A recent series of papers [1-3] have prompted me to write about the cancer stem cell (CSC) hypothesis, since during the last years there has been a lot of controversy regarding the existence, function and clinical implications of cancer stem cells. This confusion stems (no pun intended) from the lack of clarity in the field nowadays, arising mainly from misconceptions regarding the origin and function of these cells. On top of all of this is the confusion derived from media-hype and some not-so knowledgeable scientific journalists.
1.Background
The classical view of tumor biology is that transformed cells, which carry mutations that confer them selective advantages under certain conditions, divide continuously forming a homogeneous tumor. This concept entailed the idea that every clone of the original tumor proliferates indefinitely as an autonomous entity within the whole malignant cell population, and if removed from the tumor and placed somewhere else it could generate a new tumor.
The cancer stem cell hypothesis challenges the aforementioned idea by stating that there is a distinct subset of cells within the whole population capable of initiating and sustaining the growth of the tumor. The descendants of these tumor stem cells are the so-called “tumor bulk”, which are only short lived cells. This then means that it is only these ‘cancer stem cells’ that could lead to the formation of new tumors.
2. Experimental evidence from different models of cancer
2.1 Leukemia
The evidence for this hypothesis came from the group led by John Dick [4], which showed that acute myeloid leukemia (AML) cells differ in their tumor initiating abilities. The experimental approach was straightforward: sorting the cells of the whole tumor through FACS, and then injecting different subpopulations into immunocompromised mice. They later followed which subpopulation was able to reconstitute the original tumor and saw that a small fraction of them had this ability.
The subpopulations arise from using surface markers to separate them. I will come back to this point later to point out the technical problems and advantages associated to this approach).
This pioneering work showed that tumors possess a hierarchical organization, and suggested the existence of cancer stem cells. It is noteworthy that at this point the authors only referred to tumor initiating cells (the term cancer stem cell was coined later).
2.2 Solid tumors
Early work on the hematopoietic system (mainly through the clear characterization of surface markers) allowed tracing of populations with high accuracy. In the case of solid tumors much less is known about the differentiation process, and even less is known about surface markers that characterize each stage. Furthermore, FACS analysis is much more complicated due to the disaggregation step that must be performed (which can alter the surface markers).
Despite the lack of clear ways to trace populations, characterization of CSCs has been done for several types of solid tumors including breast cancer, pancreatic cancer, brain tumors and colon cancer [5-8].
Usually the approach used in most of these studies is based on the usage of known CSC markers from some type of tumor, to separate populations in another one. This rationale has proven useful in some cases, however it cannot be generalized:
-CD44 was known to be a marker of leukemic stem cells and it has been recently shown to be also a marker for breast cancer stem cells.
-CD133 was known to be a marker of glioblastoma stem cells, yet in colon cancer it has been shown to be a marker of a broader population, thus biasing the results.
In general, more knowledge about the dynamics of tissue hierarchy in both normal and pathological conditions will give rise to better tools for understanding potential populations of cancer stem cells in solid tumors.
3. Unresolved issues
3.1 Origin
Several authors claim that the term “cancer stem cell” is inaccurate since not only stem cells can give rise to cancer. This statement is incorrect. The cancer stem cell denomination is given only on a functional basis, which means that these tumor initiating cells have stem-cell properties (self-renewal and the ability to generate all lineages within the tumor), not that they exclusively arise from stem cells.
A recent work by the Clevers group [9] shows that only intestinal stem cells bearing the Lgr5 surface marker are capable of initiating adenomas, the earliest stage of colorectal cancer. The most interesting observation was that differentiated Lgr5- cells were unable to initiate tumors. Whether Lgr5+ cells within the tumor are maintained up until late-stage cancer remains unknown, but this study shows that for this model of tumor the substrate of cancer initiation is indeed an adult stem cell.
