REVIUW MUSCULOSCELETAL SYSTEM

BIOCHEMISTRY OF BONE & MUSCLE

Dr. Syahrijuita, M.Kes

BIOCHEMISTRY DEPARTMENT
Faculty of Medicine Hasanuddin University
2018
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 Standar Kompetensi Dokter
Permasalahan / Keluhan:
 Nyeri sendi
 Sakit punggung
 Nyeri Pinggang
 Nyeri otot
 Bengkak
 Sendi (Kaku,bengkak, kelainan bentuk
 Gerakan terbatas
 Patah tulang, dll
Kompetensi Dokter Indonesia
• Tingkat Kemampuan 1
(Mengenal gejala klinis,mendiagnosis,rujuk)
• Tingkat Kemampuan 2
(Mampu mendiagnosis,rujuk,menindak ljt
sesudahnya)
• Tingkat kemampuan 3
• 3a.Mendiagnosis, R/ pendahuluan,rujuk
• bukan kasus darurat
Kompetensi Dokter Indonesia
• Tingkat Kemampuan 3b
(Mendiagnosis, R/ pendahuluan,rujuk kasus
gawat darurat )

Tingkat Kemampuan 4a
( Mendiagnosis  menangani sampai tuntas)
4b. Tingkat mahir ( setelah entrenship)
 MUSCULOSKLETAL
• Dislokasi pada sendi ekstremitas 4
• Tenosynovitis supuratif 4
• In growing toe nail 4
• Paronychia 4
• Lipoma 4
• Fraktur 3B Osteomyelitis 3B
• Arthritis 3A
• Osteoarthritis 3A Fraktur clavicula 3A
Osteoporosis 3A
• Fraktur clavicula 3A
• Osteoporosis 3A
• Trauma of joint 3A
• Achilles tendonitis 3A
• Rupture of achilles tendon 3A
• Ulkus pada tungkai 3A
• Fraktur patologis 2
• Fractures and dislocations of spine 2
Primary bone tumors 2
• Bone metastasis 2
• Kista ganglion 2 Spina bifida 2
• Kyphosis 2
• Lordosis 2
• Spondylitis, spondylodiscitis 2
• Hernia of nucleus pulposus 2
Spondylolisthesis 2
• Spondylolysis 2
• Rheumatoid arthritis 3A
• Fraktur clavicula 3A
• Osteoporosis 3A Trauma of joint 3A
• Achilles tendonitis 3A
• Rupture of achilles tendon 3A
• Ulkus pada tungkai 3A
• Fraktur patologis 2
• Fractures and dislocations of spine 2
• Primary bone tumors 2
• Bone metastasis 2
• Kista ganglion 2
• Spina bifida 2
• Scoliosis 2
• Kyphosis 2
• Lordosis 2
• Spondylitis, spondylodiscitis 2
• Hernia of nucleus pulposus 2
Spondylolisthesis 2
• Spondylolysis 2
• Dislocation of hip 2
• Ligamentous lesions of hip 2
• Lesion of meniscus, medial and lateral 2
• Tarsal tunnel syndrome 2
• Instability of ankle 2
• Osteogenesis imperfecta
• Rickets, osteomalacia 1 Achondroplasia 1
• Fibrous dysplasia 1
• Osteosarcoma 1
• Ewing sarcoma 1
• Sacrococcygeal teratoma 1
• Hip dysplasia 1
• Femoral head necrosis 1 Rhabdomyosarcoma
1
• Leiomyoma 1
• Leiomyosarcoma 1 Liposarcoma 1
Fibromatosis 1 Fibroma 1 Fibrosarcoma 1
 KIPDI 2012
• 1 Artritis, osteoartritis 3A
• 2 Fraktur terbuka, tertutup 3B
• 3 Fraktur klavikula 3A
• 4 Fraktur patologis, 2
• 5 Fraktur dan dislokasi tulang belakang 2
• 6 Dislokasi pada sendi ekstremitas 2
• 7 Osteogenesis imperfekta 1
• 8 Ricketsia, osteomalasia 1
• 9 Osteoporosis 3A
• 10 Akondroplasia 1
• 11 Displasia fibrosa 1
• 12 Tenosinovitis supuratif 3A
• 13 Tumor tulang primer, sekunder 2
• 14 Osteosarkoma 1
• 15 Sarcoma Ewing 1
 Kipdi 2012
• 16 Kista ganglion 2
• 17 Trauma sendi 3A
• 18 Kelainan bentuk tulang belakang (skoliosis, kifosis, lordosis) 2
• 19 Spondilitis, spondilodisitis 2
• 20 Teratoma sakrokoksigeal 2
• 21 Spondilolistesis 1
• 22 Spondilolisis 1
• 23 Lesi pada ligamentosa panggul 1
• 24 Displasia panggul 2
• 25 Nekrosis kaput femoris 1
• 26 Tendinitis achilles 1
• 27 Ruptur tendon achilles 3A
• 28 Lesi meniskus, medial dan lateral 3A
• 29 Instabilitas sendi tumit 2
• 30 Malformasi kongenital (genovarum, genovalgum, club foot, pes planus) 2
 KIPDI 2012
• 31 Claw foot, drop foot 2
• 32 Claw hand, drop hand 2
• Otot dan Jaringan Lunak
• 33 Ulkus pada tungkai 4A
• 34 Osteomielitis 3B
• 35 Rhabdomiosarkoma 1
• 36 Leiomioma, leiomiosarkoma, liposarkoma 1
• 37 Lipoma 4
• 38 Fibromatosis, fibroma, fibrosarkoma 1
ACHONDROPLASIA
DUCHENNE MUSCULAR
DYSTROPHY
 Duchenne Muscular Dystrophy
• A severe recessive X-linked
• Rapid progression of muscle degeneration
• Eventually loss of ambulation  death
• Prevalent is one in 4000 males
• In general  male. Carriers  female
• Female if father & mather affected
• Mutation in the dystrophin gene Xp 21 
codes for the protein dystrophin  structure
stability to dystroglycan complex (DGC) 
located on the cell membrane
 MARFAN SYNDROME
• Genetic disorder off connectic tissue 
(fibrilin-1)
• Unussually tall with long limbs & long thin
finger
• Dominant gen FBN1
• Defects on the heart valve & aorta,
lung,eyes,spinal.skeleton & hard palate
• Indicate 1/ 3000 -5000,1/20.000 birth
• Long limbs, dislocated lenses, aortic root
dilation,arachnodactily
 Myasthenia Gravis
• An autoimmune neuromuscular disease
• Fluctuating muscle weakness &
fatiguability
• Weakness is caused by circulating antibody
 block Ach reseptor at post synaptiv NMJ
• Inhibiting the stimulate effect of the NT
Ach
• Incidence 3- 30 cases / million
• R/ cholinesterase inhibitors or
immunosuppressants
 Myasthenia Gravis
Sign & Symptoms

