Target Discovery and Validation Reviews and Protocols

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Keratin Transgenics and Knockouts 207 Fig. 3. (A) Epidermolysis bullosa simplex (EBS) evoked by mutations in K5 and also K14. (B) Meesmann’s corneal dystrophy elicited by mutations in K12. (C) Mutations in the keratin K6b and also other keratins are likely to trigger epidermolytic hyperkeratosis (EHK). (D) K4 mutations are reported to be responsible for white sponge nevus. (E) Pachyonychia congenita caused by mutations in K6a, K6b, and also K17. (F) Ablation of K5 in mouse causes EBS and neonatal death (21). (G) Total loss of K10 in the suprabasal epidermis in neonatal mice is without signs of fragility or wound healing response (75). There is free access to the pictures A to E, showing patients suffering from the mentioned syndromes on the World Wide Web. Pictures F and G are derived from the corresponding publications and slightly modified.
208 Vijayaraj, Söhl, and Magin filament organization, which we cannot refer to because of space limitations. For these modifications, more detailed literature is recommended (22–24). 1.1.3. Keratin Gene Expression and Regulation Today, it is commonly accepted that in simple as well as stratified epithelia, keratin genes are expressed in a “pairwise” manner. An acid type I keratin protein always attaches to a basic type II keratin to assemble a dimeric structure (8). Although redundant expression of further type I and type II keratins in different epithelia readily occurs, expression also takes place in this already mentioned pairwise manner. But what regulates this distinct pairwise turning-on and -off of different type I and II keratin genes? The human K18 keratin gene (~10 kb) (25) serves as a prime example of what might influence the transcriptional control of a keratin gene. Regulatory elements (Alu sequences and four putative SP1 binding sites) surrounding the seven coding exons as well as an AP-1 consensus site in exon 6 interacting with Ets-1 elements in intron 1 have been demonstrated to be involved in the copy number-dependent and position-independent transgenic expression of hK18. Additionally, two differentially methylated CpGs islands have been found in the first intron enhancer (26–28). Recently, taking this knowledge into consideration, Oshima and colleagues verified the coincidence of both hK18 transgene expression and that of different reporter genes in addition to the gene coding for the Cre-recombinase subcloned together with an internal ribosome entry side (IRES) immediately downstream of exon 7 (29). Results from the paradigmatic expression of the human K18 transgene imply that putative transcription factor binding sites merely identified in the (core)promoter might be not sufficient to explain the specific and pairwise expression pattern of keratin genes (30–32). In internal so-called “simple” epithelia, K8 and K18 form the pair that is predominantly expressed from embryonic day (ED)2.5 on (32) and that is complemented by K7, K19, K20, and K23 in most epithelia starting at ED3.5 (32). Generally, these keratins seem to be able to replace for K8 and K18, provided that they are expressed in the same cell type (33,34). In stratified epithelia, the prominent keratins are K5 and K14, which are complemented by different amounts of K15 and K17 in their basal layer (21,35,36). The upper parts of the epidermis maintain K5 and K14 as proteins, probably because of their long half-lives, but when keratinocytes start to differentiate they express highly abundant K1 and K10, accompanied by K1b, K2e, and K9 present in upper spinous and granular keratinocytes, particularly exposed to stress (37,38). Under conditions of proliferation or differentiation such as keratinocyte migration and wound healing, however, the so-called reinforcement keratins K6a, K6b, K6e, and K6hf as well as K16 and K17 often replace either transiently
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METHODS IN MOLECULAR BIOLOGY 360 T
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M E T H O D S I N M O L E C U L A R
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© 2007 Humana Press Inc. 999 River
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vi Preface get. Approaches to targe
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viii Contents 10 Transgenic Animal
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x Contributors SAHOHIME MATSUMOTO
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xii Contents of Volume 2 12 Validat
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2 Sioud disease pathogenesis and pe
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4 Sioud A more fruitful approach fo
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6 Sioud both transient and permanen
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8 Sioud serum biomarkers. This syne
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10 Sioud Fig. 2. Schematic of targe
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12 Sioud 13. Magin, T. M. (1998) Le
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Harnessing the Human Genome 15 The
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Harnessing the Human Genome 17 Fig.
