2/28/1990
chromosome items
chromosomes : abasic site ~ AP site : centromere : chromosome ~ chromatid, chromatin, chromosome : constitutive heterochromatin : DNA : euchromatin : facultative heterochromatin ~heterochromatin : kinetochore : nucleosome :
2/27/1990
damage repair items
damage/repair DNA : abasic site : DNA ~ DNA RNA ~ DNA damage C to T C to U ~ DNA damage by ROS : DNA repair : double strand breaks : oxidative stress and DNA damage : : : : :
decay items
decay RNA : decay DNA, RNA, protein • nonsense-mediated decay • nonstop decay • targetted genetic repair •
degradation of proteins : •• C • chaperone •• H • heat-shock proteins •• N • N-degron •• P • polyubiquitin • proteasome • protein degradation •• S • stress proteins •• U • ubiquitin • ubiquitin ligase • ubiquitin-proteasome pathway •
degradation of proteins : •• C • chaperone •• H • heat-shock proteins •• N • N-degron •• P • polyubiquitin • proteasome • protein degradation •• S • stress proteins •• U • ubiquitin • ubiquitin ligase • ubiquitin-proteasome pathway •
2/25/1990
enzymes items
enzymes : ~ cofactor : DNA polymerases : oxoG repair : RNA polymerase : AP endonuclease : base excision repair : DNA glycosylase : DNA ligase : DNA polymerases : DNA repair : Fen1
Specific Enzymes/Types : ·· A · adenylyl (adenylate) cyclase ◊ allosteric enzymes · allosteric enzymes · AP endonuclease (Ape1) ·· C · cAMP-dependent protein kinase · cyclin-dependent kinases ·· D · DAGKs · diacyl glycerol kinases · DNA glycosylase · DNA ligase · DNA Ligase I · DNA polymerases · DNA polymerase I · DNA polymerase beta · DNase IV · · E · exonuclease 1 · exosome ·· F · focal adhesion kinases (FAKs) · Fen1 · Flap Endonuclease FEN-1 · G · guanylate cyclases · guanyl cyclase ·· H · hOGG1 · hOGG1 oxoG repair ·· I · inducible transcription factors ·· L · LigIII · · M · MAP kinase · mitogen activated protein kinases · Msh2-Msh3 · MutS, MutL, and MutH ·· O · 8-oxoguanine glycosylase · oxoG repair hOGG1 ·· P · PCNA · phosphatases · phosphodiesterases · phospolipases · phospholipase C-gamma · PLC-G · protein kinase A · protein kinase C · protein tyrosine kinases (PTKs) · receptor tyrosine kinases · R · RNA polymerase · Replication factor C · reverse transcriptase · ribozymes · RNA polymerase II · RTKs ·· S · serine/threonine kinases · spliceosomal-mediated RNA trans-splicing · SMaRT ·· T · trans-splicing ribozymes ·· U · UvrD ·· X · XRCC1 ·
Specific Enzymes/Types : ·· A · adenylyl (adenylate) cyclase ◊ allosteric enzymes · allosteric enzymes · AP endonuclease (Ape1) ·· C · cAMP-dependent protein kinase · cyclin-dependent kinases ·· D · DAGKs · diacyl glycerol kinases · DNA glycosylase · DNA ligase · DNA Ligase I · DNA polymerases · DNA polymerase I · DNA polymerase beta · DNase IV · · E · exonuclease 1 · exosome ·· F · focal adhesion kinases (FAKs) · Fen1 · Flap Endonuclease FEN-1 · G · guanylate cyclases · guanyl cyclase ·· H · hOGG1 · hOGG1 oxoG repair ·· I · inducible transcription factors ·· L · LigIII · · M · MAP kinase · mitogen activated protein kinases · Msh2-Msh3 · MutS, MutL, and MutH ·· O · 8-oxoguanine glycosylase · oxoG repair hOGG1 ·· P · PCNA · phosphatases · phosphodiesterases · phospolipases · phospholipase C-gamma · PLC-G · protein kinase A · protein kinase C · protein tyrosine kinases (PTKs) · receptor tyrosine kinases · R · RNA polymerase · Replication factor C · reverse transcriptase · ribozymes · RNA polymerase II · RTKs ·· S · serine/threonine kinases · spliceosomal-mediated RNA trans-splicing · SMaRT ·· T · trans-splicing ribozymes ·· U · UvrD ·· X · XRCC1 ·
2/24/1990
2/23/1990
evolution items
evolution : allele ~ Basic mechanisms of evolution ~ Biological Evolution ~ Beyond Darwin and Neo-Darwinism ~ Bottleneck ~ Conjugation ~ Conserved & Consensus ~ Deletion~ Duplication ~ Epistasis ~ Genetic drift ~ Gene flow ~ genome and proteome ~ Founder effect ~ Horizontal Gene Transfer ~ Insertion ~ Inversion ~ Meiosis ~ Mendel's Laws ~ mispairing ~ Modern synthesis ~ Non-disjunction ~ Persistence of functional gene duplicates ~ Phyletic gradualism ~ Population Genetics and Formulae ~ Punctuated equilibria ~ Recombination ~ Speciation ~ Substitution ~ Transduction ~ Transformation ~ Translocation ~
2/22/1990
genome items
genome : allele : codon : conserved & consensus, consensus sequence : DNA : enhancer : exon : genes : genome : insulator : intron : LINEs ~ long interspersed elements ~ long terminal repeats ~ LTRs : Okazaki fragments : open reading frame ORF : promoters : repressor : response elements : self-splicing : silencers : short interspersed elements ~ silencers ~ SINEs ~ splice-sites : spliceosome : transposable elements :
