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Phenotypic plasticity in canine mammary tumours (Eva Hellmén, 12 June 2014)

It is with very great interest I read your article on phenotypic plasticity in normal breast derived epithelial cells. We have several reports on similar findings in canine mammary tumours. I can strongly recommend you to take part of them and you are most welcome to contact me on this matter. read full comment

Comment on: Sauder et al. BMC Cell Biology, 15:20

Correction of my name. (Omar Akbari, 07 February 2014)

I would like to correct my name to include the middle initial (S). Current: Omar Akbari Correction: Omar S. Akbari Thanks omar read full comment

Comment on: Oliver et al. BMC Cell Biology, 11:101

Correction to legend Figure 6 (Armando Aranda-Anzaldo, 28 February 2011)

The legend to Figure 6 must say: (a-l) instead of (a-o) read full comment

Comment on: Rivera-Mulia et al. BMC Cell Biology, 12:3

Funding Record Number (benjamin alman, 30 July 2010)

The Canadian Institute for Health Research, Research Funding Number for this work is 15136. read full comment

Comment on: Poon et al. BMC Cell Biology, 10:38

Thiol Reactivities in GPCRs (Richard Lanzara, 18 April 2008)

The sensitivity of some G protein-coupled receptors to S-nitrosothiols suggests the presence of at least one or more free thiol groups. The varying reactivities of these free thiols also suggest very complex mechanisms that regulate their redox states and reactivities with other thiol containing molecules. For example, the finding that unlike the P2Y1 receptor, which has 2 essential disulfide bridges in its extracellular domains, the P2Y12 receptor has 2 free cysteines in its extracellular domains (Cys17 and Cys270), both of which are the targets of thiol reagents and the active metabolites of clopidogrel, which forms disulfide bridges with Cys17 and/or Cys270 in the P2Y12 receptor and thereby inactivates the receptor ( Ding Z, Kim S, Dorsam RT, Jin J, Kunapuli SP. Inactivation of the human... read full comment

Comment on: Kokkola et al. BMC Cell Biology, 6:21

Bronchiolitis obliterans is the missing link of the response to macrolides therapy in human respiratory epithelial cells injury induced by sulfur mustard (Mostafa Ghanei, 12 July 2007)

The article on "Inhibition of sulfur mustard-induced cytotoxicity and inflammation by the macrolide antibiotic" in the May 24, 2007 was an interesting research by Gao et al. The study demonstrates that roxithromycin has inhibitory effects on the cytotoxicity and inflammation provoked by sulfur mustard in human respiratory epithelial cells. It suggests that macrolide antibiotics may serve as potential vesicant respiratory therapeutics through mechanisms independent of their antibacterial activity [1]. Although, pathophysiological processes of sulfur mustard inhalation injury is not well understood, indeed, all aspects of different disorders are various presentations of a single underlying disease and bronchiolitis is the original nature of the pathology in these patients. Recent pathological... read full comment

Comment on: Gao et al. BMC Cell Biology, 8:17

Brooks' hypothesis on size control (Akos Sveiczer, 03 March 2005)

Nearly two years ago, Conlon and Raff (J Biol 2003, 2:7) proposed that mammalian cells do not need any checkpoint to maintain size homeostasis. An "evidence" was that cell volume increased linearly, irrespectively of cell size, under an S-phase arrest. Conlon and Raff referred to an old and clever (albeit never proved) hypothesis of Brooks (in The Cell Cycle. Edited by John PCL. Cambridge: Cambridge University Press; 1981), arguing that linearly growing cells not necessarily require any size control mechanism. Last year, Cooper (BMC Cell Biol 2004, 5:35) and we (Sveiczer A, Novak B, Mitchison JM. Theor Biol Med Model 2004, 1:12) criticised the conclusions of Conlon and Raff. We both pointed out that even if S-phase blocked cells grow linearly, it does not mean that these cells normally grow... read full comment

Comment on: Conlon et al. BMC Cell Biology, 5:36

Brooks' hypothesis on size control (Akos Sveiczer, 23 February 2005)

Nearly two years ago, Conlon and Raff (J Biol 2003, 2:7) proposed that mammalian cells do not need any checkpoint to maintain size homeostasis. An "evidence" was that cell volume increased linearly, irrespectively of cell size, under an S-phase arrest. Conlon and Raff referred to an old and clever (albeit never proved) hypothesis of Brooks (in The Cell Cycle. Edited by John PCL. Cambridge: Cambridge University Press; 1981), arguing that linearly growing cells not necessarily require any size control mechanism. Last year, Cooper (BMC Cell Biol 2004, 5:35) and we (Sveiczer A, Novak B, Mitchison JM. Theor Biol Med Model 2004, 1:12) criticised the conclusions of Conlon and Raff. We both pointed out that even if S-phase blocked cells grow linearly, it does not mean that these cells normally grow... read full comment

Comment on: Cooper BMC Cell Biology, 5:35

Control and maintenance of mammalian cell size: Rejoinder (Stephen Cooper, 30 November 2004)

Control and maintenance of mammalian cell size: RejoinderStephen Cooper, Department of Microbiology and Immunonlogy, University of Michigan Medical School, Ann Arbor, MI 48109-0620 USA (cooper@umich.edu)I appreciate the reply by Drs. Conlon and Raff to my article on Control and Maintenance of Cell Size [1]. All of the comments and points raised in their Reply are answered in the original article. That article [1] did deal with the conclusions they drew and the arguments they did make. I trust that the readers interested in this subject will read the original Conlon/Raff article [2] and my critique [1] to understand the issues. However, for the sake of clarity and efficiency I will comment on new issues raised by the reply so that the differences are clearly joined.Regarding the comment... read full comment

Comment on: Conlon et al. BMC Cell Biology, 5:36

Question of Function (Klaus Fiedler, 29 January 2004)

I suggest that a biomembrane in a solid phase does not support biosynthesis and does not allow ion channel function. The latter is directly important for signaling and vesicular traffic. read full comment

Comment on: Joly BMC Cell Biology, 5:3