On the other hand, work done in leukemia has suggested that progenitor cells (which give rise to only a subset of cells within the tissue) are also capable of tumor initiation, particularly in chronic myeloid leukemia, where although the hematopoietic stem cell carries a mutation in Wnt signaling, only the myeloid progenitors effectively give rise to tumors.
3.2 Experimental Caveats
So far the assessment of stemness remains a highly complex issue that lacks a straightforward answer (i.e. how do you quantify stemness? I welcome any ideas).
CSC quantification is done by the capability of these cells to initiate a tumor in immunocompromised mice, although this may reflect only the ability of certain cells to adapt to a foreign environment.
In fact, the Morrison group showed that depending on the murine model utilized, the frequency of alleged CSCs within melanomas derived from patients varies [10]. This suggests that the microenvironment is the limiting step and partially disproves that CSCs are a rare population within certain tumor types. This was also seen by the Strasser group utilizing murine leukemias in immunocompetent mice [11].
Although this may suggest that CSCs are not as rare as previously reported, this does not contradict in any sense the CSC hypothesis, since the idea of a rare population came from the experimental models used and may vary considerably between tumors.
In order to properly assess which subpopulation (if any) contains CSCs, the tumor initiation experiments must be done in immunocompetent animals that share the same genetic background than that of the host (the immune system plays a major role in tumor appearance and progression, so this should be integrated into the experimental framework), and serial transplantations must be done to show that this ability is retained in time by the same population of cells (serial transplantation assays are a robust method to follow the tumor initiating capacity of a population of cells in extended periods of time). Furthermore, it has to be shown that these putative CSCs are the only ones able to generate all other lineages within the tumor.
(Of course these concepts would only apply to murine tumors, but is the proof of principle from where the field can resolve most of the current issues).
3.3 Therapeutic Relevance
Whether the direct targeting of CSCs by new treatments will effectively give rise to better therapies still remains to be proven, and so it is essential to realize that, at present, this would only be an adjuvant therapy to conventional methods. The reason for this is quite clear: although the CSCs putatively maintain the growth of the tumor, it is still the bulk of the tumor which is responsible for the disease (assuming that CSCs are a minor population of course). Nevertheless, some groups have shown that targeting the CSCs could be sufficient to stop the growth of the tumor. Work done in the Frank lab showed that by targeting the melanoma stem cell marker ABCB5, they could effectively treat the progression of this disease[12]. The same was shown for CD44 in acute myeloid leukemia by the Dick lab[13].
Moreover, in a very recent paper, the group of Michael Clarke[14] showed that the CSC population in breast cancer is more resistant to radiation, and that this is due to reduced reactive oxygen species within these cells. This could partly explain why current therapies are inefficient, as treatment-resistant CSCs would lead to relapse.
Taken together, it is evident that further studies on the nature and function of CSCs for the development of new approaches against cancer, are needed.
4. Concluding Remarks
I hope that with this brief summary of the CSC hypothesis, some light has been shed in the understanding of this concept and how it may influence both basic and clinical oncology in the future.
My impression is that further work is required to understand the dynamics of tumor initiation and growth through the CSC hypothesis, but the overall evidence seems to point towards the validation of this model. Hopefully the elucidation of how CSCs regulate tumor properties will lead to better therapeutic approaches and a deeper knowledge of the basic mechanisms that control cancer origin and development.
Francisco Barriga.
5. References
1. Jordan, C. (2009). Cancer Stem Cells: Controversial or Just Misunderstood? Cell Stem Cell, 4 (3), 203-205 DOI: 10.1016/j.stem.2009.02.003
2. Rosen, J., & Jordan, C. (2009). The Increasing Complexity of the Cancer Stem Cell Paradigm Science, 324 (5935), 1670-1673 DOI: 10.1126/science.1171837
3. Visvader, J., & Lindeman, G. (2008). Cancer stem cells in solid tumours: accumulating evidence and unresolved questions Nature Reviews Cancer, 8 (10), 755-768 DOI: 10.1038/nrc2499
4. Bonnet, D. and J.E. Dick, Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell. Nat Med, 1997. 3(7): p. 730-7.
5. Al-Hajj, M., et al., Prospective identification of tumorigenic breast cancer cells. Proc Natl Acad Sci U S A, 2003. 100(7): p. 3983-8.
