
Thomas Grundström
Researcher at Umeå University
Publications - 82
Citations - 3688
Thomas Grundström is an academic researcher from Umeå University. The author has contributed to research in topics: Calmodulin & Transcription factor. The author has an hindex of 34, co-authored 80 publications receiving 3589 citations.
Papers
More filters
Journal ArticleDOI
ampC cephalosporinase of Escherichia coli K-12 has a different evolutionary origin from that of beta-lactamases of the penicillinase type
TL;DR: It is suggested that the ampC cephalosporinase as well as related cep HALsporinases form a distinct group of serine beta-lactamases that have an evolutionary origin different from that of the serine penicillinases and thus constitute a new class of beta- lactamase.
Journal ArticleDOI
Francisella tularensis inhibits Toll‐like receptor‐mediated activation of intracellular signalling and secretion of TNF‐α and IL‐1 from murine macrophages
TL;DR: F. tularensis appears capable of abrogating the TNF‐α and IL‐1 responses of macrophages induced by E. coli LPS or BLP via a mechanism that involves suppression of several intracellular pathways and is dependent on expression of a bacterial 23 kDa protein.
Journal ArticleDOI
The E. coli β -lactamase attenuator mediates growth rate-dependent regulation
TL;DR: A single base alteration within this attenuator led to a loss in the cell's ability to coordinate its content of β-lactamase with growth rate, and a mechanism through which this mode of regulation operates is suggested.
Journal ArticleDOI
Calcium/calmodulin inhibition of basic-helix-loop-helix transcription factor domains.
Brit Corneliussen,Magnus Holm,Yvonne Waltersson,Jacqueline Onions,Bengt Hallberg,A Thornell,Thomas Grundström +6 more
TL;DR: Ca2+ ionophore selectively inhibits transcriptional activation by Ca2+/CaM-sensitive bHLH proteins in vivo, implying that Ca2-loaded CaM can directly influence transcription through differential CaM inhibition of b HLH domains.
Journal ArticleDOI
Smad and AML proteins synergistically confer transforming growth factor beta1 responsiveness to human germ-line IgA genes.
Evangelia Pardali,Xiao-Qi Xie,P Tsapogas,S Itoh,Kostas I Arvanitidis,C H Heldin,P. ten Dijke,Thomas Grundström,P Sideras,P Sideras +9 more
TL;DR: It is demonstrated that intracellular Smad proteins mediate activation of the Iα1 promoter by TGF-β, which provides a canapé of interspersed high and low affinity sites for Smad and AML factors, some of which are indispensable for T GF-β responsiveness.