Index and dictionary

For the index to the biology section I thought I'd include a dictionary. Unless you all contribute to it, I doubt it will grow to be very useful, as I don't have the time. So get on with it! If you do add something, please include references to primary literature or, if unavailable, to textbooks.

A

• Active site. Surface region of enzyme at which substrate binds and catalysis occurs.^[1]
• ADP. See adenosine diphosphate.
• Alexia. Neurological lesion causing inability to read.^[2]
• Allele. One of multiple versions of a single gene, each with unique sequences but residing at the same locus. Different alleles of the same gene may or may not have the same phenotype. Diploid cells may have two different alleles (heterozygous) or two copies of the same allele (homozygous). Arise by mutation.^[3]
• AMP. See adenosine monophosphate.
• Amphoteric. Electrolyte capable of acting both as acid and base.^[4]
• Angioblast. Mesoderm cells that form blood vessels.^[5]
• Angiogenesis. Generation of new capillaries. Endothelial cells of existing vessels invade neighbouring cells. Unregulated angiogenes leads to a variety of diseases. Angiogenesis is required for tumour development.^[6]
• Antibody. Molecule produced by the immune system which reacts with spicific antigen epitope, e.g. Immunoglobulin.^[1] Also used in many research protocols.^[7]
• Argonaute. Family of scaffold proteins involved in RNA silencing. Bring enzymes, mRNA and short regulatory RNAs together.^[8]
• ATP. See adenosine triphosphate.
• Auxotroph. Mutant prokaryotic strain that requires different growth conditions from wild-type or parent strain (prototroph), esp. nutrients which the prototype synthesis itself.^[9]
• Axonal transport. Movement of essential materials from the body to the synapse of a neuron. Motor proteins move along the cytoskeleton transporting vesicles, etc. Disruption of axonal transport has been suggested to be a cause or symptom of some neurodegenerative diseases.^[10]

B

• Bacteriophage. Virus which reproduces inside bacteria and lyses the cell upon maturation.^[9]
• Binary fission. Asexual reproduction in which cell divides into two equal daughter cells.^[9]
• Biotin. Molecule used as a non-radioactive label in molecular research, e.g. probes, subtractive hybridisation, etc. Can be attached, e.g. to dUTP. Recognised by streptavidin, avidin, etc, enzymes.^[7]
• Blastocyst. Stage of mammalian embryonic development corresponding to the blastula, during which the embryo implants into the uterine wall.^[5]
• Blastoderm (blastodisc). Embryonic stage after blastula, in which embryo is a solid layer of cells.^[5]
• Blastospore. Spore produced by budding.^[9]
• Blastula. Embryonic stage following cleavage in which the embryo is composed of an epithelial layer of cells with a fluid filled cavity. In mammals, this stage is called the blastocyst stage.^[5]
• BPA. See bisphenol A.
• Buffer. Solution with a definite pH which alters little with the addition of an acid or base. Usually consists of a solution of the salt of a weak acid in the free acid.^[4]

C

• CaMK. See calmodulin-dependent kinase.
• cAMP. See cyclic adenosine monophosphate.
• Capsid. Protein coat of virus.^[7]
• Carboxyl. -CO₂H group.^[4]
• Catalayse. Enzyme whose principle action is the catalysis of 2H₂O₂ —> 2H₂O + O₂, oxidising the enzyme's haem iron group as an intermediate. Found throughout eukaryota. Mammals have a ~60kDa homotetrameric catalayse. Named by Loew in 1900, it played an important role in early investigations into the nature of enzymes.^[11]
• CDK. See cyclin dependent kinase.
• Clathrin. Cytoplasmic protein involved in endocytosis, golgi support and intracellular trafficking. Forms a heterohexamer "triskeleton" structure of threee light and three heavy chains, which interact with lipid membranes and produce clathrin lattices to support vesicle formation.^[12][13]
• cMYC. See MYC.
• CNS. See central nervous system.
• cJun N-terminal kinase (JNK). A member of the MapK family of signalling pathways. Activated primarily by cytokines and environmental stress. Upregulates cJun, part of the AP1 TF.^[14]
• Compartment. Area of embryo descended from a small population of founder cells showing cell-lineage restriction and developing as a unit.^[5]
• Competent. Bacterial culture following treatment to improve transformation efficiency.^[7]
• CREB. See cAMP response element binding protein.
• Cyclin dependent kinase (Cdk). Group of heterodimeric protein kinases with various roles in the regulation of the cell cycle. Composed of Cdk and cyclin subunits. Misregulated in some cancers.^[15]
• Cytoskeleton. Network of protein polymers (microtubules, actin microfilaments and intermediate filaments) which provides shape and rigidity to the cell, essential for movements such as muscle contraction and cell division. Also assists movement of some organelles and molecules, such as signals, around the cell.^[16]

D

• DBPR. Double blind peer review.
• Dermatome. Region of somite that gives rise to dermis.^[5]
• Down's syndrome. See trisomy 21.

