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| 장 소 : 대구 인터불고호텔 2층 컨벤션홀 | |||||||||||||||||||||||||||||||||||||||||
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http://dec.dip.or.kr/
2009년 8월 30일 일요일
DEC 2009 (대구 국제 임베디드 컨퍼런스)
http://dec.dip.or.kr/
2009년 8월 25일 화요일
Nobel Science Essay 접수 확인 & 에세이 전문
정말 왠종일 자료만 모으다가, 글 쓰는건 오늘 하루만에 후다닥 끝낸 것 같다.
글을 보니, 참 형편없게 썼더라 [....]
다음에 쓸 기회가 있다면 좀 더 시간을 들여서 퇴고 시간을 많이 잡아야 할 것 같다.
1.우선적으로 생각할 것은 영어 용어는 가급적이면 한글로 고쳐쓰되, 꼭 영어를 써야 할 경우엔
괄호 안에 영어 용어를 기입해주고 앞에는 한글로 작성해 주는 것.
2.에세이는 보고서가 아니기 때문에, 나의 생각을 많이 반영 해 줘야 한다는 것.
그래도 이번 에세이를 쓰면서 세포 자살 메커니즘에 대해 좀 더 심도있게 알게 됐고, 전혀 생물과는 거리가 먼 사람이야! 라고 외치고 다녔던 나인데 한동안 이 에세이를 준비하면서 생물에 어느정도 흥미를 가지게 된 것 같다.
안그래도 HOUSE M.D 덕분에 의학쪽에는 많은 관심이 있었는데, 이번 기회로 생물에 안주던 관심을 주게 되니 뭐 생물님 좋은거 아닌가요?ㅋㅋㅋㅋ
여하튼, 원고 끝내고 나니 허무하고 멍하고 그렇다.
퇴고하는데 많은 도움을 준 잔류감각언니, 너무너무 고마워ㅠ_ㅠ
그리고 한글용어 관련해 도움 준 본2횽아도 고맙고.
제일 고마운건 우리 희수오래비♥ 쌤 고마워요 으헤헤'ㅁ'
다음번에 이런 기회가 있다면 정말 더 잘해보고 싶다.
이제 노벨 에세이가 슬슬 마무리 되었으니, 플라피를 다시 끄적여봐야겠다.
에세이 전문 보기
2009년 8월 20일 목요일
Activation-induced cell death - Apoptosis
Activated T-cells express CD95(Fas) upregulated surface expression of CD178(Fas L) and can secrete a soluble form of CD178. Death of the activated cell results when either soluble or surface CD178 interacts with CD95.
좀 더 부연설명을 하자면 antigen이 백혈구에 존재하는 T-cell에 붙으면 보통은 T-cell은 면역체계를 작동시켜 들어온 Antigen을 다른 세포들과 상호협동작용을 통해 없애버린다. 그러나 오래된 T-cell이나 특별한 Cytotoxic의 특성을 가진 Virus가 침투해 감염된 T-cell은 스스로 위의 분해과정을 거쳐서 자가 분해를 해 버린다. 이게 자살 기작의 가장 기본적인 원리이다.
Key word - Nucleotid, MHC class, CD8+, CD4+, T-cell - 이 기작을 더 자세히 공부하려면 이런 내용들을 이해해야 한다.
이까지 오래비 블로그에서 퍼옴.
그림 진짜 잘그리셨다고 생각......(움찔)
─────────────────────────────────────────────
*뉴클레오티드
위키백과 ― 우리 모두의 백과사전.
뉴클레오티드는 핵산을 구성하는 단위체이다. 다음과 같이 염기-당-인산의 결합으로 이루어져 있다.
- 염기: DNA의 경우 아데닌, 구아닌(오각 링과 육각 링으로 구성; 퓨린 계열), 시토신, 티민(육각 링으로 구성; 피리미딘 계열)으로 되어 있으며 RNA의 경우는 티민 대신 우라실이 들어간다.
- 당: 탄소 5개로 구성된 5탄당이다. DNA의 경우 디옥시리보오스, RNA의 경우 리보오스로 되어 있다.
- 인산: H3PO4이나 보통 핵산분자 안에서는 두 개의 산소로 각각 당과 결합하며 남는 두개의 산소에는 금속 이온(보통 마그네슘 2가 이온)이 붙어 있다. 이 인산 때문에 핵산은 강한 산성을 띤다.