• Muscle become progressively weakness

during activity & improve after periods of
rest
• Eye &eyelid movement, facial expressions,
chewing, talking & swallowing
• The onset sudden,
• Often symtoms are intermittent
OSTEOGENESIS IMPERFECTA

• Called = Brittle bone disease 

substaining multiple broken bones in child
• Causes a defect in the production of
collagen type I
• Type I collagen is found in bone, sclera,
ligament & teeth
• It’s a dominant mutation
• Is due a genetic mutation in the gene to
produce Collagen
OSTEOGENESIS IMPERFECTA
Signs & Symptoms
• Bone fragility, scoliosis
• Tooth defect, loose ligaments
• Bluish sclera, hearing deficits
• Dll

• R/: Biphosphanates & Ca suplements

• R/ genetic & Growth Hormon
Regulation of Calcium Homeostasis
 REVIEW BIOKIMIA
SEORANG IBU BERUSIA 40 TH SUDAH SETAHUN
TERAKHIR MENGALAMI NYERI PADA SENDI
TERUTAMA SENDI LUTUT. TADI MALAM DIA
MENGHADIRI PESTA PERKAWINAN.DIA SEMPAT
MELAHAP 2 MANGKOK COTO DAN 2 EMPING.
TADI PAGI DIA SUDAH TIDAK MAMPU
BERJALAN KARENA NYERI YANG HEBAT PADA
KEDUA SENDI LUTUTNYA. WARNANYA
KEMERAHAN DISERTAI BENGKAK .

27
 PERTANYAAN
• APA DIAGNOSIS IBU TERSEBUT ? DDNYA?
• APA HUBUNGAN ASAM URAT DENGAN NYERI
PADA KEDUA LUTUTNYA?
• BERAPA KADAR ASAM URAT YANG NORMAL
DALAM DARAH?
• PEMERIKSAAN APA LAGI YANG PERLU DAN
INTERPRETASINYA.
• BAGAIMANA BIOSINTESIS ASAM URAT
• BAGAIMANA PENATALAKSANAAANNYA

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BIOSINTESIS ASAM URAT

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 Biochemistry of Bone
Sub topic:

 Extracellular Matrix
Bone
Cartilage

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 Learning Objectives

• Describe structure, function of the ECM

(kolagen; elastin, noncollagenous
proteins,proteoglicans)
• Describe the chemical composition of the
bone and process of mineralization
• Describe the chemical composition of the
cartilage
• Describe the phatology of genetic diseases
from errors in the synthesis or turnover ECM
component, bone and cartilage
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 EXTRACELLULAR MATRIX
• A complex network of secreted macromolecules
located in extra cellular space
• Associated chronic diseases such as: arthritis,
ateroclerosis, cancer and fibrosis
• Including:
-Collagens: provide tensile strength connect the
different constituents of the ECM
-Adhesive proteins: elastin, laminin,fibronectin
-Proteoglicans:space filling

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 Functions ECM
• Provides mechanical contact between cells
• Forms structures with spesial mechanical
properties : bone, cartilage, tendons and joints
• Filtering properties of the kidneys
• Insulated cells and tissue from one another
• Guides cells by forming pathway embryonic
development
• Cosmetic industry:ageing

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 COLLAGENS
Major and primery structural in the ECM,>30%
total protein in the body
Morethan 20 different types
Tensile, strength and flexibility
Triple helical structure (formed by folding of 3
peptide chains)
Chains size : 600 – 3000 amino acid
Repeating sequence of collagens:(Gly – X – Y)n
Synthesis in RER, Golgi Apparatus, ECM

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Collagens

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 Functions of Collagens:

1. Numerous hereditary genetic defect

2. Impact on the skleton, joints,
tendons,skins, eyes,etc
3. Disturbances in collagens synthesis
exp:loss of teeth, bleeding,skin damage
Vit C deficiency( Scurvy)

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 HEREDITARY GENETIC DEFECTS OF COLLAGENS

Gen / Enzym Diseases

Osteogenesis imperfecta
Col 1 A1 ; 1 A2 Osteoporosis
Sindrom Ehlers – Danlos Tipe VII A; VII B
 Heavy Chondrodisplasia
Col 2 A1
 Osteosrthitis
Col 3 A1 Sindrom Ehlers – Danlos Tipe IV
Col 4 A1 - 4 A6 Sindrom Alport (termasuk bentuk autosomal atau X
Col 7 A1 Epidermolis bulosa distrofi
Col 10 A1 Chondiodisplasia mettaplasia Schmid
Hidroksilase Lisil Syndrom Ehlers – Dddanlos Tipe V
Prokolagen
Syndrom Ehlers – Dddanlos Tipe VII C
Proteinase – N

Syndrom MenKes (def. C)

Hidroksilase Lisil

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 ELASTIN

• Flexibility required for functions of :blood

vessels, lungs, ligament,skin, ECM
• The predominant protein of elastic fibers
• Only one gene
• A polypeptide 750 amno acid
• Tropoelastin  RER

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The Difference Collagens and Elastin

No Collagen Elastin
1. Multigen One gen
2. Triple Heliks Monomer crosslink
3. (Gly – X – Y )n Not

4. Hidroksilin Not

5. Not
Carbohidrat

6. Aldol intra molecular Demosin intra molecular

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 FIBRILIN
Protein (glicoprotein) = 350 kDa ;
imunohistokimia
Sindrom Marfan:
• mutasi gen (cromosom 15) for fibrilin;
dominan autosomal
• Lens Dislokation (ektopia lentis)
• hiperextensibilitas of joint; aracnodactili
(kerangka dan jari-jari panjang); tunika
media aorta weakness (dilatation of aorta
ascendens)
Mutasi gen (cromosom 5) ; aracnodactili
congenital contractur

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 SCEMATIC FIBRONECTIN
(7 Domain Fungsional)

Heparin Heparin Fibrin B

Fibrin A
Kolagen DNA Sel A B Sel B

Fibronektin pada Reseptor RGD ( Arg-Gli-Asp)

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 LAMININS

• Laminins are a family of noncollagenous in

basement membranes.
• Heterotrimeric molecules,large 850 kDa
• Interact with cells through multiple binding sites
• Has a central role in formation of crosslinks laminin and
type IV collagens

ENTAKTIN
• Binding at laminin
• Glikoprotein mengandung RGD
• Important at glomerulus filtration
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 PROTEOGLICANS

• are gel-forming components of the ECM

• Composeof peptide chains containing
covalently bound sugars
• Have a repeating disaccharide unit, an amino sugar and
a uronic acid:GLICOAMINOGLICANS
• Sindekan : Betaglikan; serglisin; perlekan,
Agrekan (tipe utama kartilago); versikan,
dekorin; biglikan; fibromodulin.