E

• E2. See estradiol.
• E2F. Family of eukaryotic transcription factors which regulate the cell cycle and apoptosis. 9 known isoforms from 8 genes. Six are regulated by Rb (notably E2F1), four by Cyc A/cdk2, and several interact with other transcription regulators. Form homo- or heterodimers, often with DP.^[17]
• Ectoderm. One of the three triploblast germ layers. In vertebrates, develops into skin and nervous system.^[5]
• eIF. See eukaryotic initiation factor.
• Endoderm. One of the three triploblast germ layers. In vertebrates, develops into gut, liver and lungs.^[5]
• Environmental sex determination (ESG). Determination of the sex of an individual by an environmnetal variable rather than a purely genetic mechanism (GSD). Environmental cues vary depending on species and may include the density or sex ratio of the existing population, or physical variables such as temperature.^[18]
• Ephrins and Eph receptors. Membrane bound ligand-receptor pair involved in development and cancer. Implemented in segmentation, cell migration, angiogenesis and axon guidence, as well as cancers. Receptors are sub-family of RTKs. 16 receptors and 8 ligands known. Forward and reverse signal transduction.^[19]
• ER. See endoplasmic reticulum or estrogen receptor.
• ErbB (also "HER" - human epidermal growth factor receptor - in humans). Family of receptor tyrosine kinases with four members. Respond to growth factors such as EGF, signalling through a wide variety of pathways. Have an important role in development, and implemented in many diseases including cancers and neurological disorders. Large: 170–185 kDa.^[20]
• ErbB-2 (also: HER-2, esp. in humans; Neu, esp. in rodents). Member of the ErbB family of receptor tyrosine kinases. Thought to be an orphan, with no binding to EGF, the principal ligand family for ErbB receptors, but being the preferential dimerisation partner for other ErbB receptors. Overexpressed in some breast cancers, treated with herceptin antibody.^[21]
• ERE. See Estrogen response element.
• ERK. See Extracellular signal-regulated kinase.
• ESD. See Environmental sex determination.
• Estrogen receptor (ER). Receptor for steroidal hormone estrogen. Two genes, ESR1 and ESR2 encode multiple splice variants of ERalpha and ERbeta, which form hetero- and homodimers. ER acts both as a signal transducer and a transcription factor for genes with the ERE promotor. Situated in nucleus and cytoplasm, with evidence of membrane association. Effects include regulation of prolactin production and cell cycle, and a role in cancers, particularly breast cancer.^[22]
• Estrogen response element (ERE). Regulatory element recognised by estrogen receptors.^[22]
• Extracellular signal-regulated kinase (ERK), aka classical MAPK. The best known members of the mitogen-activated protein kinase (MAPK) family of protein kinase signal transducers. Two isoforms, ERK-1/2 aka p42/44-MAPK. The ERK cascade involves Ras, Raf, MEK and ERK, and regulates several transcription factors and signal transducers, including p90 rsk, ELK, and estrogen receptors. The term is also sometimes used as a synonym for the entire MAPK family.^[23]

F

• Farnesoid X receptor (FXR, NR1H4). Nuclear non-steroidal receptor and transcription factor with several known ligands. Has been implemented in bile acid homeostasis, lipoprotein and glucose metabolism, hepatic regeneration, intestinal bacterial growth and hepatotoxin response. Conserved in vertebrates. Alpha gene with four alternatively spliced variants, and beta gene.^[24]
• FGF. See fibroblast growth factor.
• Footprinting. Identification of protein-binding sites on DNA by searching for phosphodiester bonds which can not be cleaved by DNase I.^[7]
• FXR. See farnesoid X receptor.