또한 아데닌이 들어가 만들어진 뉴클레오타이드는 고리형으로 만들어져 세포 내 신호전달에 쓰이기도 하며, 인산기가 세개 연달아 붙은 ATP는 생명체 내의 에너지원으로 사용된다.
가장 일반적인 뉴클레오티드들
*MHC class I
From Wikipedia, the free encyclopedia
Schematic representation of MHC class I
There are two primary classes of major histocompatibility complex (MHC) molecules, MHC class I and MHC class II. MHC class I molecules are found on every nucleated cell of the body (and thus not on red blood cells). Their function is to display fragments of proteins from within the cell to T cells, so that healthy cells will be left alone and cells with foreign proteins will be attacked by the immune system. Because MHC class I molecules present peptides derived from cytosolic proteins, the pathway of MHC class I presentation is often called the cytosolic or endogenous pathway.[1]
*MHC class II
From Wikipedia, the free encyclopedia
Schematic representation of MHC class II
MHC (major histocompatibility complex) Class II molecules are found only on a few specialized cell types, including macrophages, dendritic cells and B cells, all of which are professional antigen-presenting cells (APCs).
The peptides presented by class II molecules are derived from extracellular proteins (not cytosolic as in class I); hence, the MHC class II-dependent pathway of antigen presentation is called the endocytic or exogenous pathway.
Loading of class II molecules must still occur inside the cell; extracellular proteins are endocytosed, digested in lysosomes, and bound by the class II MHC molecule prior to the molecule's migration to the plasma membrane.
*CD8
From Wikipedia, the free encyclopedia
CD8 (cluster of differentiation 8) is a transmembrane glycoprotein that serves as a co-receptor for the T cell receptor (TCR). Like the TCR, CD8 binds to a major histocompatibility complex (MHC) molecule, but is specific for the class I MHC protein.[2] There are two isoforms of the protein, alpha and beta, each encoded by a different gene. In humans, both genes are located on chromosome 2 in position 2p12.
*T세포 [T cell]
요약
흉선에서 유래하는 림프구로 면역에서의 기억능력을 가지며 B세포에 정보를 제공하여 항체 생성을 도울 뿐만 아니라 세포의 면역에 주된 역할을 한다.
본문
면역활동에서 중요한 역할을 담당하는 림프구에는 그 기원과 기능이 서로 다른 2개의 그룹이 존재한다고 보는 것이 지배적인 견해이다. 골수(bone marrow)의 간세포(幹細胞)가 림프구로 분화하는 경우에는 다음 두 가지가 있다.
흉선(胸腺)의 상피세포에서 특수한 내부 환경과 흉선의 액성인자(液性因子)에 의해 림프구로 분화하는 경우와, 흉선과는 관계없이 골수에서만 림프구로 분화하는 경우가 있다. 이 양자는 여러 점에서 이질적이므로 전자를 흉선(thymus)에서 유래하는 림프구, 즉 T세포라 하고, 후자를 골수에서 유래하는 림프구, 즉 B세포라고 한다.
T세포는 흉선에서 교육을 받아 크게 세 가지 종류의 T세포로 나뉘는데, 살해 T세포(killer t-cell), 도움 T세포(helper T-cell), 조절 T세포(regulatory T cell)가 그것이다. 이들은 세포 표면에 있는 단백질 분자에 의해 구분이 되는데, 살해 T세포의 경우 CD8이, 도움 T세포의 경우 CD4가, 조절 T세포의 경우 CD4와 CD25가 발현되어 있어 구별이 가능하다. 외부에 세균과 같은 항원이 들어왔을 때, 도움 T세포가 사이토카인(cytokine)과 같은 특정 물질을 분비하여 살해 T세포와 B세포의 활성을 증대하면 살해 T세포는 병원체에 감염된 세포들을 죽이게 되며, B세포는 항체를 분비하여 항원의 활성을 저해한다. 이때, 조절 T세포는 면역활동을 적절히 조절하는 것으로 알려져 있다.
주사형(走査型) 전자현미경으로 양자를 형태학적으로 관찰하면, T세포의 표면은 비교적 평평하고 매끄럽게 보이는 데 비하여 B세포의 표면에는 돌기가 많이 나 있다. 또 투과형(透過型) 전자현미경으로 관찰하면, T세포에는 집합성 농밀체(濃密體:dense body)가 있고 B세포에는 산재성 농밀체가 있어 주목된다. 기능면에서 보면 B세포는 항체 글로불린의 생성에 관여하고, T세포는 면역에서의 기억능력 및 항원에 오염된 세포를 파괴하는 능력을 가지며, B세포에 정보를 제공하여 항체 생성을 돕기도 한다. T세포는 림프절 방피질부(旁皮質部)와 지라의 중심동맥 주위에 분포하는데, 이 부위를 '흉선의존영역'이라고 한다.
