Histo Cell Fates

Front 1

Proliferation
Quiescence
Differentiation
Senescence
Programmed Cell Death

Back 1

-Cell Division
-Cell is capable of dividing but currently isn't going through cell cycle
-process in which a cell becomes differentiated
-cell is functional but cannot undergo division
-cell dies in response to stimuli

Front 2

Cell Cylce

Back 2

G1-cell grows
S-Cell reolicates DNA
G2-Cell grows and prepares for mitosis
M-mitosis
G0-exit from cell cycle-quiescence

Front 3

cyclin-dependent protein kinase (cdk)

Back 3

phosphorylates specific proteins activating or inactivating them. Requires cyclin

Front 4

Cyclin

Back 4

bind to activate cdk's

Front 5

cyclinD/cdk4

Back 5

activates cells to pass restriction point and enter s phase
-phosphorylates RB becomes dissociated from E2F that controls genes for DNA synthesis, at end of G1 allows for DNA transcription

Front 6

cyclinA/ cdk 1,2

Back 6

activates DNA replication complexes leading through S phase, stmulates cyclin B production

Front 7

cyclin B/cdk1

Back 7

Mitosis Promoting Factor
-Histone packing
-phosphorylates lamins

Front 8

Check points
-G1/S
-G2/M
-M

Back 8

-damaged DNA results in stabilization of p53 which leads to inhibition of cyclin D/cdk4 activity.
-prescence of unreplicated DNA stops cycle before entrance into M
-improper spindle formation stops cycle at metaphase preventing missegregation of chromatids

Front 9

Prophase

Back 9

-Loss of Nucleolus
-Lamins are phophorylated
-chromosomes condense bound at centromere by cohesin
-migration of centrosome to poles

Front 10

Metaphase

Back 10

-Kinetochore formed on centromere, serves as attatchment point for microtubules
-mitotic spindle formed
--Astral, polar and kinetochor microtubules
-alignment of chromosomes
-Kinetochore microtubules attatch and release seperase which cleaves link btwn sister chromatids

Front 11

Anaphase

Back 11

-A) Kinetochore MT's shorten do to kinesin begins chromosome seperation
-B) polar MT's elongate and seperate two spindle poles further seperating chromosomes

Front 12

Telophase

Back 12

-Chromosomes are released from mitotic spindle
-lamins are dephosphorylated
-cell elongates
-actin and myosin contractile ring forms

Front 13

Cytokineseis

Back 13

Cleavage using actin myosin contractile ring
nucleolus reforms

Front 14

Stem Cells
-Todipotent
-Pleuropotent
-multipotent
-unipotent

Back 14

-capable of producing any cell in body
-capable of producing all differentiated cells of a specific line
-produces a limited number of cell types in a lineage
-produces only one cell type progenitor cells

Front 15

Transient Amplifying

Back 15

not fully differentiated, but are commited to a specific differentiated type. Divie rapidlyonly about 7 divisions

Front 16

Terminally Diferentiated

Back 16

endpoint of cell differentiation

Front 17

Senescence

Back 17

-metabollically active cell that cannot divide
-safeguard against cancer
-depletion of telomeres at the end of chromosomes
-plays a role in aging

Front 18

Telomerase

Back 18

a reverse trasncriptase that adds nucleotide repeats to the end of a chromosome from an associated RNA template. Not present in most cell types except stem and cancers

Front 19

Cell Death (apoptosis)
-function

Back 19

-removes cells that have migrated to the wrong place
-response to mutagen/carcinogen exposure
-turnover of terminally differentiated cells

Front 20

Apoptosis Morphology

Back 20

-condensation of nuclei, loss of cell junctions, cytoplasm becomes eosinophillic
-cell nucleus fragments into apoptotic bodies
apoptotic bodies are taken up by neighboring cells or macrophages
-no inflamation

Front 21

Apoptotic Mechanisms

Back 21

Intrinsic-growth factor withdrawal, DNA damage, inappropriate growth signals, low O2
-Extrinsic- death inducing ligands bind to death receptors and these produce apoptotic signal

Front 22

Intrinsic apoptosis

Back 22

-Bax/Bad/BCL-XS are produced by death signals, disrup BCL2 funtion in mitochondria
-BCL2 disfunction leads to mitochondria dysfunction and release of cytochrome c into cytoplasm
-cytochrom c and Apaf1 bind to caspase 9 in a huge complex that initiates caspase 3-causes apoptosis

Front 23

Extrinsic apoptosis

Back 23

-Death receptors activate intracellular messenger FADD
-FADD complexes with caspase 8/disc death inducing signal that initiates caspase-3 activation

Front 24

Caspase Activation

Back 24

-Caspase cysteine containing active site proteases cleave tetrapeptide sequence that contains aspartic acid
-Caspase 8,9 serve as activators cleaving and activating executioner caspases like caspase 3 that cut up the cell

Front 25

Caspase Targets

Back 25

-Nuclease complex cleaves DNA into nucleosome lengths
-Nuclear Lamins
-Gelsolin cleavage cuts up actin cytoskeleton
-DNA repair and replication enzymes prevents DNA repair
-BCL2 cut up and reinforces apoptotic signal

Front 26

Necrosis

Back 26

Cell Death
-Stimulated by injury or infection
-nuclei becomes condensed and some condensation of organelles
-cell swells and plasma membrane bursts
-leakage of intracellular contents leads to inflamatory response

Front 27

Protoncogenes

Back 27

-Stimulate proliferation
-inhibit cell death
-inhibit senescence
-inhibit differentiation

Front 28

Tumor Suppressors

Back 28

-Inhibit proliferation
-Trigger Cell Death
-Trigger senescence
-Stimulate Differentiation-example-p53 and RB