G

• G protein. Class of signalling molecules. Monomeric or heterotrimeric. Monomeric and alpha subunits have GTPase activity: signalling is activated by an exchange of GDP for GTP, and deactivated by cleavage of GTP. Usually membrane associated. Some trimeric G proteins are coupled to seven transmembrane domain receptors.^[25]
• Gastrulation. Movement of the endoderm and mesoderm from the surface to the interior of the gastrula stage vertebrate embryo.^[5]
• Genetic imprinting. See genomic imprinting.
• Genetic sex determination (ESD). Determination of an individual's sex by a sex chromosome or sex determining gene without environmental cues. Alternative is ESD. Sex determination in mammals is genetic using sex chromosomes.^[18]
• Genomic imprinting. Mechanism in animals, esp. mammals, in which the version of the two copies of a gene to be expressed is determined by the sex of the parent from which they are inherited. In gametogenesis certain genes are silenced by epigenetic mechanisms in one sex only.^[26]
• Germ layer. System of classifying the tissues of the early embryo. Each layer gives rise to a different set of organs, with some exceptions. Vertebrates have three germ layers (triploblasts).^[5]
• Grb2. See growth factor receptor-bound protein 2.
• Growth factor receptor-bound protein 2 (Grb2). Adaptor protein in the signalling between receptor tytosine kinases and Ras. SH2 domain binds to activated RTK, SH3 domain binds to SOS.^[27]
• GSD. See genetic sex determination.

H

• Harvesting (in mol. res.). Collection of cells from culture for next stage of an experiment, usually by centrifugation.^[7]
• Hedgehog (hh). Family of intercellular signals which signal over long and short distances to the patched receptor. Involved in development of left-right (a)symmetry, neural tube and somite patterning, and most organs; and implemented in many cancers. Three isoforms in mammals, one in zebrafish and flies.^[28]
• HER. See ErbB.
• HER-2. See ErbB-2.
• Heterochromatin protein 1 (HP1). Family of proteins involved in stable heterochromatin production. Binds to tail of histone 3 when it is methylated at Lys 9.^[29]
• HH. See Hedgehog.
• Homeobox gene. See Hox gene.
• Homeotic selector gene. See Hox gene.
• Homeotic transformation. Mutation affecting a Hox gene which causes abnormal development, in the form of a body segment zone developing the phenotype of a different segment.^[30]
• Hox genes (Homeobox genes, Homeotic selector genes). Family of transcription factors which determine the identities of the segmentation zones of the anterior-posterior axis of Bilateral animals. Contain homeobox concensus sequence. Arranged in hox clusters on the chromosome. Mutations may lead to homeotic transformation in which a segment develops the phenotype of another segment.^[30]
• HP1. See heterochromatin protein 1.
• Hyperkinesis. Excessive motor activity.^[2]
• Hyperplasia. Abnormal enlargement of tissue/organ by cell division, excluding tumours (neoplasia).^[2]
• Hypertelorism. Abnormal separation of paired organs, esp. the eyes, usually congenital.^[2]
• Hypertrophy. Abnormal enlargement of tissue/organ by enlargement of cells.^[2]
• Hypertropia. Eyes at different levels, with squint.^[2]
• Hypochromia. Abnormally pale, e.g. RBCs with low haemoglobin, or iris lacking pigment.
• Hypotonia. Relaxed or underdeveloped muscles.^[2]

I

• Immunoglobulin (Ig). Antibody produced by plasma cells and recognised by T lymphocytes. Multiple classes, the major ones being A, D, E, G and M. ~23 and >=53 kDa light and heavy chain subunits. Antigen specificity due to huge variation at N-terminal produced by alternative splicing.^[1]
• Imprinting. See genomic imprinting.
• Inclusion body. Insoluble crystalline accumulation of protein in cell. Can form when using expression systems to produce large quantities of a foreign or engineered protein.^[7]

J

• JAK. See janus kinase.
• JNK. See cJun N-terminal kinase.

K

• Karyotype. Set of metaphase chromatid pairs. Can be stained to show banding of heterochromatin and therefore identify each chromosome and any chromosome abnormalities.^[3]
• kDa. See Dalton.
• Kinase. Any of a diverse range of enyme families which phosphorylate (add phosphate groups to) proteins, lipids, etc. Protein kinases are ubiquitous in intracellular signalling, often in cascades of multiple kinases.^[25][31]
• Kinetochore. Plate-like protein structure at the centromere of eukaryotic chromosomes which attaches to the microtubules of the mitotic spindle and is visible from late-prophase. ^[1]
• Klinefelter's syndrome. Disomy or partial disomy of the X chromosome in males (XXY). Testicular germ-cell aplasia, some mental retardation common, often taller than average.^[3][2]
• Km. See Michaelis constant.
• KSR. See kinase suppressor of ras.

