1. Getting Your Science in Print
A Publisher’s Perspective
Sharon Schendel
U.S. Editorial Office
The Biochemical Journal
2. Why should I publish?
• Communicate your results to the scientific
community
• Create a version of record that is available in
public repositories (e.g. PubMed Central)
• Subject your study to peer review
Validates your results
Suggests ways to strengthen your data
• Further your scientific career
3. How does the publishing process
work?
Start with the Journal Editorial Office:
• Field/Solicit submissions from authors
• Process submitted papers
• Assess manuscript suitability for the journal
• Initiate/Monitor the review process
• Prepare papers for online and print publication
• Deposit accepted manuscripts in PubMed Central
(where applicable)
5. Journal Review Models
Cell, Science, Nature
Staff Editor (usually Ph.D.)
makes initial assessment
Paper rejected
without review
Paper sent to
reviewers
Rejected
Accepted!
Resubmit
elsewhere
Consideration
by sister journal
My
Paper
7. Comparison of models
Publication Model Cost Accessibility
Open Access
High >$1,000 No restrictions
Reader Pays
Low-to-nothing Restricted to
subscribers (for first
12 months)
Hybrid
Author choice Author choice
9. Impact Factor
• Reported by Institute of Scientific Information (ISI)
• Value that expresses the average number of citations
of papers published in a given journal
• Calculated over a two year period and reported as a
four digit value, e.g. Biochem J. IF= 4.897
• 2010 IF = Cites in 2010 of 2008 & 2009 articles
Total # of 2008 and 2009 articles
10. Author metrics
• H-factor is a “personal” impact factor that
measures productivity and impact of
publications.
• A researcher with an h-index of 7 indicates that
s/he has seven papers that have been cited at
least seven times.
• Cons: Favors older researchers; does not give adequate weight to
highly cited papers; some fields are less highly cited.
11. Some other sites of interest for metrics
• Faculty of 1000: Experts identify articles of high
interest: www.f1000.com
• Google Scholar: literature search that lists
number of times a paper is cited:
www.scholar.google.com
• ResearcherID: ISI service where authors can
manage their publication portfolio, check
citations and h-factor: www.researcherid.com
13. Think about the title
• Make the title concise but informative
• Which title would you choose?
a) The effect of alcohols on the JAK/STAT signaling
pathway to nuclear NFkB activation. Part 3 – the
influence of xylitol.
b) Xylitol inhibits STAT3 activation of NFkB.
c) Xylitol influences inflammation.
14. Consider what the reviewers want
• Novelty
• Mechanistic information
• Concise text that tells a good story
• Technique variety
15. Consider what the journals want
• Novel, high impact studies
• Suggestions for reviewers
• Brief, informative titles
• Concise abstracts
16. A few notes about Abstracts…
• The abstract is the initial point of contact with
your paper, both before and after publication
• Journals often email abstracts to potential
reviewers
• The abstract is what will appear in literature
databases
17. Two distinct signalling cascades target the NF-κB regulatory factor c-IAP1 for
degradation
Csmos RA, Wright CW, Galban S, Oetjen KA, and Duckett CS
Biochemical Journal (2009, Vol. 420 pp. 83-91)
The cellular Inhibitor of Apoptosis factor c-IAP1 has recently emerged as a negative regulator
of the non-canonical NF-kB signalling cascade. While synthetic IAP inhibitors have been
shown to trigger the autoubiquitinylation and degradation of c-IAP1, less is known about the
physiological mechanisms by which c-IAP1 stability is regulated. Here we describe two
distinct cellular processes that lead to the targeted loss of c-IAP1. Recruitment of a TRAF2:c-
IAP1 complex to the cytoplasmic domain of the Hodgkin’s/anaplastic large cell lymphoma-
associated receptor, CD30, leads to the targeting and degradation of the TRAF2:c-IAP1
heteromer through a mechanism requiring the RING domain of TRAF2, but not c-IAP1. In
contrast, the induced autoubiquitinylation of c-IAP1 by IAP antagonists causes the selective
loss of c-IAP1, but not TRAF2, thereby releasing TRAF2. Thus, c-IAP1 can be targeted for
degradation by two distinct processes, revealing the critical importance of this molecule as a
regulator of numerous intracellular signalling cascades. (150 words)
Background
Purpose
Results
Conclusions
Abstract Example
18. Paper Sections
• Abstract
• Introduction: relate your study to previous knowledge
• Materials and Methods: Allow others to reproduce
your experiments. Describe only those methods
unique to your study.
• Results: Summarize the results
• Discussion: Interpret (but do not repeat) results and
how they relate to current knowledge. Describe how
your results might lead to new research directions.
19. Prepare your figures
Keep the labels legible and the accompanying legends brief
Figure 2 MALT1 activation
(A, B, C) Different salts and buffer additives were screened for MALT1 activating potential. Full-length (150 nM) and
catalytic domain MALT1 (4 µM) were assayed in 50 mM HEPES, pH 7.5, 10 mM DTT, 1 mM EDTA, supplemented as
depicted (A and B) or in 50 mM HEPES, 100 mM NaCl, 0.9 M sodium citrate, pH 7.5, supplemented as depicted (C). (D) 500
nM full-length MALT1-WT was assayed in buffers with varying citrate concentration, supplemented with full-length
catalytic mutant as depicted. The experiments were repeated three (A, B, C) or two times (D), respectively. Mean values
and SEM are shown. (From Hachmann et al. Biochemical Journal 2012 (Vol. 443 pp. 287-295)