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Harnessing the Human Genome 23 The
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Harnessing the Human Genome 27 repr
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Harnessing the Human Genome 29 14.
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Harnessing the Human Genome 31 45.
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34 Imoto et al. (4,5), and Bayesian
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36 Imoto et al. 2. Materials Two ty
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38 Imoto et al. Fig. 3. Graphical v
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40 Imoto et al. Fig. 5. Result of t
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42 Imoto et al. p(D |G) = ∫ p(D,
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44 Imoto et al. β k (k = 1,…,q j
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46 Imoto et al. Fig. 7. Partial res
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48 Imoto et al. Fig. 8. Strategy to
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50 Imoto et al. Fig. 9. (continued)
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52 Imoto et al. Table 3 List of Roo
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54 Imoto et al. 5. De Hoon, M. J. L
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56 Imoto et al. 39. Kamimura, T., S
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58 Beaty et al. cytotoxic drugs and
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60 Beaty et al. Fig. 1. Principles
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62 Beaty et al. oligonucleotide mic
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64 Beaty et al. 3. The 12% polyacry
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66 Beaty et al. 2.3.3. Protein Stai
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68 Beaty et al. 3.1.3. Labeling of
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70 Beaty et al. 1 µL of the anneal
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72 Beaty et al. 4. Phenol:cholorfor
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74 Beaty et al. 19. Wash twice with
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76 Beaty et al. The Following Volum
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78 Beaty et al. using a protein ass
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80 Beaty et al. 6. Shake the gel fo
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82 Beaty et al. Fig. 2. Preparation
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84 Beaty et al. search in. A widely
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86 Beaty et al. 3. Kern, S. E., Hru
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88 Beaty et al. 34. Peters, D. G.,
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5 Molecular Classification of Breas
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Molecular Profiling of Breast Cance
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Fig. 2. (Continued) the right ident
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6 Discovery of Differentially Expre
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Gene Target Discovery 117 In the fi
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Gene Target Discovery 119 sequences
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Gene Target Discovery 121 There is
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Gene Target Discovery 123 digestion
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Gene Target Discovery 125 Fig. 1. P
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Gene Target Discovery 127 5. Sargen
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Gene Target Discovery 129 41. Berry
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132 Matsumoto, Miyagishi, and Taira
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144 Fig. 1. The ribozyme-expression
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146 Sano and Taira 5. 10X L (low-sa
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148 Sano and Taira ribozymes may cl
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150 Fig. 3. A system for the identi
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152 Sano and Taira 4. Notes 1. We r
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9 Production of siRNA- and cDNA-Tra
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258 Skovseth, Küchler, and Haralds
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270 Iversen and Sørensen witnessed
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272 Iversen and Sørensen Fig. 1. P
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274 Iversen and Sørensen the core
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14 An Overview of the Immune System
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Overview of Immune System 279 diffe
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Overview of Immune System 281 Fig.
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Overview of Immune System 283 then
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Overview of Immune System 285 expre
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Overview of Immune System 289 solub
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Overview of Immune System 291 amino
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Overview of Immune System 293 (unre
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Overview of Immune System 297 the c
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Overview of Immune System 299 (44).
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Overview of Immune System 301 demon
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Overview of Immune System 307 some
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Overview of Immune System 309 sera
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Overview of Immune System 313 measu
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Overview of Immune System 315 42. H
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Overview of Immune System 317 74. D
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15 Potential Target Antigens for Im
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Tumor Antigen Discovery 321 develop
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Tumor Antigen Discovery 323 panel b
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Tumor Antigen Discovery 325 16. Joc
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16 Identification of Tumor Antigens
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Immunoproteomics 329 by “shot gun
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Immunoproteomics 331 isoelectric fo
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Immunoproteomics 333 3. 2D-PAGE is
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17 Protein Arrays A Versatile Toolb
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Protein Arrays 337 Table 1 Classifi
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Protein Arrays 339 fractions from c
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Protein Arrays 341 combinatorial sc
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Protein Arrays 343 The ideal proteo
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Protein Arrays 345 18. Cekaite, H.
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Protein Arrays 347 49. Yuko Kawahas
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Index 349 Index A Acetyl-CoA carbox
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Index 351 conditional by using FRT
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Index 353 Recombinant tumor antigen
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