L

• Linkage. Proximity of two genes on a chromosome. Linkage affects whether the genes will be separated by recombination in meiosis. Historically used to produce maps of genes on chromosomes, but now largely redundant.^[3]

M

• Macromolecule. Molecule with a high molecular weight, generally 10kDa and above. Usually a polymer.^[4]
• MAD2. Mitotic checkpoint, associated with kinetochores and spindle formation. Upregulated by Rb and thought to cause aneuploidy in cancers.^[32][33]
• Major histocompatibility complex (MHC). Part of the immune system. Scaffolds which present peptide antigens to T lymphocytes. MHC genes are highly polymorphic, and each individual has a unique MHC. T cell recognition of foreign MHC proteins is involved in transplant rejection.^[1]
• MAP kinase. See Mitogen-activated protein kinase.
• MAPKAP-K1. See ribosomal s6 kinase.
• Mesoderm. One of the three triploblast germ layers. In vertebrates, develops into skeleton, muscle, kidney, heart, blood.^[5]
• MHC. See Major histocompatibility complex.
• Michaelis constant. Substrate concentration at which rate of reaction is half of maximum (Vmax / 2). Inversely indicative to affinity of enzyme for substrate.^[4]
• Microarray. Research technique which uses hybridisation to analyse thousands or millions of genes at a time. Usually a pair of transcriptomes, or less commonly genomes, are tagged with different coloured fluorescent dies and added to a slide with an array of oligonucleotides representing specific genes. Quantitative differential expression is shown by the resulting differences in fluorescence.^[34]
• microRNA (miRNA). Endogenous short non-coding RNAs involved in RNA interference. Involved in regulation of gene expression and defence against infection by tagging complementary mRNAs for digestion. Hybridise to complementary sequences and form complexes with RISCs. Produced by DCR from a stem-loop precursor.^[35][36]
• Mitogen-activated protein kinase (MAPK, MAP kinase). Family of signalling proteins found in many pathways. The term "Extracellular signal-regulated kinase" (ERK) is often used as a synonym for MAP kinase, but is also used specifically for a subset of MAP kinases (p42/p44 MAPK, aka ERK1/2). MAP kinases are activated by phosphorylation of Thr and Tyr in domain VIII by MAP kinase kinases, e.g. MEK, and ultimately by signals from e.g. RTKs. MAPKs activate nuclear TFs, and may affect other cytosolic proteins and kinases.^[1][37][38]
• Monomer. Relatively small and simple molecule which can be polymerised or telomerised by forming a chain with other monomers.^[4]
• Morula. Early stage of mammalian development during which embry is a solid ball of cells.^[5]
• cMyc. Signal involved in the regulation of cell cycle, cell growth, differentiation, apoptosis, transformation, genomic instability, and angiogenesis.^[39]

N

• Necrosis (type III cell death). Cell death occuring in pathology, lacking the charactoristic progression of apoptosis and autophagy. Cell and organelles swell and membranes rupture. Originally thought to be uncontrolled, but evidence now suggests some specific programs are involved.^[40]
• Neu. See ErbB-2.
• Neurofibromatosis ("von Recklinghausen disease"). Slow growing benign or malignant tumours of nervous system, may cause spinal deformity, congenital tibial dysplasia, and excessive bone and soft-tissue growth. Single gene autosomal dominant. Two types, NF1 and NF2, with differing phenotypes. NF1 = 17q11.2; NF2 = 22q12.2. 30-50% occur spontaneously.^[41]
• NSAID. See non-steroidal anti-inflamatory drug.

O

• Oestrogen. See Estrogen.
• Oestrogen receptor. See Estrogen receptor.
• Oligomer. Polymer composed of only a small number of monomers.^[4]
• Oncogene. Genes determining tumour growth, usually modifications of normal genes (proto-oncogenes), sometimes viral.^[3][2]

P

• p53. Tumour suppressive TF. Activates cell cycle arrest, DNA repair, senescence and apoptosis in response to DNA damage, telomere loss, oxidative stress and oncogene activation.^[42][43]
• PAI. See pathogenicity island.
• Parkinson's disease. Neurological disease charactorised by progressive loss of motor control causing trembling and impaired movement. Rarely seen under the age of 50. Loss of dopamine producing brain cells and protein aggregation in neurons have been implemented in the development of the disease, but the ultimate cause may vary, with mutations associated with some cases.^[44][45]
• Pathogenicity island (PAI). A bacterial mobile genomic island, usually containing several genes, which can convey pathogenicity by horizontal transfer. Virulence genes are often grouped in several PAIs distributed throughout the genome. Most are 10-200kb.^[46]
• Philadelphia chromosome (Ph). Result of balanced translocation t(9;22)(q34;q11.2), producing the bcr-abl fusion gene and tumourigenesis in chronic myelogenous leukemia.^[47]
• Phytohormone (plant hormone). Plant growth regulators. Most are chemically unlike animal hormone. Includes abscisic acid, auxin, brassinosteroids, cytokinin, ethylene, gibberellins, and jasmonic acid.^[48]
• Plant hormone. See phytohormone.
• Polymer. Large molecule made of multiple relatively small subunits (monomers), e.g. in a chain. May be a single monomer repeated (e.g. starch), or a random or specific sequence of different monomers (e.g. DNA and proteins). Often macromolecules. Form by addition or condensation polymerisation.^[4]
• Pseudogene. A section of DNA showing sequence similarity to known genes, but containing mutations precluding the production of functional products, thus categorised as "junk DNA". Some may be transcribed, but have no functional product, while some sequences initially thought to be non-functional pseudogenes have been implicated in RNA interferance.^[49]