6. Dalerba, P., et al., Phenotypic characterization of human colorectal cancer stem cells. Proc Natl Acad Sci U S A, 2007. 104(24): p. 10158-63.
7. Li, C., et al., Identification of pancreatic cancer stem cells. Cancer Res, 2007. 67(3): p. 1030-7.
8. Singh, S.K., et al., Identification of human brain tumour initiating cells. Nature, 2004. 432(7015): p. 396-401.
9. Barker, N., et al., Crypt stem cells as the cells-of-origin of intestinal cancer. Nature, 2009. 457(7229): p. 608-11.
10. Quintana, E., et al., Efficient tumour formation by single human melanoma cells. Nature, 2008. 456(7222): p. 593-8.
11. Kelly, P.N., et al., Tumor growth need not be driven by rare cancer stem cells. Science, 2007. 317(5836): p. 337.
12. Schatton, T., et al., Identification of cells initiating human melanomas. Nature, 2008. 451(7176): p. 345-9.
13. Jin, L., et al., Targeting of CD44 eradicates human acute myeloid leukemic stem cells. Nat Med, 2006. 12(10): p. 1167-74.
14. Diehn, M., et al., Association of reactive oxygen species levels and radioresistance in cancer stem cells. Nature, 2009. 458(7239): p. 780-3.
Tuesday, June 30, 2009
Cancer Stem Cells: the root of all evil?
A recent series of papers [1-3] have prompted me to write about the cancer stem cell (CSC) hypothesis, since during the last years there has been a lot of controversy regarding the existence, function and clinical implications of cancer stem cells. This confusion stems (no pun intended) from the lack of clarity in the field nowadays, arising mainly from misconceptions regarding the origin and function of these cells. On top of all of this is the confusion derived from media-hype and some not-so knowledgeable scientific journalists.
Monday, June 29, 2009
Let's relaunch the Molecular and Cell Biology Blog Carnival
While looking around the Blog Carnival site for the Cancer Research Blog Carnival, I thought I'd give it a chance and look if there was a carnival on molecular biology.And there was one, the "Molecular and Cell Biology Carnival", but it was discontinued last December, after only 5 issues.
So, crazy idea here... let's relaunch the Carnival! There are lots of Molbio articles at Researchblogging, so there is a core of articles that could in principle be included in the Carnival. It'll take some time to advertise that the Carnival is back in business, but it just may work. I'm not sure why the Carnival was discontinued the first time, but I guess it was because of a lack of articles (or of willing hosts). This would be the main issue to tackle if we are thinking of relaunching it. That's why we should start by advertising the carnival a lot before anything else. Researchblogging can be a good place to search for potential contributors and hosts.
If the problem was indeed the lack of articles, we could consider launching it only every two months, so articles could pile up.
So, what do you think.... should we give this a chance?
[Image credit: Exothermic]
Note added: Now that I think of it, while it is a good idea to give it two months for the articles to pile up, this would result in some articles being 'too old' by the time Carnival followers get them... any other ideas on how to increase the number of articles submitted?
Thursday, June 25, 2009
Farewell to the King
Well, it's not all about molbio around here...
I actually had the chance to see him live here in Santiago, several years ago.
A video of one of my favorite MJ songs:
Image credit: CNN (http://edition.cnn.com/)
Tuesday, June 23, 2009
More videos from the Biotech companies...
I've posted a series of funny (and geeky) videos from different biotech companies promoting their new technologies and equipment before [See Commercials in life science research: Roche, BioRad does it again... and Another (geeky) science commercial] in which I've commented on the pros of their production.From what is really becoming a "video battle" between companies, I bring you another series of videos, although two are more music videos than short stories.