- ⓒ 두산백과사전 EnCyber & EnCyber.com, 무단 전재 및 재배포 금지 -
From Wikipedia, the free encyclopedia
Schematic representation of MHC class II
MHC (major histocompatibility complex) Class II molecules are found only on a few specialized cell types, including macrophages, dendritic cells and B cells, all of which are professional antigen-presenting cells (APCs).
The peptides presented by class II molecules are derived from extracellular proteins (not cytosolic as in class I); hence, the MHC class II-dependent pathway of antigen presentation is called the endocytic or exogenous pathway.
Loading of class II molecules must still occur inside the cell; extracellular proteins are endocytosed, digested in lysosomes, and bound by the class II MHC molecule prior to the molecule's migration to the plasma membrane.
*CD8
From Wikipedia, the free encyclopedia
CD8 (cluster of differentiation 8) is a transmembrane glycoprotein that serves as a co-receptor for the T cell receptor (TCR). Like the TCR, CD8 binds to a major histocompatibility complex (MHC) molecule, but is specific for the class I MHC protein.[2] There are two isoforms of the protein, alpha and beta, each encoded by a different gene. In humans, both genes are located on chromosome 2 in position 2p12.
| *T세포 [T cell] | |
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http://en.wikipedia.org/wiki/Apoptosis
http://ko.wikipedia.org/wiki/뉴클레오티드
http://en.wikipedia.org/wiki/MHC_class_I
http://en.wikipedia.org/wiki/MHC_class_II
http://en.wikipedia.org/wiki/CD4
http://en.wikipedia.org/wiki/CD8
http://100.naver.com/100.nhn?docid=156771
영어......................... 젠장. ㅠ_ㅠ 나도 이해하고싶다.
2009년 8월 19일 수요일
The Nobel Prize in Physiology or Medicine 2002 - Presentation Speech (Eng+Kor)
Presentation Speech
Presentation Speech by Professor Urban Lendahl of the Nobel Committee at Karolinska Intitutet, December 10, 2002.
Translation of the Swedish text.
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| Professor Urban Lendahl delivering the Presentation Speech for the 2002 Nobel Prize in Physiology or Medicine at the Stockholm Concert Hall. Copyright © Nobel Web AB 2002 Photo: Hans Mehlin |
Your Majesties, Your Royal Highnesses, Ladies and Gentlemen,
We have all begun our lives in a seemingly modest way – as the fertilised egg cell, a tenth of a millimetre in size. From this small cell, the adult human being develops, with its hundred thousand billion cells, through cell division, cell differentiation and by formation of the various organs. To only make new cells is however not sufficient, certain cells must also die at specific time points as a natural part of the growth process. Think for example about how we for a short period during foetal life have web between our fingers and toes, and how this is removed by cell death.
The importance of cell differentiation and organ development was understood by many, but progress was slow. This was largely an effect of our complexity, with the large number of cells and many cell types – the forest could not be seen because of all the trees. Could the task to find the genetic principles be made simpler? Were there a species simpler than humans, but still sufficiently complex to allow for general principles to be deduced?
Sydney Brenner in Cambridge, UK, took on the challenge, and his choice was the nematode Caenorhabditis elegans. This may at first seem odd, a spool-shaped approximately 1 millimetre long worm with 959 cells that eats bacteria, but Brenner realised in the early 1960s that it was, what we today would call, "loaded with features". It was genetically amenable and it was transparent, so that every cell division and differentiation could be directly followed in the worm under the microscope. Brenner demonstrated in 1974 that mutations could be introduced into many genes and visualised as distinct changes in organ formation. Through his visionary work, Brenner created an important research tool. The nematode had made into the inner circle of research.
John Sulston came to Brenner's laboratory in 1969. He took advantage of that cell divisions could be followed under the microscope and assembled the cell lineage in the worm, showing which cells are siblings, first and second cousins. He found that cell divisions occurred with a very high degree of precision, the cell lineage was identical between different individuals. He also realised that certain cells in the lineage always died at a certain time point. This meant that programmed cell death was not a stochastic process, but rather occurred with a very high degree of precision. During the course of this work Sulston identified the first gene important for the cell death process: nuc-1.
