Project Ideas:

• Program immune system cells to recognize and destroy cancer.

Killer T cells

• Program Cells to recognize cancer

Extracellular-- established

Intracellular-- how to do?

• Artificial cell?

Convert complex virus (vaccinia) to independent entity

• Cyborg cell (contains cybernetic components that interface directly with the cell).

Make cells that incorporate nanoparticles

That have interfaces to electronics/electrode

That have interfaces to nanomotors

Spicule-like structures to act as nano-injectors, or light transmitters, or both!

Scaffolding incorporating exotic materials (e.g. gold) assembled/disassembled by the cell forsome purpose (protection, electrostatic properties, etc.)

Relevant information:

http://www.pnas.org/content/101/33/12096.full (biomineralization)

http://en.wikipedia.org/wiki/Brain-computer_interface

http://books.google.com/books?id=L9JQknQXtJgC&pg=PA283&lpg=PA283&dq=cell+scaffold+synthetic&source=bl&ots=DoRsTouMz6&sig=Sd5jOCSnWmL6-6YcO_FmPRK3Ieo&hl=en&ei=CjggSsbLN6fgsgPs2t2OBA&sa=X&oi=book_result&ct=result&resnum=7#PPA284,M1 (scaffold design)

http://www.ncbi.nlm.nih.gov/pubmed/9556760 (more scaffolding)

http://books.google.com/books?id=LXeE5soHiWMC&pg=PA48&lpg=PA48&dq=cell+synthetic+polymer&source=bl&ots=pyTKTVVVIf&sig=fw9qTvoI1SvTXOYqTPFy6kcPHpE&hl=en&ei=7T4gSt-TLoTGtAOPubT0Aw&sa=X&oi=book_result&ct=result&resnum=6 (cell encapsulation stuff)

http://www.mrs.org/s_mrs/sec_subscribe.asp?CID=2273&DID=80942&action=detail (spicules as opticle fibers)

http://www.springerlink.com/content/bj51562302q84121/ and http://portal.acm.org/citation.cfm?id=1361246.1385056 (spicules as blueprints for biofabrication)

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TWB-4RJSJ2V-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=f06995d2f9f498218dab236295ee28da (synthetic polymers on a cell membrane)

http://www.bu.edu/abl/files/tibtech_simpson.pdf (general synthetic biology)

http://pubs.acs.org/doi/full/10.1021/cr030698%2B?cookieSet=1 (gold nanotech)

http://www.bio-medicine.org/medicine-news-1/Scientists-look-at-syringe-assembly-in-plague-bacteria-12885-1/ (bacterial syringe)

https://www.researchgate.net/publication/5823872_Bioencapsulation_of_living_bacteria_(Escherichia_coli)_with_poly(silicate)_after_transformation_with_silicatein-alpha_gene (bioencapsulation)

• Biofilm that can be placed over wounds to seal them, and also prevents scarring/infection.

Need to make sure that biofilm is not immunogenic.

Promote formation of identical skin tissue

Speed up healing process

• Mammalian skin cells that are more resistant to damage from UV radiation.
• Hybrid cells which are less specialized but more versatile in function.

Make cells that regenerate damaged tissue (think of ultimate model in neoblasts from planaria)

• Cells that can recognize long dsRNA and not attack them. Just an idea(Could you be more specific? --am, immune cells?, what kind of dsRNA (for RNAi?),for what purpose (to minimize inflammation?)

• turn off oncogenes through RNAi
• Cell redifferentiation
• Increase nutritional value of food by inserting vitamin plastids
• Fight obesity by decreasing feeling of hunger: increasing leptin production/ blocking ghrelin production
• Lower blood glucose levels: overexpression of insulin-receptor genes
• Alter expression of genes that control the absorption of essential substances (such as calcium, other minerals and vitamins, fats, certain proteins, etc.)