2/21/1990
protein items
Specific proteins/types : ·· C · cAMP receptor binding protein · cofactor · core histones H2A, H2B, H3, and H4 · CRE-binding protein CREB · cytokines ·· E · elongation factor EF ·· G · general transcription factors ·· H · helicases : Helicase II · heterochromatin · histone · HP1 · I · inducible transcription factors · L · · LexA repressor ·· M · mCAT2 receptor · motor proteins ·· N · nucleosome ·· P · PcG proteins · PCNA · Polycomb group · proteome ·· R · RecA · regulatory proteins · repressor proteins · Receptor Tyrosine Kinases (RTKs) · ribosomes · RPA ·· S · serine rich (SR) splicing factors · silencers · Ski7p · small nuclear ribonucleoproteins (snRNPs) · spliceosome · SR (serine rich) splicing factors ·· T · TATA binding protein · TBP · trans-acting factors · trithorax group (trxG) ·· U · ubiquitin (Ub) · UPF1 UPF2 · upstream transcription factors
RNA processing items
processing : capping : polyadenylation : pre-mRNA splicing : RNA processing : pre-mRNA splicing : : : : : :
2/20/1990
regulation items
regulation : alternative splicing : epigenetics : gene regulation : nonsense-mediated decay : nonstop decay : response elements : RNA processing : spliceosome : transcription : transcription factors : transcription initiation : termination of transcription
Gene regulation ensures that the genes of differentiated, somatic cell lines are normally repressed, and are only expressed when their products are required. Failure of gene regulation and uncontrolled proliferation is a feature of malignancies and arises through carcinogenic mutations.
Gene induction permits gene expression (derepression), and gene induction mechanisms ultimately involve regulatory proteins that bind to a regulatory DNA gene locus to induce or upregulate gene expression, which involves transcription, pre-mRNA splicing, and translation. Other regulatory proteins bind to repressor sequences to downregulate gene expression. Regulatory proteins bind to segments of DNA and bring about gene regulation. Most gene regulation proteins are single proteins, often homodimers or homotetramers, which bind to two ligands: a. a metabolic intermediate, and b. a cis-acting gene regulation element. Trans-acting factors are usually protein factors control gene expression by binding to cis-acting sequences, which are DNA sequences in the vicinity of the structural portion of a gene, and which are required for gene expression. Regulatory proteins are targetted for early degradation at the proteasome by the ubiquitin-mediated protein degradation pathway. Some control of gene expression is tissue-specific and other control mechanisms are pleiotropic because they affect varied tissues.
Proto-oncogenes promote cell proliferation – these are genes coding for growth factors, transcription factors, and trans-membrane receptors for signal transduction by growth factors, and estrogens. Oncogenes are mutated proto-oncogenes, which drive excessive cell proliferation in the absense of tumor suppressors.
Defective RNAs are removed by nonsense-mediated decay and RNA is continuously degraded by nonstop decay. Apoptosis is essential, programmed cell death. Sublethal stressors cause repression of housekeeping genes and activation of stress genes that code for stress proteins and molecular chaperones. Heat shock response is an important homeostatic mechanism that enables cells to survive a variety of environmental stresses. These heat shock proteins function in multi-protein complexes as molecular chaperones and assist in the proper protein folding of stress damaged proteins, and stabilization of other cellular proteins. Severely damaged proteins are degraded. When DNA is damaged, cell-cycle checkpoints employ signal transduction pathways to arrest the cell cycle, pending repair. If damage to DNA or proteins is too severe, apoptosic pathways are activated.
Regulation of metabolism is primarily determined by separation of enzymes and metabolites in separate compartments, by feedback control of activity (allosteric) or synthesis of inducible/repressible enzymes. Chemical cofactors are non-proteinaceous substances that assist enzymes in performing catalytic actions. Molecular genetic cofactors are activators or repressors.
Gene regulation ensures that the genes of differentiated, somatic cell lines are normally repressed, and are only expressed when their products are required. Failure of gene regulation and uncontrolled proliferation is a feature of malignancies and arises through carcinogenic mutations.