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 Glicosaminoglican Function
• Component struktural extracellular matrix
• Facilitated cell migration (HA)
• Turgor of tissue, pressure of cartilag
• Filter of matrix
• Cornea transparantion transparansi (KS
dan DS) dan sklera (DS)
• Anticoagulan
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 Nama/na Cacat Enzim Metabolit
ma lain Urine
MUKOPOLISAKARIDOSIS
Hurler; MPS I/α - l Iduronidase Dermatan/hep
Schele ; aran Sulfat
Hurler-
Schele
Hunter ; Iduronat Sulfatase Idem
MPS II
Santilippo Sulfamidase;α-N- Heparan Sulfat
A;MPS II AA Asetilglukosaminidase
Sabfilippo Asetil transferase Idem
B;MPS IIIB
Sanfilippo Galaktosa-6-Sulfatase Idem
C; MPS C
Morquio A; Β-galaksosidase Keratan sulfat
MPS IV A c6-SO4
Morquio B; Arilsulfatase-B Keratan Sulfat
MPS IFB
Maroteaux- Idem Dermatan
ammy; MPS Sulfat
VI
Sly; MPS Β-glukoronidase Dermatan/hep
VII aran sulfat C4-
C6-SO4
MUKOLIPIDOSIS
Siadolis/ML Sialidase/Neurraminidase Fragmen
I glikoprotein
Penyakit Sel UDP-N-asetilglukosamina; Idem
–I; ML II (glikoprotein) N-
Asetilglukosaminifosfo
transferase
Polidistrofip ML II tapi defisiensi tidak idem
seudo lengkap
Hurler; MLh
1 50
 Bone

• Bone: Type I collagen and

hidroksiapatit
• cartilago: Type II collagen and
Proteoglicans

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 The Difference Osteoclast and
osteoblast
Osteoclast Osteoblast
Multinuclear cell mononuclear cell
Stean cell: hemopoetik Prekursor mesenkim
pluripoten pluripoten
Function: Forming of bone.
Function: resorption of bone (ostoeid) and mineralisation
– arrange Ca++ dan PO4 via
membran
Have alkalifosfatase –
anorganic phosphate

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53
 Influencing Factors of
oteoclast/osteoblast

Activator of ostoeblast:
• PTH
• 1,25 dihidroksicole calciferol
• T3; T4
• hGH : IGF - 1
• PGE2
• TGFβ
• Estrogen

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Inhibitor of Osteoblast : Kortikosteroid
Activator of osteoclast :
• PTH
• 1,25 dihidroksicole calciferol
• IL-1 ; IL-6
• TNF
• TGFα
Inhibitor of Osteoclast
• Calcitonin
• Estrogen
• TGFβ
• INFα
• PGE2

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 Phatology of Genetic Metabolism of Bone and
Cartilage
Diseases:
1. Dwarfisme: Growth Hormon Deficiency .
2. Rikets ; vitamin D Deficiency (children)
3. Osteomalasia : vitamin D Deficiency (adult)
4. Hiperparatiroidism : resorption of bone
5. Osteogenesis imperfekta ; mutasi gen Col 1 A1 dan
Col 1 A2 – sinthesis and stucture of Colagen I
6. Osteoporosis : pasca menopause (>>) and induced
mutasi gen Col 1 A1 dan Col 1 A2 (<<)
7. Osteoarthistis : mutasi gen Col 1 A1 (<<)
8. Chondrodisplasia : Mutasi gen Col 2 A1
9. Sindrom Pfeifer: Mutasi gen FGFR1 (resepor
pertumbuhan fibroblas 1)
10. Sindrom Jackson – Weiss dan Crouzon ; Mutasi gen
code FGFR2
11. Achondroplasia Tanatoforik ; Mutasi gen Kode 1
FGFR3
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 Cartilage Proteins:
Protein Collagen:
Tipe II :90 – 98% artikular cartilage : 3 rantai α1 (II)
V; VI; IX; XC; XI; IX and II cross binding
XI helped arraging of diameter fiber type II

Non Collagen :
Proteoglicans ;
• Agrecan : major
• Non agrecan ; in some type of cartilage
• DS – PG I (biglican)
• DS – PG II ( decorin)
Chondronectin : binding type II at surface of cartilage,
Ancorin C II : binding type II at surface of Chondrosit.