* Cell regeneration - if we can make cells that can mimic the nervous system cells in the central nervous system it could be potentially helpful for paralyzed patients; or cells that can mimic the behavior of motor neurons so that there may be cures for ALS patients

* cells that can take over the function of hair cells in the ear. it would be a better alternative to those with impaired hearing

• http://www.jneurosci.org/cgi/content/full/jneuro;23/11/4395

* cells that can aid in bone regeneration or cartilage regeneration

* cells that can grow hair to treat male pattern baldness

* cells to make biofuels (they're using algae right now)

* cells that can absorb CO2 (maybe stuff the cells into the exhaust pipe) and help solve global warming!

* cells that can eat up plaque build-up in arteries or destroy LDL-cholesterol

* induced pluripotent cells

• Cells that have transposons whose transposase recognizes specific gene bp sequences and can interrupt that gene: like some harmful genes
• Cells that can make polymers like rubber
• Cells that block Th1 and Th2 factors to help children with asthma

• transposonarticle.pdf: transposonarticle.pdf

• Brainstorming_Ideas_List_#1.doc: Brainstorming_Ideas_List_#1.doc

• JBO020502.pdf: JBO020502.pdf

• Dunn_-_1996_-_Mammalian_cell_binding_and_transfection_mediated_b.pdf: Dunn_-_1996_-_Mammalian_cell_binding_and_transfection_mediated_b.pdf

• Eriksson_et_al_-_2007_-_Tumor_specific_phage_particles_promote_tumor_regre.pdf: Eriksson_et_al_-_2007_-_Tumor_specific_phage_particles_promote_tumor_regre.pdf

• Harel-Levi_et_al_-_2008_-_Human_genomic_site-specific_recombination_catalyze.pdf: Harel-Levi_et_al_-_2008_-_Human_genomic_site-specific_recombination_catalyze.pdf

• Lu_and_Collins_-_2009_-_Engineered_bacteriophage_targeting_gene_networks_a.pdf: Lu_and_Collins_-_2009_-_Engineered_bacteriophage_targeting_gene_networks_a.pdf

• Sapinoro_et_al_-_2008_-_Fc_receptor-mediated,_antibody-dependent_enhanceme.pdf: Sapinoro_et_al_-_2008_-_Fc_receptor-mediated,_antibody-dependent_enhanceme.pdf

• pathogenarticle.pdf: Bacterial injection

• Müller_et_al_-_2008_-_Bioencapsulation_of_living_bacteria_(Escherichia_c.pdf: Müller_et_al_-_2008_-_Bioencapsulation_of_living_bacteria_(Escherichia_c.pdf

• [[http://www.regensci.org/twiki/pub/IGEM2009/BrainStorming/Wiens_et_al_-_2009_-_The_role_of_the_silicatein-%5balpha%5d_interactor_sili.pdf][Wiens_et_al_-_2009_-_The_role_of_the_silicatein-[alpha]_interactor_sili.pdf]]: Wiens_et_al_-_2009_-_The_role_of_the_silicatein-[alpha]_interactor_sili.pdf

• Müller_et_al_-_2009_-_Sponge_spicules_as_blueprints_for_the_biofabricati.pdf: Müller_et_al_-_2009_-_Sponge_spicules_as_blueprints_for_the_biofabricati.pdf

• phagemid.pdf: phagemid.pdf

• filamentousbacteriophage.pdf: filamentousbacteriophage.pdf

• chemokinesreceptor.pdf: chemokinesreceptor.pdf

Possible Receptors

PTHrP

The parathyroid hormone-related protein receptor(PTHRP) is expressed in breast cancer bone metastases and promotes autocrine proliferation in breast carcinoma cells.