Robert Horvitz came to work with Brenner and Sulston in 1974. Horvitz started a systematic search for genes controlling programmed cell death. He identified the key genes for the cell death process proper. The discovery of these central death genes, ced-3, ced-4 and ced-9, changed the view on programmed cell death from something rather obscure to a process with a strict genetic programme. Horvitz also showed that there are human homologues to the death genes in the worm and that those have corresponding functions – the cell death machinery had deep evolutionary roots.
This year's Nobel Prize celebrates the Joy of Worms. Brenner's almost prophetic visions from the early 1960s of the advantages of this model organism have been fulfilled. It has given us new insights into the development of organs and tissues and why specific cells are destined to die. This knowledge has proven valuable, for instance, in understanding how certain viruses and bacteria attack our cells, and how cells die in heart attack and stroke.
Sydney Brenner, Robert Horvitz and John Sulston.
Your discoveries concerning the genetic regulation of organ development and programmed cell death have truly opened new avenues for biological and medical research. On behalf of the Nobel Assembly at Karolinska Institutet I wish to convey to you our warmest congratulations and I ask you to step forward to receive the Nobel Prize from the hands of His Majesty the King.
Copyright © The Nobel Foundation 2002
한글 해석
The Nobel Prize in Physiology or Medicine 2002 - Illustrated Presentation
| The Nobel Prize in Physiology or Medicine 2002 | |
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The Nobel Assembly at Karolinska Institutet has awarded the Nobel Prize in Physiology or Medicine jointly to Sydney Brenner, Robert Horvitz and John Sulston for their discoveries concerning "genetic regulation of organ development and programmed cell death". By using the nematode Caenorhabditis elegans as a model system, the Laureates have identified key genes regulating these processes. They have also shown that corresponding genes exist in higher species, including man. |
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Introduction | |||||||||||
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The human body consists of hundreds of cell types, all originating from the fertilized egg. During the embryonic
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Sydney Brenner realized, in the early 1960s, that the
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Robert Horvitz used C. elegans to investigate whether We now know that most genes involved in controlling | ||
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| John Sulston | |||
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John Sulston developed techniques to study all cell As a result of these findings, Sulston discovered that specific | ||
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| The Implications of the Discoveries | ||||
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The introduction of C. elegans as a novel experimental model system, the characterization of its invariant cell lineage, and the possibility to link this to genetic analysis have proven valuable for many research disciplines. For example, this is true for developmental biology and for analysis of the functions of signalling pathways in multicellular organisms. Research on programmed cell death is intense. Knowledge in this field has helped us to understand the mechanisms by which some viruses and bacteria invade and manipulate our cells. Some diseases, like cancer and certain autoimmune conditions, are characterized by a reduction in cell death, leading to the survival of cells normally destined to die. Many treatment strategies against cancer are based on stimulation of the cellular "suicide programme". This is an interesting and challenging task to further explore in order to reach a refined manner to induce cell death in cancer cells. We also know that in AIDS, neurodegenerative diseases, stroke and myocardial infarction, cells are lost as a result of excessive cell death. For instance, current research suggests that it is possible to reduce the damage caused by myocardial infarction and stroke by using drugs restraining programmed cell death. |
Credits and References for the 2002 Nobel Poster for Physiology or Medicine
Scientific Advisors, Professors at Karolinska Institutet:Hans Jörnvall - Physiological Chemistry, Secretary of the Nobel Assembly
Urban Lendahl - Genetics
Sten Lindahl - Anesthesiology, Chairman of the Nobel Committee
Sten Orrenius - Toxicology
Art Director:
Urban Frank
Medical Writer:
Anders Nystrand
Printed by:
DB Media AB, Stockholm, Sweden 2002
Copyright © 2002:
The Nobel Committee for Physiology or Medicine
at Karolinska Institutet, SE-171 77 Stockholm, Sweden
Web Adapted Version:
Nobelprize.org
Every effort has been made by the publisher to credit organizations and individuals with regard to the supply of photographs and illustrations. The publishers apologize for any omissions which will be corrected in future editions.
http://nobelprize.org/nobel_prizes/medicine/laureates/2002/illpres
The Nobel Prize in Physiology or Medicine 2002 - Prizewinners
"for their discoveries concerning 'genetic regulation of organ development and programmed cell death'"
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 1/3 of the prize |
1/3 of the prize |
1/3 of the prize |
| United Kingdom | USA | United Kingdom |
| The Molecular Sciences Institute Berkeley, CA, USA |
Massachusetts Institute of Technology (MIT) Cambridge, MA, USA |
The Wellcome Trust Sanger Institute Cambridge, United Kingdom |
| b. 1927 (in Union of South Africa) |
b. 1947 | b. 1942 |
Titles, data and places given above refer to the time of the award.