Gene induction permits gene expression (derepression), and gene induction mechanisms ultimately involve regulatory proteins that bind to a regulatory DNA gene locus to induce or upregulate gene expression, which involves transcription, pre-mRNA splicing, and translation. Other regulatory proteins bind to repressor sequences to downregulate gene expression. Regulatory proteins bind to segments of DNA and bring about gene regulation. Most gene regulation proteins are single proteins, often homodimers or homotetramers, which bind to two ligands: a. a metabolic intermediate, and b. a cis-acting gene regulation element. Trans-acting factors are usually protein factors control gene expression by binding to cis-acting sequences, which are DNA sequences in the vicinity of the structural portion of a gene, and which are required for gene expression. Regulatory proteins are targetted for early degradation at the proteasome by the ubiquitin-mediated protein degradation pathway. Some control of gene expression is tissue-specific and other control mechanisms are pleiotropic because they affect varied tissues.
Proto-oncogenes promote cell proliferation – these are genes coding for growth factors, transcription factors, and trans-membrane receptors for signal transduction by growth factors, and estrogens. Oncogenes are mutated proto-oncogenes, which drive excessive cell proliferation in the absense of tumor suppressors.
Defective RNAs are removed by nonsense-mediated decay and RNA is continuously degraded by nonstop decay. Apoptosis is essential, programmed cell death. Sublethal stressors cause repression of housekeeping genes and activation of stress genes that code for stress proteins and molecular chaperones. Heat shock response is an important homeostatic mechanism that enables cells to survive a variety of environmental stresses. These heat shock proteins function in multi-protein complexes as molecular chaperones and assist in the proper protein folding of stress damaged proteins, and stabilization of other cellular proteins. Severely damaged proteins are degraded. When DNA is damaged, cell-cycle checkpoints employ signal transduction pathways to arrest the cell cycle, pending repair. If damage to DNA or proteins is too severe, apoptosic pathways are activated.
Regulation of metabolism is primarily determined by separation of enzymes and metabolites in separate compartments, by feedback control of activity (allosteric) or synthesis of inducible/repressible enzymes. Chemical cofactors are non-proteinaceous substances that assist enzymes in performing catalytic actions. Molecular genetic cofactors are activators or repressors.
2/19/1990
RNA items
RNAs : RNA : mRNA : nuclear speckles : miRNAs : pre-mRNA : tRNA : ribozymes in repair of RNA and DNA : snoRNAs : trans-splicing ribozymes and therapeutics : : :: : :
2/18/1990
replication items
replication & reproduction : C ¤ carcinogenesis • centrioles ~ chromatid, chromatin, chromosome ~ constitutive heterochromatin · ~ cyclin-dependent kinases ~ D DNA RNA ~ DNA ligases ~ DNA polymerases ~ E euchromatin ~ F facultative heterochromatin ~ G genes ~ general transcription factors ~ genetic template ~ genome ~ H helicases ~ heterochromatin constitutive heterochromatin facultative heterochromatin ~ histone ~ I inducible transcription factors ~ K kinetochore ~ L • lamins ~ M mRNA ~ N nucleic acids ~ nucleobases & nucleosides & nucleotides ~ nucleosome ~ nucleotide • nuclear membrane • nuclear lamina • nuclear pore • nucleolus • nucleus ~ O open reading frame ORF ~ P polyadenylation ~ post-transcriptional modulation ~ preinitiation complex~ pre-mRNA ~ pre-mRNA splicing ¤ proliferation ~ R replication ~ replicative transposition (type I) ~ reproduction ~ RNA polymerase ~ S • spindle ~ splice-site ~ spliceosome ~ T TATAA box ~ TBP ~ template ~ transcription ~ transcription factors ~ transcription initiation ~ termination of transcription ~ tRNA ~ translation ~ transposable elements ~ U upstream transcription factors ~
2/17/1990
research items
research : Research techniques : Research Articles :RNAs : RNA : mRNA : nuclear speckles : miRNAs : pre-mRNA : tRNA : ribozymes in repair of RNA and DNA : snoRNAs : trans-splicing ribozymes and therapeutics : : :
2/16/1990
signaling items
CELL SIGNALING : • • A • adhesion and signaling • • C • cAMP-dependent protein kinase • chemotaxis • • E • ERKs • • F • focal adhesion • • G • GPCRs • GPCR families • • H • hormones • • M • MAP Kinase • mitogen activated protein kinases • MAPK signaling cascade • MAPK responses • • N • Nitric Oxide • neurotransmission • neuronal interconnections • • P • PKA · protein kinase A • PKC • phosphotransfer-mediated signaling pathways • Protein Kinase Signaling Networks • protein kinase A • protein kinase C • protein tyrosine kinases • PTKs • • R • receptor tyrosine kinases • Rho GTPases • RTKs • • S serine/threonine kinases • signaling gradients • signal transduction • signaling and adhesion • • T • TGF-β • two-component systems •
splicing items
splicing : alternative splicing : cis versus trans-acting factors : epigenetics : pre-mRNA splicing : self-splicing : splice-site : spliceosome : : : :