http://www.ncbi.nlm.nih.gov/pubmed/12592371

Parathyroid hormone-related peptide (PTHrP? ) has a high homology with the N-terminal portion of the parathyroid hormone (PTH). The gene of PTHrP? is complex and can generate by alternative splicing at least three mature peptides containing 139, 141 and 173 amino acids. PTHrP? acts via a common receptor with PTH but also via specific receptors. In physiological circumstances, PTHrP? is produced locally in many normal tissues where it has autocrine/paracrine functions, particularly during embryonic development, growth regulation and differentiation of many cellular types. PTHrP? has endocrine action on bone and kidney. The humoral hypercalcemia of malignancy is mainly mediated by PTHrP? . Most hypercalcemic patients with solid tumors have increased plasma PTHrP? , whereas PTHrP? is not detectable in healthy subjects. During treatment with bisphosphonates, elevated plasma levels of PTHrP? are associated with a weak response. PTHrP? has also a significant role in the pathophysiology of bone metastases . PTHrP? can induce a local osteolysis near the bone metastases, which favours their progression and thus participates in the autocrine regulation of tumor growth. In breast cancer, PTHrP? is detected in about 60% of primary tumors and in more than 70% of bone metastases, whereas only 17% of nonbone metastases express PTHrP? . A higher expression of PTHrP? and its mRNA 1-139, is positively correlated with an invasive tumor phenotype and the development of bone metastases. PTHrP? is an effector of transforming growth factor (TGFbeta) in the development and progression of osteolytic bone metastases. TGFbeta, which is released in bone matrix during osteolytic resorption, enhances tumor cells PTHrP? production. Then, PTHrP? stimulates bone resorption and develops tumor cells metastatic potential. Thus a feedback loop exists between carcinoma cells and the bone microenvironment, leading to a vicious circle. http://www.ncbi.nlm.nih.gov/pubmed/11741801?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=4&log$=relatedreviews&logdbfrom=pubmed

IFN-\x{03b3} (IP-10)/CXCL10

Interferon--inducible protein-10 (IP-10)/CXCL10 is a CXC chemokine that attracts T lymphocytes and NK cells through activation of CXCR3, the only chemokine receptor identified to date that binds IP-10/CXCL10. We have found that several nonhemopoietic cell types, including epithelial and endothelial cells, have abundant levels of a receptor that binds IP-10/CXCL10 with a K _d of 1\x{2013}6 nM. Surprisingly, these cells expressed no detectable CXCR3 mRNA. Furthermore, no cell surface expression of CXCR3 was detectable by flow cytometry, and the binding of ¹²⁵I-labeled IP-10/CXCL10 to these cells was not competed by the other high affinity ligands for CXCR3, monokine induced by IFN-/CXCL9, and I-TAC/CXCL11. Although IP-10/CXCL10 binds to cell surface heparan sulfate glycosaminoglycan (GAG), the receptor expressed by these cells is not GAG, since the affinity of IP-10/CXCL10 for this receptor is much higher than it is for GAG, its binding is not competed by platelet factor 4/CXCL4, and it is present on cells that are genetically incapable of synthesizing GAG. Furthermore, in contrast to IP-10/CXCL10 binding to GAG, IP-10/CXCL10 binding to these cells induces new gene expression and chemotaxis, indicating the ability of this receptor to transduce a signal. These high affinity IP-10/CXCL10-specific receptors on epithelial cells may be involved in cell migration and, perhaps, in the spread of metastatic cells as they exit from the vasculature. (All of the lung cancer cells we examined also expressed CXCR4, which has been shown to play a role in breast cancer metastasis.) CXCR3-negative endothelial cells may also use this receptor to mediate the angiostatic activity of IP-10/CXCL10, which is also expressed by these cells in an autocrine manne

http://www.jimmunol.org/cgi/content/abstract/167/11/6576

EGF

Recombinant human ribonuclease 1 (RNasel) was chemically linked to recombinant human epidermal growth factor (EGF). The cytotoxicity of this conjugate was assayed using MTT assay. The EGF-RNase conjugate showed dose-dependent cytotoxicity against breast and squamous cell carcinomas overexpressing the EGF receptor (EGFR). The cytotoxicity of the conjugate correlated positively with the level of EGFR expression by each cell line. These results suggest that the EGF-RNase conjugate is a more effective anticancer agent with less immunogenicity and toxicity than conventional chimeric breast cancer toxins.

