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Errata
Tremblay et al. HES1 is a novel interactor of the Fanconi anemia core complex. Blood.
2008;112(5):2062-2070.
On page 2064 in the September 1, 2008, issue, there is an error in
Figure 1A. Lanes indicating interactions between HES1 constructs
and FA proteins are inverted. The correct Figure 1 is shown.
On page 2067, under the section “HES1 is required for MMC
resistance and FANCD2 monoubiquitination” (which begins on
page 2066), there are errors in the first sentence of the last
paragraph that reads, “Among all FA complementation groups,
only cells with mutations in the downstream components
(FANCD1/BRCA2, FANCJ/BRIP1/BACH1, and FANCN/
PALB2) have an impaired Rad51 foci phenotype.38,43” The
correct sentence should read: “Among all FA complementation
groups, only cells with mutations in the downstream components (FANCD1/BRCA2 and FANCN/PALB2) have an impaired
Rad51 foci phenotype.37-39,43”
Figure 1. FA proteins interact with HES1. (A) Yeast-2-hybrid assay with HES1 and FA proteins. Yeast strain AH109 was cotransformed with HES1 constructs expressing full-length or
truncated HES1 protein with FA proteins as indicated and assayed for interaction as described in “Yeast-2-hybrid.” A positive interaction is indicated as ⫹. Negative controls included
pGBK-HES1 cotransformed with pGADT7 empty vector. (B) FA core complex components coimmunoprecipitate with HES1. 293T cells were cotransfected with HA-tagged HES1 and FA
coding vectors and were subjected to immunoprecipitation (IP) with either anti-FANCA antibodies, anti-HES1 antibodies, or control IgG. IP was analyzed by SDS-PAGE and Western
blotting using the indicated antibodies. (C) Co-IP of endogenous proteins from 293T cell extracts using anti-HES1 or anti-FANCA antibodies. (D) Coomassie gel staining of endogenous
protein extracts of 293T cells subjected to IP using anti-HES1 antibodies. Major bands were extracted from gel slices and the indicated proteins were identified by mass spectrometry.
Klibi et al. Blood diffusion and Th1-suppressive effects of galectin-9–containing exosomes
released by Epstein-Barr virus–infected nasopharyngeal carcinoma cells. Blood.
2009;113(9):1957-1966.
On pages 1957 and 1965 of the February 26, 2009, issue, the
seventh author’s last name is incorrectly listed as Sylvestre L. E.
Moulec and incorrectly initialized as S.L.E.M. in the Authorship
Contribution. The correct name is Sylvestre Le Moulec and initials
are S.L.M. The errors were corrected in the online version, which
now differs from the print version.
Schmitz et al. Response: Intrathecal methotrexate and central nervous system events. Blood.
2009;114(9):1999-2000.
On pages 1999 and 2000 of the August 27, 2009, issue, there are
errors in the second letter in Correspondence.
On page 1999, in the first paragraph of the Schmitz et al
Response there is an error in attribution. Due to a miscommunication, the authors believed they were responding to a letter to the
editor from Brugières and colleagues, rather than a letter from
Pierre-Yves Dietrich. The first and second sentences of the Schmitz
et al letter should read: “We thank Dr Dietrich for his comments
and for pointing out the additional information coming from the
Brugières et al study in children and adolescents with anaplastic
3974
large-cell lymphoma.1 The author raises important questions,
which we would like to answer as follows:”
On page 2000, the name “Dietrich” should replace “Brugières et al”
in the seventh sentence of the last paragraph. The correct sentence
should read: “Although the low number of such patients in our trial
precluded a statistical analysis of whether at least these patients may
have benefited from intrathecal MTX we agree with Dietrich that
intrathecal MTX was of limited value in the population at large and
should no longer be administered, particularly if the side effects are
taken into account.”
BLOOD, 29 OCTOBER 2009 䡠 VOLUME 114, NUMBER 18
From www.bloodjournal.org by guest on June 15, 2017. For personal use only.
2009 114: 3974
doi:10.1182/blood-2009-08-240986
Klibi et al. Blood diffusion and Th1-suppressive effects of galectin-9−
containing exosomes released by Epstein-Barr virus−infected
nasopharyngeal carcinoma cells. Blood. 2009;113(9):1957−1966.
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