Photos: Copyright © The Nobel Foundation
The Nobel Prize in Physiology or Medicine 2002 - Press Release
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Press Release
7 October 2002
The Nobel Assembly at Karolinska Institutet has today decided to award
The Nobel Prize in Physiology or Medicine for 2002 jointly to
Sydney Brenner, H. Robert Horvitz and John E. Sulston
for their discoveries concerning "genetic regulation of organ development and programmed cell death"
Summary
The human body consists of hundreds of cell types, all originating from the fertilized egg. During the embryonic and foetal periods, the number of cells increase dramatically. The cells mature and become specialized to form the various tissues and organs of the body. Large numbers of cells are formed also in the adult body. In parallel with this generation of new cells, cell death is a normal process, both in the foetus and adult, to maintain the appropriate number of cells in the tissues. This delicate, controlled elimination of cells is called programmed cell death.
This year's Nobel Laureates in Physiology or Medicine have made seminal discoveries concerning the genetic regulation of organ development and programmed cell death. By establishing and using the nematode Caenorhabditis elegans as an experimental model system, possibilities were opened to follow cell division and differentiation from the fertilized egg to the adult. The Laureates have identified key genes regulating organ development and programmed cell death and have shown that corresponding genes exist in higher species, including man. The discoveries are important for medical research and have shed new light on the pathogenesis of many diseases.
Sydney Brenner (b 1927), Berkeley, CA, USA, established C. elegans as a novel experimental model organism. This provided a unique opportunity to link genetic analysis to cell division, differentiation and organ development – and to follow these processes under the microscope. Brenner's discoveries, carried out in Cambridge, UK, laid the foundation for this year's Prize.
John Sulston (b 1942), Cambridge, England, mapped a cell lineage where every cell division and differentiation could be followed in the development of a tissue in C. elegans. He showed that specific cells undergo programmed cell death as an integral part of the normal differentiation process, and he identified the first mutation of a gene participating in the cell death process.
Robert Horvitz (b 1947), Cambridge, MA, USA, has discovered and characterized key genes controlling cell death in C. elegans. He has shown how these genes interact with each other in the cell death process and that corresponding genes exist in humans.
Cell lineage – from egg to adult
All cells in our body are descendents from the fertilized egg cell. Their relationship can be referred to as a cellular pedigree or cell lineage. Cells differentiate and specialize to form various tissues and organs, for example muscle, blood, heart and the nervous system. The human body consists of several hundreds of cell types, and the cooperation between specialized cells makes the body function as an integrated unit. To maintain the appropriate number of cells in the tissues, a fine-tuned balance between cell division and cell death is required. Cells have to differentiate in a correct manner and at the right time during development in order to generate the correct cell type.
It is of considerable biological and medical importance to understand how these complicated processes are controlled. In unicellular model organisms, e.g. bacteria and yeast, organ development and the interplay between different cells cannot be studied. Mammals, on the other hand, are too complex for these basic studies, as they are composed of an enormous number of cells. The nematode C. elegans, being multi-cellular, yet relatively simple, was therefore chosen as the most appropriate model system, which has then led to characterization of these processes also in humans.
Programmed cell death
Normal life requires cell division to generate new cells but also the presence of cell death, so that a balance is maintained in our organs. In an adult human being, more than a thousand billion cells are created every day. At the same time, an equal number of cells die through a controlled "suicide process", referred to as programmed cell death.
Developmental biologists first described programmed cell death. They noted that cell death was necessary for embryonic development, for example when tadpoles undergo metamorphosis to become adult frogs. In the human foetus, the interdigital mesoderm initially formed between fingers and toes is removed by programmed cell death. The vast excess of neuronal cells present during the early stages of brain development is also eliminated by the same mechanism.
The seminal breakthrough in our understanding of programmed cell death was made by this year's Nobel Laureates. They discovered that specific genes control the cellular death program in the nematode C. elegans. Detailed studies in this simple model organism demonstrated that 131 of totally 1090 cells die reproducibly during development, and that this natural cell death is controlled by a unique set of genes.