Q

• Q banding (Quinacrine banding, mepacrine stain). Pattern of dark and light bands on metaphase spreads when stained with the fluorescent dye quinacrine, used to identify chromosome aberrations. Shows bands of high A-T content. Generally redundant due to G and R banding.^[1][2]

R

• RAMP. See receptor activity modifying protein.
• Rb (retinoblastoma). Tumour suppressor and cell cycle regulator. Binds to the E2F transcription factor preventing transcription and initiatiating heterochromatin formation, thus arresting the cell cycle. When phosphorylated by cyclin dependent kinases, transcription, and thus the cell cycle, is able to proceed. Damage to Rb, or an upstream signal, may cause cancer. Named after retinoblastoma, a cancer in which it is mutated or missing.^[50]
• Receptor activity modifying protein (RAMP). Single transmembrane domain proteins which dimerise with G-protein coupled receptors to assist in function and/or localisation.^[51]
• Receptor tyrosine kinase (RTK). Superfamily of single transmembrane domain receptors with inherant kinase activity. Upon ligand binding they typically dimerise (some are always dimers but change conformation) and cross/auto-phosphorylate one or more tyrosine residues of the intracellular domain, activating intracellular signalling, typically including the PKC and MAPK pathways. Includes many growth factor receptors.^[31]
• Rhombomeres. Compartments in the hindbrain of vertebrate embryos. Divided along anterior-posterior axis, influenced by ephrin signalling and displaying unique Wnt1 and Notch signalling.^[52]
• ribosomal s6 kinase (rsk, p90rsk), aka MAPK-activated protein kinase-1 (MAPKAP-K1). 90 kDa serine/threonine protein kinase signal transducer activated by ERK. Regulates glycogen synthase kinase 3 (GSK3); L1 CAM (neural cell adhesion); Son of Sevenless (Ras exchance factor); Myt1 (inhibitor of cdc2); cAMP response element-binding protein (CREB); estrogen receptor-α (ERα); IκBα/NFκB; and c-Fos.^[53]
• RNA silencing. Group of mechanisms which regulate gene expression and protect against viruses, transposons, etc. Prevent translation, and usually reduce mRNA half-life. Includes RNA interference, antisense suppression, quelling (fungi, algae), and post-transcriptional silencing and co-suppression (plants),^[54]
• rsk. See Ribosomal s6 kinase.
• RTK. See receptor tyrosine kinase.

S

• SAGE. See serial analysis of gene expression.
• SBPR. Single blind peer review.
• Sedimentation coefficient. Velocity at which particle sediments in centrifuge, expressed in Svedbergs (10^-13).^[55]
• Serial analysis of gene expression (SAGE). Research technique which identifies and quantifies the mRNAs in a transcriptome by sequencing ~14 bases at the 3' UTR of the transcripts.^[56]
• siRNA. See Small interference RNA.
• Small interference RNA (siRNA, sometimes "short ..."). Endogenous or exogenous short non-coding RNA participating in RNA interference in a similar mechanism to miRNAs. 21-25-nt in length. Produced by DCR from a double stranded precursor. Used in molecular biology research to produce gene knockdown models.^[35]
• STAT. See signal transducer and activator of transcription.
• Sticky end. Single stranded extension to a double stranded DNA molecule. Can hybridise to complementary sequences, and are therefore used in many research protocols.^[7]
• Subtractive hybridisation. Method of discovering sections of DNA unique to one genome or transcriptome.^[57]
• Svedberg (S). Unit of sedimentation coefficients.^[55]

T

• TGF. See transforming growth factor.
• TNF. See tumour necrosis factor.
• Triploblast. Ovum or early embryo with three germ layers. Vertebrates have triploblast embryos.^[5]
• Trisomy 21 ("Down's syndrome", hist. "mongolism"). Trisomy or partial trisomy of chromosome 21. Phenotype includes mental retardation, abnormal facial charactoristics, abnormal genetal development, short and broad hands, below average height, sterility and life expectancy of 40. 1.43 per 1000 live births, but correlated with maternal age. Named for J.L. Down, 1866.^[2][3]
• Type I cell death. See apoptosis.
• Type III cell death. See necrosis.

