BIO 311 Exam 3 Questions and Answers | Latest
Update | 100% Correct.
Mitochondria Structure
-Have a preferred location in cells
-Are associated with microtubules
-Associated with ER membrane-regulates Ca2+
-37 genes
Mitochondria Energy Production
Glycolysis-Pyruvate-Krebs Cycle-ETC-ATP
Krebs cycle(citric acid cycle)
second stage of cellular respiration, in which pyruvic acid is broken down into carbon dioxide in
a series of energy-extracting reactions
located in the mitochondrial matrix
Possibilities why Mito. keep their 37 genes
Mito. Gene proteins are hydrophobic
Genes must be regulated
Mitochondria Outer Membrane
Porin-Voltage Dependent anion channel, passes molecules up to 5000 proteins. Large aqueous
channel in outer mito. membrane
PIGBOS-Communicates with Endoplasmic Reticulum(ER), Regulates UPR
,PIGBOS and UPR
PIGBOS activates UPR when the number of unfolded proteins builds up in the cell. UPR lowers
this number.
Less PIGBOS = More UPR = Cell death
Mitochondria Inner Membrane
"Glue" for ETC
Cardiolipids- 4 legged phospholipids that binds electron transport complexes together
Increases membrane resistance
-pH(H+) differential
-Vm = -200mV
ATP/ADP antiporter and phosphate transporter
Phosphoenolpyruvate carboxylase
Plays critical roll in C4 plants and carbon dioxide assimilation
Mitochondrial Fusion
Two Mitochondria fusing into one
Possibilities to why:
Maintain homogenous pool of mitochondria
restore damages mitochondria
mitochondrial localization
Mitochondrial Fision
,One Mitochondria splits into two
Possibilities to why:
Distribute mitochondria to daughter cells
Eliminate damaged portion
Tunneling nanotubes
Small tube that connects to cells together
Why?:
Transport mitochondria
Microtubules + F. Actin microtubules to maintain structure
Mitochondrial Triggered Intrinsic Apoptosis
Occurs when Mitochondria are stressed(chemo, radiation)
Process:
Mitochondria Permeability transition Pore opens
BaK/Bax enter
Cytochrome C releases and binds to APAF-1
Steps: Procaspace a - Caspace 9 - Procapase 3 - Caspace 3 - Cell death
TRAIL death receptors
use Caspace 8 to trigger apoptosis through a non-mito. mediated pathway
Extrinsic
, Over-expression of Bcl-2 blocks Mitochondrial Triggered Intrinsic Apoptosis
Signs of tumor
resistance to cancer treatment
Genasense
bcl-2 antisense oligonucleotide and targets Bcl-2 mRNA
Obatoclax
Small molecule Bcl-2 inhibitor
Venetoclax
BCL-2 inhibitor
Synta Pharmaceuticals
developing and commercializing small molecule drugs to treat cancer and chronic inflammatory
diseases.
Elesclomol
Synta Pharmaceuticals
targets ETC
Increases ROC and causes apoptosis in cancer cells by activating APTP through an increase in
reactive O2 species
Cyclosporin A
Blocks MPTP which decreases Apoptosis possibility
Used to prevent organ rejection post transplant
Update | 100% Correct.
Mitochondria Structure
-Have a preferred location in cells
-Are associated with microtubules
-Associated with ER membrane-regulates Ca2+
-37 genes
Mitochondria Energy Production
Glycolysis-Pyruvate-Krebs Cycle-ETC-ATP
Krebs cycle(citric acid cycle)
second stage of cellular respiration, in which pyruvic acid is broken down into carbon dioxide in
a series of energy-extracting reactions
located in the mitochondrial matrix
Possibilities why Mito. keep their 37 genes
Mito. Gene proteins are hydrophobic
Genes must be regulated
Mitochondria Outer Membrane
Porin-Voltage Dependent anion channel, passes molecules up to 5000 proteins. Large aqueous
channel in outer mito. membrane
PIGBOS-Communicates with Endoplasmic Reticulum(ER), Regulates UPR
,PIGBOS and UPR
PIGBOS activates UPR when the number of unfolded proteins builds up in the cell. UPR lowers
this number.
Less PIGBOS = More UPR = Cell death
Mitochondria Inner Membrane
"Glue" for ETC
Cardiolipids- 4 legged phospholipids that binds electron transport complexes together
Increases membrane resistance
-pH(H+) differential
-Vm = -200mV
ATP/ADP antiporter and phosphate transporter
Phosphoenolpyruvate carboxylase
Plays critical roll in C4 plants and carbon dioxide assimilation
Mitochondrial Fusion
Two Mitochondria fusing into one
Possibilities to why:
Maintain homogenous pool of mitochondria
restore damages mitochondria
mitochondrial localization
Mitochondrial Fision
,One Mitochondria splits into two
Possibilities to why:
Distribute mitochondria to daughter cells
Eliminate damaged portion
Tunneling nanotubes
Small tube that connects to cells together
Why?:
Transport mitochondria
Microtubules + F. Actin microtubules to maintain structure
Mitochondrial Triggered Intrinsic Apoptosis
Occurs when Mitochondria are stressed(chemo, radiation)
Process:
Mitochondria Permeability transition Pore opens
BaK/Bax enter
Cytochrome C releases and binds to APAF-1
Steps: Procaspace a - Caspace 9 - Procapase 3 - Caspace 3 - Cell death
TRAIL death receptors
use Caspace 8 to trigger apoptosis through a non-mito. mediated pathway
Extrinsic
, Over-expression of Bcl-2 blocks Mitochondrial Triggered Intrinsic Apoptosis
Signs of tumor
resistance to cancer treatment
Genasense
bcl-2 antisense oligonucleotide and targets Bcl-2 mRNA
Obatoclax
Small molecule Bcl-2 inhibitor
Venetoclax
BCL-2 inhibitor
Synta Pharmaceuticals
developing and commercializing small molecule drugs to treat cancer and chronic inflammatory
diseases.
Elesclomol
Synta Pharmaceuticals
targets ETC
Increases ROC and causes apoptosis in cancer cells by activating APTP through an increase in
reactive O2 species
Cyclosporin A
Blocks MPTP which decreases Apoptosis possibility
Used to prevent organ rejection post transplant