http://www.springerlink.com/content/a3151006356l0175/

TARP

Previously, we showed that prostate and prostate cancer cells express a truncated T-cell receptor chain mRNA that uses an alternative reading frame to produce a novel nuclear T-cell receptor chain alternate reading frame protein (TARP). TARP is expressed in the androgen-sensitive LNCaP? prostate cancer cell line but not in the androgen-independent PC3 prostate cancer cell line, indicating that TARP may play a role in prostate cancer progression. To elucidate the function of TARP, we generated a stable PC3 cell line that expresses TARP in a constitutive manner. Expression of TARP in PC3 cells resulted in a more rapid growth rate with a 5-h decrease in doubling time. cDNA microarray analysis of 6538 genes revealed that caveolin 1, caveolin 2, amphiregulin, and melanoma growth stimulatory activity were significantly up-regulated, whereas IL-1ß was significantly down-regulated in PC3 cells expressing TARP. We also demonstrated that TARP expression is up-regulated by testosterone in LNCaP? cells that express a functional androgen receptor. *These results suggest that TARP has a role in regulating growth and gene expression in prostate cancer cells.*

http://cancerres.aacrjournals.org/cgi/content/abstract/61/22/8122

TRAIL

The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL or Apo2L? ) is a potent inducer of death of cancer but not normal cells, which suggests its potential use as a tumor-specific antineoplastic agent. TRAIL binds to the proapoptotic death receptors DR4 and the p53-regulated proapoptotic KILLER/DR5 as well as to the decoy receptors TRID and TRUNDD. In the present studies, we identified a subgroup of TRAIL-resistant cancer cell lines characterized by low or absent basal DR4 or high expression of the caspase activation inhibitor FLIP. Four of five TRAIL-sensitive cell lines expressed high levels of DR4 mRNA and protein, whereas six of six TRAIL-resistant cell lines expressed low or undetectable levels of DR4 (²; P < 0.01). FLIP expression appeared elevated in five of six (83%) TRAIL-resistantcell lines and only one of five (20%) TRAIL-sensitive cells (²; P < 0.05). Two TRAIL-resistant lines that expressed DR4 contained an A-to-G alteration in the death domain encoding arginine instead of lysine at codon 441. The K441R? polymorphism is present in 20% of the normal population and can inhibit DR4-mediated cell killing in a dominant-negative fashion. The expression level of KILLER/DR5, TRID, TRUNDD or TRID, and TRUNDD did not correlate with TRAIL sensitivity ( P > 0.05). These results suggest that the major determinants for TRAIL sensitivity may be the expression level of DR4 and FLIP. TRAIL-resistant cells became susceptible to TRAIL-mediated apoptosis in the presence of doxorubicin. In TRAIL-sensitive cells, caspases 8, 9, and 3 were activated after TRAIL treatment, but in TRAIL-resistant cells, they were activated only by the combination of TRAIL and doxorubicin. Our results suggest: ( a) evaluation of tumor DR4 and FLIP expression and host DR4 codon 441 status could be potentially useful predictors of TRAIL sensitivity, and ( b) doxorubicin, in combination with TRAIL, may effectively promote caspase activation in TRAIL-resistant tumors.

http://clincancerres.aacrjournals.org/cgi/content/abstract/6/2/335

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a potent endogenous activator of the cell death pathway and functions by activating the cell surface death receptors 4 and 5 (DR4 and DR5). TRAIL is nontoxic in vivo and preferentially kills neoplastically transformed cells over normal cells by an undefined mechanism. Radiotherapy is a common treatment for breast cancer as well as many other cancers. Here we demonstrate that ionizing radiation can sensitize breast carcinoma cells to TRAIL-induced apoptosis. This synergistic effect is p53-dependent and may be the result of radiation-induced up-regulation of the TRAIL-receptor DR5. Importantly, TRAIL and ionizing radiation have a synergistic effect in the regression of established breast cancer xenografts. Changes in tumor cellularity and extracellular space were monitored in vivo by diffusion-weighted magnetic resonance imaging (diffusion MRI), a noninvasive technique to produce quantitative images of the apparent mobility of water within a tissue. Increased water mobility was observed in combined TRAIL- and radiation-treated tumors but not in tumors treated with TRAIL or radiation alone. Histological analysis confirmed the loss of cellularity and increased numbers of apoptotic cells in TRAIL- and radiation-treated tumors. Taken together, our results provide support for combining radiation with TRAIL to improve tumor eradication and suggest that efficacy of apoptosis-inducing cancer therapies may be monitored noninvasively, using diffusion MRI.

