Cells are made up of 3 things :

Enzyme lamine, H3a akan memfosforilasi

Cell membrane , nucleus, cytoplasm. Nucleus isinya
nuclear envelope shg lapisan itu dissolving.
DNA material. DNA : double stranded containing 46
chromosome (23 maternal, 23 paternal)
Sentrosom  microtubules organization
Sifat dari sel :
b. Metaphase
 Labile cell : Stratified squamous cell yg terus Microtubules organization akan take place di
proliferasi contonya di epidermis, GI tract, vagina, both of the poles – polar microtubules
urinary tract, HSC in bone marrow constantly
undergo proliferation. Microtubules connect to each kinetochore &
 Stable cell : jadi dia diem aja di G1 phase karna dia align it in the middle
ga harus proliferasi terus, kcuali ada triger/stimulus
dmn dia harus tumbuh. Contonya liver/ hepatosit,
epitel dari kidney tubules, alveolar of the lungs.
 Permanent cell /amitotic : setelah lewatin cell cyle
dia ga akan bs ulang cell cycle lagi apapun stimulus
nya contohnya neurons , skeletal muscle, cardiac
muscle

Cell cycle
1. G1 – gap/ growth 1 phase (preparation)
Synthesis organelles, proteins, enzymes dan repair
thymidine dimers preparing for cell mitosis.
G1 / S Checkpoint
2. S phase – synthetic
DNA replication, dimana di maintain oleh enzyme
DNA polymerase 1 dan 3 spy bikin dna nya gasalah
Metaphase checkpoint
c. Anaphase
Splitting of the chromatid and sisted chromatid
to each of the poles using the motor proteins
dynein and kinesin to direct the chromatid
towards the microtubules.

Kurleb 6 jam APC : anaphase promoting complex yg

mencegah securin bind dng superese shg
3. G2 – gap/growth 2 phase cohesion broke down dan chromatid separate.
Bahannya sdh tersedia, chromosome jumlahnya sdh
96 (46x2) d. Telophase
Chromatid condensed become loose again
Spy bs mitosis butuh volume sel yg cukup, shg Forming a cleavage forrow  squeezing of the
disini volume sel membesar dan volume sitoplasma cytoplasma into 2 separate cells
jg meningkat
5. Cytokinesis
Kurleb 2 hours The cell already finish of dividing into 2 cells with
the DNA 2n (46 Chromosome each)
G2/M checkpoint
Now the cells already finish the cell cycle, proiliferative
Fase interfase = G1 – S- G2 cell can undergo cell cycle again back to interphase, but
other cell can go to G0 phase – dormant phase, but in
4. M – mitosis phase
certain circumstances under stimulus it can go back to
a. Prophase
interphase. But amitotic cell they cant under any other
condensing chromatin
stimulus to go back to cell cycle.
Klo sblm sel itu mitosis chromatin nya itu
loose, jadi disini dibikin condensed (chromatin Stimulus to proliferation of cells :
= dna + histone protein)
 gabisa fosforilasi RB protein shg proliferasi lanjut
terus, E2F ga copot shg inhibit proliferasi (klo
copot kan dia bs stimulate gene yg pro cell cycle)

 BAX gene – pro-apoptotic gene teraktivasi klo

misal DNA mistake terlalu parah gabisa di repair

 Growth factors / mitogen – different Growth

factor receptor  activate enzymes of
transcription factor  stimulate proliferative
genes.

Proliferative genes MYC, FOS, JUN  producte

TF  activate cyclin gene  produce cyclin
protein (D,E,A,B)

Another gene make cyclin dependent kinase

(CDK 1,2,3,4,6) & with cyclin protein mreka
bergabung  drive the cell cycle

 E2F yg udh copot dari RB protein  stimulate

another gene spy drive proliferation

Inhibition of proliferation of cells :

 Tumor suppressor gene  make retinoblastoma

protein , bound to E2F  inhibit binding of
receptor and drive proliferation of cells
But C+CDK complex fosforilate the RB protein
shg E2F lepas /copot dari RB protein stimulate
other gene to pro cell cycle

 ATM gene  fs nya utk read DNA spy tau DNA

nya rusak / ngga, ada mismatch / ngga.

Mismatch + / Ada DNA rusak  ATM gene

stimulate MDM-2 utk stop inhibit P53  gene
P53 bs kerja  stimulate other gene  Undergo
DNA repair

 Gene MDM-2 - E3 Ubiquitin complex  brakes

of the P53 yg menginhibit P53 spy ga terus2an
stimulate other gene utk DNA repair.

 P53 jg stimulate other gene yaitu P15,16,17,18,21

 produce protein CDK-Inhibitor yg inhibit
Cyclin dependent kinase shg stop proliferasi, +