U

• Ubiquitin (Ub). Small protein which forms polyUb chains attached to lysine or the N-terminus of proteins to tag them for proteolysis. Also participates in signal transduction.^[58]
• Uracil. Pyrimadine base found in RNA. Equivalent to thymine of DNA.^[3]

V

• Vector (vehicle). DNA molecule used in transformation/transfection to transfer and replicate gene(s) in the host cell. Usually plasmids, viruses or artificial chromosomes.^[7]
• VEGF. See vascular endothelial growth factor.
• Vehicle. Syn. Vector.

W

• Western blot (Western transfer). Research technique using current to transfer protein from an electrophoresis gel to a nitrocellulose or PVDF membrane, e.g. for detection with antibodies. Named after Southern blots.^[7]
• Wnt (Wingless-int). Family of extracellular signalling molecules, and the intracellular pathways they activate. Binds to frizzled receptor. Crucial to development, esp. body axis and cell polarity, and involved in some cancers.^[59]

Z

• Zygote. Fertilised egg.^[5]

References

1. a,b,c,d,e,f,g  Lodish, H., D. Baltimore, A. Berk, S.L. Zipursky, P. Matsudaira & J. Darnell. 2000. Molecular Cell Biology. W.H. Freeman. (Verified, JAD, 2007-01-14).
2. a,b,c,d,e,f,g,h,i,j,k  Lennox, B. and M.E. Lennox. 1988. Heineman Medical Dictionary. Oxford: Heineman Medical Books. (Verified, JAD, 2007-01-29)
3. a,b,c,d,e,f,g  Russell, P.J. 2003. iGenetics. Benjamin Cummings. (Verified, JAD, 2007-01-29)
4. a,b,c,d,e,f,g,h  Sharp, D.W.A. 1990. Dictionary of Chemistry. Penguin. (Verified, JAD, 2007-02-02)
5. a,b,c,d,e,f,g,h,i,j,k,l,m,n  Wolpert, L., R. Beddington, T. Jessel, P. Lawrence, E. Meyerowitz, J. Smith. 2002. Principles of Development. Oxford University Press. (Verified, JAD, 2007-01-28).
6. ^   Liekens, S., E. De Clercqa and J. Neyts (2001). Angiogenesis: regulators and clinical applications. Biochemical Pharmacology 61:253-270 Full text. (Verified, JAD, 2007-04-20)
7. a,b,c,d,e,f,g,h,i,j  Brown, T.A. 1996. Gene Cloning (3rd ed). London: Chapman & Hall. (Verified, JAD, 2007-01-29)
8. ^  Parker, J.S. and Barford, D. 2006. Argonaute: a scaffold for the function of short regulatory RNAs. Trends in Biochemical Sciences 31(11):622-630 (doi). (Verified, JAD, 2007-02-05)
9. a,b,c,d  Volk, W.A. 1996. Microbiology (7th ed). NY: HarperCollins.
10. ^   Duncan, J.E. and L.S.B. Goldstein (2006). The Genetics of Axonal Transport and Axonal Transport Disorders. PLOS Genetics 2:e124 Full text.
11. ^   Kirkman, H.N. and G.F. Gaetani (2006). Mammalian catalase: a venerable enzyme with new mysteries. Trends in Biochemical Sciences 32:44-50 Full text. (Verified, JAD, 2007-02-05)
12. ^   Anna Young (2007). Structural insights into the clathrin coat. Seminars in Cell & Developmental Biology 18:448-458 Full text. (Verified, JAD, 2007-09-17)
13. ^   Ian G. Mills (2007). The interplay between clathrin-coated vesicles and cell signalling. Seminars in Cell & Developmental Biology 18:459-470 Full text. (Verified, JAD, 2007-09-17)
14. ^   Westona, C.R. and R.J. Davis (2007). The JNK signal transduction pathway. Current Opinion in Cell Biology 19:142-149 Full text. (Verified, JAD, 2007-04-16).
15. ^  Malumbres, M and M. Barbacid. 2006. Cell cycle kinases in cancer. Current Opinion in Genetics & Development 17(1):60-65. doi (Verified, JAD, 2007-04-16)
16. ^   {{{authors}}} (2004). The Cytoskeleton In Vivo. PLoS Biology 2:e100 Full text. (Verified, JAD, 2007-02-04)