First, a rock ballad for Roche xCelligence:
Little cells, resting on your plate, tell me how you feel down there, inside?
There is another (more rocker) video for this system here
Then, you can "Reach that Peak" with this video from Agilent.
you are my mass spec girl, I'm your mass spec boy...
Lastly, check out a funny video promo for Agilent Total RNA Isolation Mini Kit here
Share these videos around in your lab! Let us know if you find more of these videos...
Long overdue post on John Mattick's visit
As you may recall, John Mattick visited us last May (for a week) [John Mattick is coming to Chile] and even though I've been meaning to write a post regarding his visit, I've been swamped with work and never got down to doing it.
Let me just say that not only he does some very interesting and mind-broadening science, but he also is simply a great guy! I was in charge of his visit so I got to spend a lot of time with him. With a couple of fellow grad students we organized a visit to downtown Santiago, the seaside city of Viña del Mar and (of course) we also went to a local bar to celebrate a great week. Also, we had a faculty dinner which gave the opportunity to some Professors to meet John in a social environment. All these extracurricular activities were great to get to know such a interesting and wise man talk about scientific life, research, and all you can think of.
He gave a faculty seminar (see title below) and a couple of classes to first-year grad students (entitled “The genome is the transcriptome” and “The role of non coding RNA in epigenetics, development, cognition and cell biology”), where we got a sneak preview to his until then, soon-to-be published article in Nature Genetics entitled "Tiny RNAs associated with transcription start sites in animals".
Further, thanks to his willingness to meet with some very eager faculty members, some very interesting collaborations were started (in fact, one that will possibly allow me go to Australia next year).
I know some fellow bloggers have some very strong words regarding John's work and ideas, but I would strongly recommend that they met with him first and discuss them. Ultimately, that's the beauty of science. He is a great speaker to invite to your school, considering how hot RNA research is right now, and also a very interesting person.
It's amazing how much else is there to learn about gene expression regulation and the importance of RNA in these processes.
Here's a pic after his faculty seminar entitled "The human genome as an RNA machine".
He gave a faculty seminar (see title below) and a couple of classes to first-year grad students (entitled “The genome is the transcriptome” and “The role of non coding RNA in epigenetics, development, cognition and cell biology”), where we got a sneak preview to his until then, soon-to-be published article in Nature Genetics entitled "Tiny RNAs associated with transcription start sites in animals".
Further, thanks to his willingness to meet with some very eager faculty members, some very interesting collaborations were started (in fact, one that will possibly allow me go to Australia next year).
I know some fellow bloggers have some very strong words regarding John's work and ideas, but I would strongly recommend that they met with him first and discuss them. Ultimately, that's the beauty of science. He is a great speaker to invite to your school, considering how hot RNA research is right now, and also a very interesting person.
It's amazing how much else is there to learn about gene expression regulation and the importance of RNA in these processes.
Here's a pic after his faculty seminar entitled "The human genome as an RNA machine".
Friday, June 19, 2009
The 2008 Journal Citation Report is in!
The 2008 release of Journal Citation Reports is in (the IF report for a certain year, is released the following year). If it weren't for twitter I would have never known, mainly because every journal is promoting themselves through it. Score for twitter! (Please note: the image on the left will make sense in a second).Anyway, you know how I feel about the IF [for example see here] and I've talked about the special care one has to have with it before, so I don't want you to get the impression that just because I'm posting the news I think we should all live our lives around the IF (which of course, I don't... don't be silly). The list, however, is a highlight so we are bringing some details right to your RSS reader (if you follow us through one of those).
Not many surprises on the top (considering ALL journals), with some medical (CA-CANCER J CLIN, NEW ENGL J MED) and review journals holding on to most of the top 10 positions (including some biology related journals like NAT REV MOL CELL BIO, ANNU REV IMMUNOL) but also of interest is Nature with an amazing 31.434 and Cell with a 31.253 (8th and 9th, respectively) way over Science at 28.103. Also, I didn't know Nature Genetics was doing so well (30.259!).