Breast cancer continues to be a major health problem worldwide despite recent advances in its diagnosis and treatment ( 1). Novel cytotoxic and hormonal agents have emerged from an improved understanding of oncogenesis and the biology of the mammary gland. Ionizing radiation is an important treatment modality for breast cancer as well as many other cancers ( 1). As an integral part of breast-conserving treatment, radiotherapy reduces the incidence of local and regional recurrences. Ionizing radiation can damage cells directly by interacting with critical cellular targets or indirectly by generating free radicals ( 2). Regardless of the mechanism, radiation-induced damage often triggers the endogenous suicide machinery of cells ( 3, 4).

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) (also known as APO-2L) is an apoptosis-inducing member of the tumor necrosis factor (TNF) gene family that includes TNF, CD95 Ligand (CD95L? ), and lymphotoxin-\x{03b1} (LT- \x{03b1}), among others. TNF family members are homotrimeric molecules that function by interacting with, trimerizing, and thus activating their respective cell-surface receptors. A subset of these type II transmembrane proteins activate the cell death pathway ( 5, 6). They transduce the apoptotic signal by engaging death receptors that belong to a subfamily of the TNF receptor gene superfamily and include TNFR1, CD95, death receptor (DR3), DR4, DR5, and DR6 ( 6). One of the prototypic and best-characterized death receptor\x{2013}death ligand pairs is CD95 and CD95L? (also known as the Fas/APO-1 system) ( 7, 8).

In the CD95 pathway, ligand-induced activation of the receptor causes recruitment of the intracellular death adapter molecule FADD (Fas-associated death domain protein) ( 9, 10), which can then engage the death protease caspase 8 ( 11, 12). By facilitating the proximity of zymogen molecules, FADD triggers caspase 8 autoactivation, hierarchically controlling the activation of downstream caspases and ultimately manifesting in the apoptotic phenotype ( 13). In an analogous fashion, TRAIL binds to the death receptors DR4 and DR5 ( 14, 15). Homologs of the FADD\x{2013}caspase 8 axis likely dictate the suicide response emanating from DR4 and DR5 ( 14). Interestingly, TRAIL also binds DcR1? (decoy receptor 1) and DcR2? , two related decoy receptors that fail to signal cell death ( 14\x{2013} 17). Functionally, TRAIL has been shown to preferentially kill transformed cell lines over normal cells ( 18). Various theories have emerged to explain this discrepancy, including differential expression levels of death receptors, decoy receptors, and death inhibitors ( 19).

Although TNF and CD95L? induce apoptosis of cancer cells, systemic administration of either agent is toxic to mice. Because of its ability to activate the proinflammatory transcription factor NF-\x{03ba}B, TNF infusion causes a lethal septic-shock like state in mice ( 20, 21). Activation of the CD95 pathway in vivo causes massive liver damage consequent to CD95-mediated hepatocyte apoptosis ( 22, 23). Unlike TNF and CD95L? , TRAIL is nontoxic systemically, enhancing its potential as a cancer therapeutic ( 18). Recent studies have shown that systemic administration of TRAIL can slow the growth and, in some cases, induce regression of tumor cell xenografts ( 18, 24). TRAIL, as a selective killer of tumor cells, has also received considerable press ( 25) and is currently in preclinical trials.

