biochem tidbits

TF that binds to CAAT box (a promoter)

TF that binds to promoter region

TF that binds to TATA box (promoter)

chrom 16

• alpha thalessemia: results in severe anemia and death
• note-alpha globin is oxygen carrying component of Hb

two beta globins and two alpha globins, 4 heme groups

chrom 11

sickle cell anemia

yolk sac

fetal dev

alpha, beta, delta globin

modified RNA base in T loop of tRNA; linkage btw uracil and ribose is changed from C-N bond to C-C bond

T loop of tRNA; modified RNA base

modified RNA base; deaminated adenine base whose nucleoside is inosine

pseudouridine and nucleosides w/ 2'-O-methylribose

linked to mRNA via 5'-5' triphosphate linkage to first transcribed nucleotide

polyA signal (site of cleavage), binding sites for prot, binding sites for miRNA, siRNA, and reg RNA

enz w/ endonucleolytic activity that remove the primer in lagging strand synth

DNA clamp prot; processivity factor for DNA pol delta by encircling DNA as a trimer which creates a topological link to the genome

TTAGGG

single origin of replication in prok; 245 bp long w/ conserved seq (four 9-bp repeats and three 13-AT rich bp repeats)

initiation factor in prok DNA synth; binding cooperative (once one DnaA binds to a OriC repeat, tons of others bind)

acts on three AT rich regions of OriC

binds to open OriC in prok; delivered by DnaC; completes pre-priming complex; has helicase activity

primase for prok DNA synth

termination seq in DNA repl in prok; when bound to Tus prot, terminates DNA synth

Ter sites; will arrest a rep fork approaching the Ter site from one direction but will allow unimpeded fork mvmt through the Ter site from other direction

ribonuc that degrades the RNA from RNA-DNA hybrids in rt of RNA template; func as endonuc and exonuc

group-specific antigen; codes for core and structural prot of retrovirus (i.e. viral capsid)

codes for rt, protease, and integrase; synth viral DNA and integration into host DNA after infection

codes for retroviral coat prot; plays role of entry of virion into host cell

dimer RNA; cap at 5' and polyA at 3'; has terminal noncoding regions and internal coding regions

forms a direct repeat at both ends of genome

non-coding region, first part of genome to be rt; forms 3' end of provirus genome

18nt complementary to 3' of specific tRNA primer used by virus to begin rt

long, non-transL region downstream of transC start site and present at 5' of all virus mRNAs

short A/G run; initiates strand synth in rt

non-coding region; forms 5' end of provirus after rt; contains promoter elements used in transC of provirus

"retroviruses that contain oncogenes"; viral DNA incorporates a section of host DNA (contains genes for growth promotion called proto-oncogenes) into its own DNA; increased transC caused by LTRs of virus cause increased growth of infected cell

2 +ssRNA

bind to basic promoter seq facilitating RNA binding

bind to seq distant from basic promoter and have specific roles

• 1. modulate efficiency of initiation
• 2. mediate signal response
• 3. regulate gene exp
• 4. bind other reg prot

• 1. internal promoter-binding sites for TF and RNA pol 3
• 2. transcription products contain promoter (start pt upstream of promoter)

CAAT and G/C box; fixed position/orientation but located distally upstream from TATA (core promoter element)

TF that binds to TATA core promoter element; binding of RNA pol follows

elements in transC that are not covalently linked to DNA

CAAT binding prot; trans acting element

TF; trans acting element; binds to promoter

binds to TATA box; TF; trans acting element

thalassemia, colorectal cancer, IGF-1, SCIDs, reduced globin chain synth in alpha/beta thalessemia

symptoms: degeneration of skin, joints, kidneys, nervous system, photosensitive rashes on face and extremities

cause: presence of Ab to U1snRNP

• participates in:
• DNA damage repair
• ubiquitination
• transC reg

defect in its alt splicing results in breast/ovarian cancer

accumulation of immature granulocytes, cancer of blood and bone marrow, fatique, susceptible to infection, tend to bleed