The model organism C. elegans
Sydney Brenner realized, in the early 1960s, that fundamental questions regarding cell differentiation and organ development were hard to tackle in higher animals. Therefore, a genetically amenable and multicellular model organism simpler than mammals, was required. The ideal solution proved to be the nematode Caenorhabditis elegans. This worm, approximately 1 mm long, has a short generation time and is transparent, which made it possible to follow cell division directly under the microscope.
Brenner provided the basis in a publication from 1974, in which he broke new ground by demonstrating that specific gene mutations could be induced in the genome of C. elegans by the chemical compound EMS (ethyl methane sulphonate). Different mutations could be linked to specific genes and to specific effects on organ development. This combination of genetic analysis and visualization of cell divisions observed under the microscope initiated the discoveries that are awarded by this year's Nobel Prize.
Mapping the cell lineage
John Sulston extended Brenner's work with C. elegans and developed techniques to study all cell divisions in the nematode, from the fertilized egg to the 959 cells in the adult organism. In a publication from 1976, Sulston described the cell lineage for a part of the developing nervous system. He showed that the cell lineage is invariant, i.e. every nematode underwent exactly the same program of cell division and differentiation.
As a result of these findings Sulston made the seminal discovery that specific cells in the cell lineage always die through programmed cell death and that this could be monitored in the living organism. He described the visible steps in the cellular death process and demonstrated the first mutations of genes participating in programmed cell death, including the nuc-1 gene. Sulston also showed that the protein encoded by the nuc-1 gene is required for degradation of the DNA of the dead cell.
Identification of "death genes"
Robert Horvitz continued Brenner's and Sulston's work on the genetics and cell lineage of C. elegans. In a series of elegant experiments that started during the 1970s, Horvitz used C. elegans to investigate whether there was a genetic program controlling cell death. In a pioneering publication from 1986, he identified the first two bona fide "death genes", ced-3 and ced-4. He showed that functional ced-3 and ced-4 genes were a prerequisite for cell death to be executed.
Later, Horvitz showed that another gene, ced-9, protects against cell death by interacting with ced-4 and ced-3. He also identified a number of genes that direct how the dead cell is eliminated. Horvitz showed that the human genome contains a ced-3-like gene. We now know that most genes that are involved in controlling cell death in C. elegans, have counterparts in humans.
Of importance for many research disciplines
The development of C. elegans as a novel experimental model system, the characterization of its invariant cell lineage, and the possibility to link this to genetic analysis have proven valuable for many research disciplines. For example, this is true for developmental biology and for analysis of the functions of various signaling pathways in a multicellular organism. The characterization of genes controlling programmed cell death in C. elegans soon made it possible to identify related genes with similar functions in humans. It is now clear that one of the signaling pathways in humans leading to cell death is evolutionarily well conserved. In this pathway ced-3-, ced-4- and ced-9-like molecules participate. Understanding perturbations in this and other signaling pathways controlling cell death are of prime importance for medicine.
Disease and programmed cell death
Knowledge of programmed cell death has helped us to understand the mechanisms by which some viruses and bacteria invade our cells. We also know that in AIDS, neurodegenerative diseases, stroke and myocardial infarction, cells are lost as a result of excessive cell death. Other diseases, like autoimmune conditions and cancer, are characterized by a reduction in cell death, leading to the survival of cells normally destined to die.
Research on programmed cell death is intense, including in the field of cancer. Many treatment strategies are based on stimulation of the cellular "suicide program". This is, for the future, a most interesting and challenging task to further explore in order to reach a more refined manner to induce cell death in cancer cells.
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| Using the nematode C. elegans this year's Nobel Laureates have demonstrated how organ development and programmed cell death are genetically regulated. They have identified key genes regulating programmed cell death and demonstrated that corresponding genes exist also in higher animals, including man. The figure schematically illustrates the cell lineage (top left) and the programmed cell death (below) in C. elegans. The fertilized egg cell undergoes a series of cell divisions leading to cell differentiation and cell specialization, eventually producing the adult organism (top right). In C. elegans, all cell divisions and differentiations are invariant, i.e. identical from individual to individual, which made it possible to construct a cell lineage for all cell divisions. During development, 1090 cells are generated, but precisely 131 of these cells are eliminated by programmed cell death. This results in an adult nematode (the hermaphrodite), composed of 959 somatic cells. |
http://nobelprize.org/nobel_prizes/medicine/laureates/2002/press.html
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