Ionizing radiation continues to have an important role in cancer treatment. Identifying biological compounds that will enhance the efficacy of radiotherapy is of tremendous interest, especially because of the existence of many radioresistant tumors. Previous studies have shown that angiostatin, an inhibitor of angiogenesis, has a combined antitumor effect with radiation ( 26). Here we show that an endogenous activator of the apoptosis pathway, TRAIL, can work in concert with radiation to eradicate breast cancer tumors. Unlike radiotherapy, TRAIL functions systemically and thus has the added benefit of targeting metastases. The molecular mechanism of the combined antitumor activity of TRAIL and radiation was also investigated.

In this study, tumor therapy is monitored noninvasively by using diffusion-weighted MRI, a sensitive imaging modality that can detect alterations in extracellular water mobility. The diffusion of water in tissue is strongly affected by fluid viscosity and membrane permeability between intra- and extracellular compartments, active transport and flow, and directionality of structures that impede or enhance mobility. As cells are damaged and killed by therapeutic interventions, the integrity of cell membranes may be compromised and the fractional volume of the interstitial space may increase because of apoptotic body formation and cell loss. These changes are expected to increase the mobility of water in the damaged tissue. Mobility of tissue water in vivo can be noninvasively quantified as an apparent diffusion coefficient (ADC) by using diffusion MRI ( 27). Detection of changes in the microscopic water environment by quanitative diffusion MRI may serve as a \x{201c}window\x{201d} to observe apoptotic activity in vivo. The ability to monitor apoptosis-inducing cancer therapy noninvasively should aid assessment of therapeutic efficacy and treatment stratification on an individual basis.

http://www.pnas.org/content/97/4/1754.full

NHRs

Induction of differentiation and apoptosis in cancer cells through ligands of nuclear hormone receptors (NHRs) is a novel and promising approach to cancer therapy. All- trans -retinoic acid (ATRA), an RA receptor-specific NHR ligand, is now used for selective cancers. The NHR, peroxisome proliferator-activated receptor \x{03b3} (PPAR\x{03b3}) is expressed in breast cancer cells. Activation of PPAR\x{03b3} through a synthetic ligand, troglitazone (TGZ), and other PPAR\x{03b3}-activators cause inhibition of proliferation and lipid accumulation in cultured breast cancer cells. TGZ (10 ^\x{2212}5 M, 4 days) reversibly inhibits clonal growth of MCF7 breast cancer cells and the combination of TGZ (10 ^\x{2212}5 M) and ATRA (10 ^\x{2212}6 M, 4 days) synergistically and irreversibly inhibits growth and induces apoptosis of MCF7 cells, associated with a dramatic decrease of their bcl-2 protein levels. Similar effects are noted with in vitro cultured breast cancer tissues from patients, but not with normal breast epithelial cells. The observed apoptosis mediated by TGZ and ATRA may be related to the striking down-regulation of bcl-2, because forced over-expression of bcl-2 in MCF7 cells cultured with TGZ and ATRA blocks their cell death. TGZ significantly inhibits MCF7 tumor growth in triple immunodeficient mice. Combined administration of TGZ and ATRA causes prominent apoptosis and fibrosis of these tumors without toxic effects on the mice. Taken together, this combination may provide a novel, nontoxic and selective therapy for human breast cancers http://www.pnas.org/content/95/15/8806.abstract

What receptor to use when phage targets cell? check which normal cells they appear on also

-cxcr4 cytokine appears on breast cancer (which normal cells?)

-interferon gamma (which normal cells?)