• 1. failure of histone acetylation
• 2. failure of granulocyte diff (due to mutations in RAR...results in transC failure)

all-trans retinoic acid (ATRA) and Trichostatin A

mutant RAR will not release HDAC activity from receptor-HDAC complex unless high amts of ATRA supplied

mutant RAR does not release HDAC at all; lots ATRA and tirchostatin A (HDAC inhib)

• add A's to 3' end of viral DNA...prolonged stability
• edit viral RNA causing frame-shift mut resulting in new viral RNA and prot

seq in intron next to 5' splice juntion; bound to by snRNPs

C-U and A-I

in mRNA; starts w/ start codon and ends w/ stop codon

YES

GTP

biochemical basis: low [heme] activates prot kinase to phosph/activate eIF-2 kinase-Pi; active eIF-2 kinase-Pi phosph eIF-2; eIF-2 is now inactive...initiation of transL in euk is inhibited

• def of Hb in red blood cell leads to anemia
• symptoms: extreme fatique, shortness of breath, headache, dizziness, susceptible to infection and arrhythmia

• measurement of blood cell size
• hematocrit levels
• Hb levels

• sm, naturally occurring prot
• alpha, beta, gamma
• anti-viral and anti-cancer moeities

interferon act enz to phosph an endonuc; endonuc-p can now degrade viral mRNAs....inhib of prot synth and viral proliferation and growth

post-transL prot modification; conv of glutamic acid to gamma-carboxyglutamic acid

req for blood clotting prot

blood is unable to clot if carboxyglutamination is not functioning properly

CF gene mut; CFTR is not properly glycosylated during post-transL modifications

collagen is stabilized by hydroxylation of prolines and lysines

post-transL modification; cov linkage of prenyl groups to anchor a prot to cell mem

neurodegenerative disorders: CJD/Mad cow, Alzheimer's, Huntington's

• Vo= [S](Vmax/Km)
• rate is directly proportional to substrate concentration

• Vo=Vmax
• rate is maximal and indep of substrate concentration

• Vo=Vmax/2
• Km is equal to substrate concentration when rxn rate is half the maximal value

indep of enz concentration; measure of binding affinity of E for S or apparent dissoc constant

Vmax=(Kcat)(ET)

greater it is, the higher aff an enz has for a substrate

used to treat Parkinson disease and depression

binds to glycopeptide transpeptidase bc its molecular shape is similar to D-Ala-D-Ala substrate

covalent bond formed btw penicillin and a Ser in the active site of enz resulting in inactivation of enz, inability of bact to synth their cell walls...bact lysis

K_m increased, V_max unchanged

• increases K_m by a factor of (1+[I]/K_i)
• new K_m: K_m^app: Km(1+[I]/K_i)

• V_max decreased, K_m unchanged
• decreases V_max by a factor of 1/(1+[I]/K_i)
• V_max^app= V_max/(1+[I]/K_i)

inhibitor only binds to ES complex (vs competitive inhibitors which resemble substrate and compete for active site of enz)

• [ES] lowered which lowers V_max (V_max=K_catE_T)
• Km lowered bc removing [ES] shifts equil of E+S to the right (bc removing the prod, [ES])....increases affinity enz has for subst

decreases both K_m and V_max by a factor of 1/(1+[I]K_i)

indication of how potent an inhibitor is

• increases slope
• x intercept moves to the right
• same y intercept

• increases slope
• x intercept stays the same
• increased y intercept

• same slope
• x intercept moves to left
• increased y intercept

competitive inhibitor example; inhib dihydrofolate reductase

formation of acyl-enz int whose formation is concurrent w/ formation of colored prod of chromogenic subst

exists as a dimer, no cat act, binds CTP

exists as a trimer, cat act, does not bind CTP

complete enz=2xC₃ and 3xR₂

• btw pairs of catalytic chains w/in cat trimer
• quindi for each catalytic trimer, there are three active sites which gives 6 active sites total per enz (two catalytic trimers per ATCase)

to make more pyrimidines...therefore if lots of purines in env then there will be lots of ATP to allost act CTPAse but if there are lots of pyrimidines then CTP will inhibit CTPase through allos inhib

act by phosphorylation of Tyr 412 which stabilizes R form; cov mod that leads to allost stabilization of R state