17. ^  DeGregori, J. and D.G. Johnson. 2006. Distinct and Overlapping Roles for E2F Family Members in Transcription, Proliferation and Apoptosis. Current Molecular Medicine 6(7):739-748. (Verified, JAD, 2007-04-27)
18. a,b  Haag E.S., Doty A.V. 2005. Sex Determination across Evolution: Connecting the Dots. PLoS Biology 3(1):e21 (doi). (Verified, JAD, 2007-02-04)
19. ^  Davy A. and P. Soriano. 2004. Ephrin signaling in vivo: Look both ways. Developmental Dynamics 232(1):1-10. (Verified, JAD, 2007-01-28).
20. ^  Nancoe, S.R. and S. Sever. 2006. ErbB receptors: new insights on mechanisms and biology. Trends in Cell Biology 16(12):607-609 (doi). (Verified, JAD, 2007-02-05)
21. ^  Olayioye, M.A., 2001. Intracellular signaling pathways of ErbB2/HER-2 and family members. Breast Cancer Res 3:385-389. doi. (Verified, JAD, 2007-03-04)
22. a,b  Cianaa, P., F. Scarlattia, A. Bisernia, L. Ottobrinia, b, A. Brenaa, A. Lanaa, F. Zagaria, G. Lucignania, b and A. Maggia. 2006. The dynamics of estrogen receptor activity. Maturitas 54(4):315-320. (Verified, JAD, 2007-01-31)
23. ^  Orton, R.J., O.E. Sturm, V. Vyshemirsky, M. Calder, D.R. Gilbert and W. Kolch. (2005. Computational modelling of the receptor-tyrosine-kinase-activated MAPK pathway. The Biochemical journal 392:249-261. doi (Verified, JAD, 2007-04-27)
24. ^  Lee1, F.Y., H. Lee, M.L. Hubbert, P.A. Edwards, and Y. Zhang. 2006. FXR, a multipurpose nuclear receptor. Trends in Biochemical Sciences 31(10):572-580 (doi). (Verified, JAD, 2007-02-05)
25. a,b  Hancock, J.T., 1997. Cell Signalling. Harlow UK: Longman. (Verified, JAD, 2007-01-29).
26. ^  Wood, A.J. and R.J. Oakey, 2006. Genomic Imprinting in Mammals: Emerging Themes and Established Theories. PLoS Genetics 2(11): e147 doi. (Verified, JAD, 2007-02-05)
27. ^  Garbay, C., Wang-Qing Liua, M. Vidala and B.P. Roques. 2000. Inhibitors of RAS signal transduction as antitumor agents. Biochemical Pharmacology 60(8):1165-1169 (Verified, JAD, 2007-03-02)
28. ^  Cross, S.S. and J.P. Bury. 2004. The Hedgehog signalling pathways in human pathology. Current Diagnostic Pathology 10(2):157-168. doi. (Verified, JAD, 2007-03-04)
29. ^  Straub, T. 2003. Heterochromatin Dynamics. PLoS Biology 1(1):e14 (doi). (Verified, JAD, 2007-02-05)
30. a,b  Pearson, J.C., D. Lemons and W. McGinnis. 2005. Modulating hox gene functions during animal body patterning. Nature Reviews Genetics 6:893-904. doi. (Verified, JAD, 2007-05-15)
31. a,b  Schenk, P.W. and B.E. Snaar-Jagalska. 1999. Signal perception and transduction: the role of protein kinases. Biochimica et Biophysica Acta 1449(1):1-24. doi. (Verified, JAD, 2007-03-04)
32. ^  Hardwick, K.C. 2005. Checkpoint Signalling: Mad2 Conformers and Signal Propagation. Current Biology 15(4):R122-R124. doi. (Verified, JAD, 2007-04-16).
33. ^  van Deursen, J.M. 2007. Rb loss causes cancer by driving mitosis mad. Cancer Cell 11(1):1-3.
34. ^  Hoheisel, J.D. 2006. Microarray technology: beyond transcript profiling and genotype analysis. Nature Reviews Genetics 7: 200-210 (doi 10.1038/nrg1809). (Verified, JAD, 2007-02-03)
35. a,b  Tang, G. 2005. siRNA and miRNA: an insight into RISCs. Trends in Biochemical Sciences 30(2):106-114. (Verified, JAD, 2007-02-02)
36. ^  Kim, V.N., Nam, J.W. 2006. Genomics of microRNA. Trends in Genetics 22(3):165-173. (Verified, JAD, 2007-02-02)
37. ^  Davis, R.J., 1993. The mitogen-activated protein kinase signal transduction pathway. The Journal of Biological Chemistry 268(20):14553-14556. (Verified, JAD, 2007-01-25)