-parathyroid related hormone protein receptor

-PPAR gamma

-her2 (take it from genentech's work, we already have the sequence synthesized - advantage, can express antibody in bacteria) not unique but is known to be involved with breast cancer and we don't have to buy it

It may not matter if receptors appear on normal cells if they don't respond to the siRNA anyway

How to get phage to bind to these receptors? Look up the ligand affinities

-Helpful if receptor gets endocytosed, want it to go in the cell

-In 2006: took antibody against her2, did genetic or chemical fusion to basic protein (positively charged) that can bind RNA, incubated w/ siRNA, got it into cells - doesn't work very well

Complicated part: delivery of siRNA, simplest way is make it so if it gets to nucleus, use eukaryotic machinery to make siRNA for you

OR T7 polymerase (delivery of extra protein)

OR find RNA phage

Two big questions: What cells to target? What RNA to knock out?

http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowFulltext&ArtikelNr=000055396&Ausgabe=227176&ProduktNr=223857 (full article on biology of HER2)

• her2article.pdf: her2 biology

Article from Andy http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2194631

HER2 Endocytosis http://books.google.com/books?id=qy1A7BtHF78C&pg=PA114&lpg=PA114&dq=her2+antibody+endocytosis&source=bl&ots=-f0upUFX16&sig=zewNRlCzY-H51s36INZwtIolxoQ&hl=en&ei=y81DSrrJD4_gsQPvn-j4DQ&sa=X&oi=book_result&ct=result&resnum=1

complete genome of a single-stranded RNA bacteriophage which infects gram-negative bacteria, has a broad host range http://jvi.asm.org/cgi/content/full/80/18/9326?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=phage&searchid=1&FIRSTINDEX=1500&resourcetype=HWFIG

• ms2article.pdf: article describing MS2 replicase

Q\x{03b2} http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WK7-4S7BDNN-7&_user=4423&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000059605&_version=1&_urlVersion=0&_userid=4423&md5=1bb3ab9430605599662bce01598fbab3

• csf1progression.pdf: CSF-1 Progressio

Function and Structure of Q\x{03b2} http://www.jbc.org/cgi/reprint/251/9/2740

Killing cancer cells by targeted drug-carrying phage nanomedicines http://www.biomedcentral.com/1472-6750/8/37

• baculovirusarticle.pdf: Using baculovirus to target mammalian cells

: Phages for targeted gene-delivery http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TCW-4JKHKX5-1&_user=4423&_coverDate=05/31/2006&_rdoc=1&_fmt=full&_orig=search&_cdi=5181&_sort=d&_docanchor=&view=c&_acct=C000059605&_version=1&_urlVersion=0&_userid=4423&md5=60d294744d118a208dc15510de724d6d#SECX5 Phages have also been proposed as potential therapeutic-gene delivery vectorsAlthough conceptually different, the rationale for using phages for this purpose is similar to that for using phages for DNA vaccine delivery \x{2013} the phage coat protects the DNA from degradation after injection, a nd the ability to display foreign molecules on the phage coat also enables targeting of specific cell types, a prerequisite for effective gene therapy.

CONFLICT end

.http://ucelinks.cdlib.org:8888/sfx_local?&url_ver=Z39.88-2004&url_ctx_fmt=info:ofi/fmt:kev:mtx:ctx&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.atitle=Quantitative+analysis+of+the+bacteriophage+Q+beta+infection+cycle&rft.auinit=K&rft.aulast=Tsukada&rft.date=2009&rft.epage=70&rft.genre=article&rft.issn=0304-4165&rft.issue=1&rft.spage=65&rft.title=Biochimica+et+Biophysica+Acta&rft.volume=1790&rfr_id=info:sid/www.isinet.com:WoK:BIOSIS&rft.au=Okazaki,+M&rft.au=Kita,+H&rft.au=Inokuchi,+Y&rft.au=Urabe,+I&rft.au=Yomo,+T&rft_id=info:doi/10.1016%2Fj.bbagen.2008.08.007

In vivo gene delivery and expression by bacteriophage lambda vectors http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2063594

• targetingantibacterialarticle.pdf: Targeting antibacterial agents using filamentous phage
• http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T76-3T14NST-1&_user=4420&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=945450150&_rerunOrigin=scholar.google&_acct=C000059607&_version=1&_urlVersion=0&_userid=4420&md5=a46de66e9e8731d23bc03802285f2bf5 (phage antibody display)

• ms2saccharomycesarticle.pdf: Production in Saccharomyces cerevisiae of MS2 virus-like particles packaging functional heterologous mRNAs