Now let's get down to business: who made the Top-20 in the Biochemistry & Molecular Biology category? (I feel like I'm on E! at the Oscars... yes.. now the image should make sense. OK maybe it wasn't funny at all).
In descending order: CELL, ANNU REV BIOCHEM1, NAT MED, ANNU REV BIOPH BIOM1, NAT CHEM BIOL,TRENDS BIOCHEM SCI1, MOL CELL, PLOS BIOL, MOL PSYCHIATR, MOL SYST BIOL, PROG LIPID RES, NAT STRUCT MOL BIOL, CURR BIOL, BBA-REV CANCER1, GENOME RES2, TRENDS MOL MED1, PLANT CELL, CURR OPIN STRUC BIOL1, CRIT REV BIOCHEM MOL1, EMBO J
1 Review journals
2This journal keeps going up in the rankings, as a reflection of the way we are approaching science at present, making use of several bioinformatics tools to mine the increasing amounts of genomic data being generated, to ask and answer important biological questions. Also, to report such data!
So how are some of the PLoS Journals doing? PLoS Biology 12,683 (and still the best ranked, and let's face it, best overall PLoS Journal), PLoS Medicine 12.185 (close second!), PLoS Pathogens 9.125, PLoS Genetics 8.883, PLoS Computational Biology 5.895, PLoS Neglected Tropical Diseases 4.172.
It is pretty awesome if you ask me. Great for PLoS and OA publishing!
We'll have to keep our eyes open in case someone gets down to do the analysis of how the OA journals did this year in the IF report. I'd be very interested in knowing if OA journals are going up in the rankings as some have suggested. Let us know shall you find such an analysis in the days to come.
The list is available through institutional subscription at Web of Science.
PS. For my plant biologists readers: Plant Cell 9.296 (and top 20 in B&MB!), The Plant Journal 6.493, Plant Physiology 6.110. Plant Physiology is getting closer!!
Wednesday, June 17, 2009
The Top 100 Journals in Biology and Medicine
I've just learned about this (although the list has been around for a while): In conjunction with SLA’s Centennial, the BioMedical & Life Sciences Division conducted a poll among its 686 members, to identify the 100 most influential journals of Biology & Medicine over the last 100 years.
Wow, that's a hard task. Lot's of journals come to mind... but let's continue with the news..
Interestingly, there was an entire section devoted to "Molecular and Cellular Biology journals, which also included Journals in Biotechnology and the Leading Multiscience Publications".
You can check the whole list here.
The "DBIO Top 10" journals were announced yesterday at the DBIO Annual Business luncheon during the Centennial Conference in Washington, DC, where Nature was awarded the first place. (OK, so maybe I made a good decision to renew my print subscription for the third year in a row). Anyway, this sounds OK to me. [You can check more details about it here: Nature wins 'journal of the century' award!]
Other journals which also made the list (and if they hadn't made it, it would have been, IMHO, a somewhat misleading poll) include Science, Cell and PNAS.
To some of my readers, it would interesting to know that Plant Physiology (but not The Plant Journal or Plant Cell) made the cut (although this may be related to their different "ages" and the fact that the scope in the early days of Plant Physiology also included fungi research).
On the other hand, I was surprised to see the EMBO Journal and the FASEB journal in the list. Not that I think they are not important journals in their fields, but I hardly consider them to be among the "most influential journals in the last 100 years".
Anyway, I'm not sure I see the point on doing such a poll, but good for Nature.
Also, I hardly think that a scientist will be influenced by this list at all, in a similar way that scientists are not (or should not) be influenced by the impact factor, when analyzing papers, but then again, I don't think this was the purpose behind making this list... so, why was this poll put together? Any thoughts?
Are the most influential journals in your field represented in this list? Check it out here.