38. ^  Cobb, M.H., T.G. Boulton & D.J. Robbins, 1991. Extracellular signal-regulated kinases: ERKs in progress. Cell Regulation, 2:965-978. (Verified, JAD, 2007-01-25)
39. ^  Oster, S.K., C.S.W. Ho, E.L. Soucie and L.Z. Penn. 2004. The myc Oncogene: MarvelouslY Complex . Advances in Cancer Research 84:81-154. doi (Verified, JAD, 2006-04-16)
40. ^  Golstein, P. and G. Kroemer, 2007. Cell death by necrosis: towards a molecular definition. Trends in Biochemical Sciences 32(1):37-43 (doi). (Verified, JAD, 2007-02-05)
41. ^  Yohay, K. 2006. Neurofibromatosis types 1 and 2. Neurologist. 12(2):86-93. (Verified, JAD, 2007-01-31)
42. ^  Papazoglu, C. and A.A. Mills. 2007. p53: at the crossroad between cancer and ageing. Journal of Pathology 211(2):124-133. (Verified, JAD, 2007-01-31)
43. ^  Helton, E.S. and X. Chen. 2006. p53 modulation of the DNA damage response. Journal of Cellular Biochemistry. 9 Oct 2006. (Verified, JAD, 2007-01-31)
44. ^  Cookson M.R. 2004. Molecules That Cause or Prevent Parkinson's Disease. PLoS Biology 2(11):e401 (doi). (Verified, JAD, 2007-02-04)
45. ^  National Institute of Neurological Disorders and Stroke. 2007. Parkinson's Disease: Hope Through Research. Accessed by JAD, 2007-02-04.
46. ^  Schmidt1, H. and M. Hensel. 2004. Pathogenicity Islands in Bacterial Pathogenesis. Clin Microbiol Rev 17(1): 14–56. doi. (Verified, JAD, 2007-04-16).
47. ^  Alvarez, R.H., H. Kantarjian, and J.E. Cortes. 2007. The biology of chronic myelogenous leukemia: implications for imatinib therapy. Semin Hematol. 44(1):S4-14. (Verified, JAD, 2007-04-14)
48. ^  Gray W.M. 2004. Hormonal Regulation of Plant Growth and Development. PLoS Biology 2(9):e311 (doi). (Verified, JAD, 2007-02-04)
49. ^  Deyou Zheng, and Mark B. Gerstein. 2007. The ambiguous boundary between genes and pseudogenes: the dead rise up, or do they? Trends in Genetics 23(5):219-224 (May 2007). doi (Verified, JAD, 2007-04-26)
50. ^  Halaban, R. 2005. Rb/E2F: A two edged sword in the melanocytic system. Cancer and metastasis reviews 24:339-356. doi (Verified, JAD, 2007-03-08)
51. ^  Parameswarana, N. and W.S. Spielman. 2006. RAMPs: the past, present and future. Trends in Biochemical Sciences 31(11):631-638 (doi). (Verified, JAD, 2007-02-05)
52. ^  Blair, S.S., 2004. Developmental biology: Notching the hindbrain. Current Biology 14(14):R570-2. (Verified, JAD, 2007-01-31)
53. ^  Morten Frödin and Steen Gammeltoft. 1999. Role and regulation of 90 kDa ribosomal S6 kinase (RSK) in signal transduction. Molecular and Cellular Endocrinology 151(1-2):65-77 doi (Verified, JAD, 2007-04-27)
54. ^  Cottrell, T.R. and T.L. Doering. 2003. Silence of the strands: RNA interference in eukaryotic pathogens. Trends in Microiology 11(1):37-43. (Verified, JAD, 2007-02-03)
55. a,b  Garrett, R.H and C.M Grisham. 1995. Biochemistry. Saunders College Publishing. (Verified, JAD, 2007-02-02)
56. ^  Wang, S.M. 2007. Understanding SAGE data. Trends in Genetics 23(1):42-50 (doi). (Verified, JAD, 2007-02-06)
57. ^  Winstanley, C. 2002. Spot the difference: applications of subtractive hybridisation to the study of bacterial pathogens. J Med Microbiol 51:459-467. (Verified, JAD, 2007-03-12).
58. ^  Kirkina, V. and I. Dikic. 2007. Role of ubiquitin- and Ubl-binding proteins in cell signaling. Current Opinion in Cell Biology 19(2):199-205. doi (Verified, JAD, 2007-04-20)
59. ^  Wieschaus, E. and N.S. Tolwinski. 2004. Rethinking WNT signaling. Trends in Genetics 20(4):177-181 (doi). (Verified, JAD, 2007-02-05)