Crystal structure of the MS2 coat protein dimer: implications for RNA binding and virus assembly: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6VSR-4CXD815-11&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=951849110&_rerunOrigin=scholar.google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=6530b2298e63e5d2bf30435323ebbd7e

RNA Bacteriophage Capsid-Mediated Drug Delivery and Epitope Presentation: http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowPDF&ArtikelNr=67930&Ausgabe=228866&ProduktNr=224031&filename=67930.pdf

Multiple presentation of foreign peptides on the surface of an RNA-free spherical bacteriophage capsid: http://vir.sgmjournals.org/cgi/reprint/74/4/541.pdf "We have produced a plasmid expression vector for the coat protein of RNA bacteriophage MS2. The vector has been modified to introduce a unique Kpni restriction site within the coat protein gene at a site corresponding to the most radially distant feature of the bacteriophage capsid, namely the top of the N-terminal fl-hairpin (between residues 15 and 16). Insertion of DNA oligonucleotides at this site allows the production of chimeric MS2 coat proteins having foreign peptide sequences expressed as the central part of the hairpin."

• immunogenic_Display_of_Diverse_peptides_of_VLP_of_ms2.pdf: Immunogenic Display of Diverse Peptides on VLP of RNA Phage MS2

M13 Phage

• Killing_cancer_cells_by_targeted_drug-carrying_phage_nanomedicines.pdf: M13 Phage antibody

• Gene_transfer_of_Hodgkin_cell_lines_via__anti-displaying_bacteriophage.pdf: M13 Phage gene transfer

• Chappel_1998_Journal-of-Immunological-Methods.pdf: Modulation of antibody display on M13 filamentous phage

• 10.1007_978-1-60327-565-119.pdf: General M13 Phage Display: M13 Phage Display in Identification and Characterization of Protein\x{2013}Protein Interactions

• aavp_vector__transgene_cassette.pdf: aavp vector protocol transgene cassette

• Grimm_2005_Methods-in-Enzymology.pdf: aav vector shrna protocol

• phage_display_protocol.pdf: Phage Display Protocol

• Raf-1_siRNA_delivery.pdf: Raf-1 siRNA sequence
• Eleminating_helper_phage_from_phage_display.pdf: Antibody display using a phage plasmid and phagemids
• aav_cassette.pdf: pTRUf3
• basicprotocolshRNA.pdf: Basic protocols for Expression Arrest\x{2122} TRIPZ lentiviral shRNAmir

Silica Section

According to the Germans, the protein Silintaphin-1 directs the enzyme silicatein in biosilicification :P -Gabe

Gabe's idea: Bind many copies of Silintaphin-1 around the phage using a protein tag and in theory the silicatein enzyme should form a silica layer around the phage.

Read Me

• silintaphin-1_directs_silicatein.pdf: Sinlintaphin-1 directs silicatein

• spongies_silicatein_and_silintaphin-1.pdf: Spongies :P Silicatein and Silintaphin -1

See Page 14? Organosilicon chemistry book: http://books.google.com/books?id=fwmffhqdAYEC&printsec=frontcover&dq=Organosilicon+chemistry+IV

• Biomimetic-silica-structures-Cha.pdf: (Jessica) silica structures
• http://www.google.com/patents?id=QXSaAAAAEBAJ&printsec=abstract&zoom=4&source=gbs_overview_r&cad=0 Method of isolating binding peptides from a combinatorial phage display library and peptides produced thereby
• http://repositories.lib.utexas.edu/bitstream/handle/2152/1317/gooche53184.pdf?sequence=2 Peptide selection using phage display
• http://www.sciencemag.org/cgi/content/full/286/5442/1129 "Polycationic Peptides from Diatom Biosilica That Direct Silica Nanosphere Formation"
• http://www.ifa.hawaii.edu/users/akboal/abjc18feb0502.pdf "Review: Silicon Metabolism in Diatoms: Implications for Growth" (check out references to other articles)