Image credit: Copyright © 2009, American College of Chest Physicians
Tuesday, June 16, 2009
My Science badges
During my (short) scientific life, I've worked in very different research projects: Alzheimer's, plant molecular biology, mRNA splicing and presently, circadian rhythms. This has had me doing research through diverse approaches and techniques, throughout the years. While some have criticized my allegedly "lack of focus", I value all of these experiences as I consider them to have helped me grow as a scientist, for example by studying biology through different perspectives, discussing science with lots of different people and attending seminars in a variety of topics, among other reasons.
So after reading about it over at Sandwalk, and considering my diverse experience in science, I've decided to join the Science Scouts ("Order of the Science Scouts of Exemplary Repute and Above Average Physique"), not only to promote this geeky funny initiative, but also (ok, mainly) as a somewhat small personal reward. Why reward, you may ask. As a Scout organization, Science Scouts awards badges for several different "achievements" in science. I just figured that working in different fields would get me more badges, considering the different things I've done, but apparently it's not the case :-P
For example, shall you clone something (and I've cloned a lot of stuff over the years), then you are awarded this nice badge:
Also, if you blog about science, they this badge is for you:
Anyway, there are lots of badges I look forward to obtaining, like the one awarded by publishing in Science or Nature.
Here are some of my other badges. Take a look at the Science Scout's site and learn what they mean.
For example, shall you clone something (and I've cloned a lot of stuff over the years), then you are awarded this nice badge:
Also, if you blog about science, they this badge is for you:
Anyway, there are lots of badges I look forward to obtaining, like the one awarded by publishing in Science or Nature.
Here are some of my other badges. Take a look at the Science Scout's site and learn what they mean.
Monday, June 8, 2009
ATP synthase and its effects on grad students
I'll never forget the first time I saw an animation of the advance of the prokaryotic replication fork (I know the post is on ATP synthase. I'll get to that in a second). It was around 2005 while I was taking a MolBio course. Bruce Alberts (with whom I would later sit down for coffee on a cold morning in Chicago two years later, to discuss life as a biologist) came to visit our University in Chile and brought with him this video from HHMI (you can see other HHMI's animations here) which I posted a few months ago while discussing a recent paper on DNA replication [Polymerase Dynamics at the Eukaryotic DNA Replication Fork].
Recently, Iddo at Byte Size Biology, pointed us to some very interesting videos, from John E. Walker’s lab, on the mechanism of ATP synthase, an enzyme capable of synthesizing ATP from ADP and Pi through a unique rotary mechanism, in which subunits move relative to one another, powered by an electrochemical gradient of H+ or Na+ across the membrane [Da Vinci, F0-F1 ATPase: a copyright-driven Update].
This is just one of them:
OK, enough with the background, and on to the REAL reason of this post: what would you get if you add geeky grad students, a camera and a seminar on the enzymatic mechanisms of ATP synthase (and maybe some beer)?
This (again, thanks Iddo!):
Sunday, June 7, 2009
And now we play the waiting game...
As some of you know, I've been away from blogging for a while (actually I've done a little blogging, highlighting some sites and collections, but little to none reviewing of primary literature) as a result of writing my PhD Thesis project: in my school, early on your 2nd year you have to submit a thesis project which you will have to present and defend in your "Qualifying Exam". This project (a ~15-20 pages document) summarizes what you will do during your PhD, providing (of course) the background and stating the hypothesis, objectives and the means by which you plan to address them.After working for over a year in my previous lab (in plant molecular biology), I decided to switch fields (for reasons I may share later) and enter the fascinating world of circadian rhythms, using fungi as model organisms. As I was already in my 2nd year, I knew that making such a decision will require a lot of work, as I would need to read a lot (and from scratch) to come up with an original (and "PI-satisfying") research project in little over a month.
Shortly after I downloaded all the articles necessary to get me into context, I realized the impact of the field: a LOT of CNS, G&D and PNAS articles flooded my folder, a view I longed since my days working in mRNA splicing in yeast in the US.
So I started reading and soon came up with an idea I felt was interesting and, more importantly, one that motivated me. So I ran it by my PI and he was totally on board with it. In fact, his words were "fascinating idea. In fact, I was kinda thinking the same thing". After deciding on a research topic, I had to read a lot more, now getting deeper on this subject and write something called a "pre-project", which is a 4-5 pages summary of your proposed project. The purpose of this pre-project is for the school to select your thesis committee accordingly. After turning that document in, they gave me ~1 month to write the final project, which had to be very detailed, particularly in the background info and the methods.
Needless to say, this resulted not only in the downloading of more and more papers, but also in the daily email from my PI stating something like "you should DEFINITELY include this paper" which is usually a 2 seconds-old (and 15 pages long) article.
In the end, and on the verge of losing it, I rationalized the reading, focused on the writing, and on my final week managed to have a draft 3 days before deadline, in my PI's inbox. After some corrections and a little fighting with Endnote, I managed to turn it in, 20 minutes before deadline, last Friday. I think it's a nice project, timely (which is a very good feature of any research project) and well-conceived (if I may praise myself a little).
As we ping-ponged the different versions of the manuscript with my PI, I realized I made a good decision not only in terms of changing labs, but in choosing my new PI: he was critical, yet supportive, never criticizing an approach or expression without providing an alternative or explaining (in some cases with extreme detail) why he thought I should think about the particular item from a different perspective or in a different way. Also, he's been in the US for this whole period (quick reminder: I'm attending grad school in Chile), but we talked and discussed ideas daily, not only through email, but also Skype!. I felt completely supported throughout this entire experience, which was great.
So, what's next? As the post title states, I now have to wait; wait for the committee to set a date for my exam. In the meantime, I keep studying and giving practice talks to my fellow lab members. Also (although I may do this less now) I've been invited to sit through (and comment on) the practice talks of some friends who are also at this stage.
I'll keep you posted!
(Image credit: Crashhanna, see here)
Microorganisms invade PLoS One
PLoS One has set up a collection of articles describing whole genome sequence and/or comparative genomics of important prokaryotic organisms [The PLoS ONE Prokaryotic Genome Collection]. They will be highlighting articles in this field and including them as part of this collection from now on, so if you are interested in Microbiology this may be a good thing to keep in you bookmarks.
(Image from Miller et al. 2007)
Thursday, June 4, 2009
New MS protocol at Nature Protocols
I've been away from blogging for a while, because tomorrow I turn in my PhD Thesis Project, and a few weeks after that, I'll be taking my qualification exam: this means that for the last few weeks I've been reading my eyes out and studying, giving me little time to review articles and other items to highlight here at MolBio Research Highlights.
As part of my project (actually as an alternative approach) I've been thinking about using mass spectrometry (MS) to identify if the particular protein I'm studying is regulated through phosphorylation (sorry, can't give more details at the time). This is great as you can sequence phosphopeptides even if they are present at very low levels.
By some coincidence, while thinking about this, Nature Protocols alerted me of their latest FREE featured paper, a new MS protocol for the detection of peptide post-translational modifications.
Here's the link and reference:
Unwin RD, et al. (2009) A sensitive mass spectrometric method for hypothesis-driven detection of peptide post-translational modifications: multiple reaction monitoring-initiated detection and sequencing (MIDAS). Nature Protocols 4,870-877.
Wednesday, June 3, 2009
Conference on Open Access
As you may know, I'm a strong supporter of Open Access and I've been promoting some of the activities regarding last year's Open Access Day and the 2009 Open Access Week at this blog [OA week will take place in October] (you can also see the banner on the right sidebar under "Coming soon").This post is just to let you know about the 1st Conference on Open Access Scholarly Publishing (COASP), which will take place in mid-September (14-16).
More info here
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