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 Major Proteins of Bone
• Collagens:
– Type I ± 90 % total protein, 2  chains
• Non Collagen
– Plasma Protein (compound))
– Proteoglican :
• CS-PG I (Biglican) : 2 GAG chains
• CS-PG II (Dicorin) : 1 GAG chains

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• 4 % compact bone remodeling every year
and 20% trabecular bone exchange
• Process bone remodelling :
– Resorption  osteoclast
– Formationosteoblast
Bone serves as store of Calsium

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 Phatology of Genetic
Metabolism at Bone and Cartilage
Diseases :
• Osteogenesis Imperfecta : Sklera tipis, tembus,
biru  Mutasi gen Col1A1 & Col1A2  sintesa
& struktur kolagen I
• Osteoporosis : bone mass per unit volume
decrese
– pasca menopause (>>)
– Mutasi gen Col1A1 dan Col1A2 (<<)
• Osteoarthritis : CS  KS & HA , mutasi gen
Col2A1 (<<)
• Achondroplasia tanatoforik : mutasi gen kode
FGFR 3
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 MUSCULOSCELETAL SYSTEM

BIOCHEMISTRY OF MUSCLE

Dr. Syahrijuita, M.Kes

BIOCHEMISTRY DEPARTMENT
FACULTY OF MEDICINE HASANUDDIN UNIVERSITY
2009

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SUB TOPIC:
Synthesis dan Hydrolysis Ach at NMJ
Muscle Proteins
Muscle Energy Metabolism

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 Learning Objectives
• Describe structure, synthetis and
hydrolysis of Ach at NMJ
• Describe muscle proteins
• Describe muscle energy metabolism

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Stucture , synthesis dan Hydrolysis
Asetilkolin pada Neuro Muskular
Junction
 Neuro Muskular Junction or motor end-plate:
location of connected neurons and muscles

 Asetilkolin (Ach) chemical structure :

(CH3)3-N+-CH2- C2H2- O-C- CH3
II
O

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ASETILCOLIN :
•The first Neuroransmitter isolated
•Synthesis at terminal presinaps
neuron colinergic
•Storage in vescile
•Secretion by exositosis

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Stage of Synthesis and Hydrolysis Ach
at NMJ
1. Synthesis Ach in sitosol neuron terminal: seb:
Kolinasetiltransferase
Asetil-KoA + Kolin  Asetilkolin + KoA

2. Ach storage in synaptic vesicles

3. Sexcretion of Ach from vesicles to sinaps cleft
and exositosis results miniatur potensial end
plate (depolarisation)
causing voltage gated Ca2+ channels to open

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4. Ach binding receptor forward passed
membran .
Na+ influks K+ eksfluks  depolarisasi
potensial action + muscle contraction
5. Ach hydrolis after receptor channels
closed:
asetilkolinesterase
Ach + H2O  Acetat + Cholin
6 Cholin recycles to terminal neuron to
resynthesis Ach

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Clinical Manifestation : miastenia gravis = antibodi
attack Ach receptor
At NMJ : Forming autoantibodi Ach receptor

Receptor damage (lysis local) by autoantibodi

results crossbinding and endositosis

Decrese of receptor clearly

Symptoms : episodic musles weakness which
innervasion by cranial neurons.

R/: Cholinesterase Inhibitor

To increase total Ach at NMJ

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Muscle Proteins
Muscle: Biochemistry mechine influens
chemical energy to mecanical/kinetic energy
Three (3) Type of muscle :
Skeletal volunter
Cardiac striated
Smooth non striated involunter

Sarcomere is the functional contractile unit

Muscle contraction : the thick and thin filaments

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 Muscle Proteins
Striated muscle : Miosin, Aktin,
tropomiosin, troponin I, T, C,
(3 major proteins )
Smooth muscle : without Troponin

Kalmodulin

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Actin :
• BM 45.000 Dalton
•Initial synthesis as actin globular
• After binding ATP dan mol Ca2+
formed Aktin F
• Double helix supercoil

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 Minor Proteins
Tropomyosin :
molekular fibrosa
2 ß and  chains
binding at helix actin F
Troponin :
3 polypeptids
Tipe T : binding with tropomiosin
Tipe I : avoid interaction myosin – actin
Tipe C : Binding Ca2+ to start contraction
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 Myosin ~ Myosin II
• Major Protein at muscle  55 %
• BM : 460.000 Dalton
• Ta. : 3 pairs protein, 1 pairs long chains
200.000 Dalton, 2 pairs short chains
20.000 Dalton
• Secunder Structure heliks with residu prolin
• Short chains have ATPase activity 
important for muscle contraction
• Molekular heksamer asimetrik

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Miosin + Tripsin 2 Meromiosin
LMM α heliks
not ATPase activity
not binding at F-aktin
HMM Fibrosa + globular
Have ATPase activity
Binding at F-aktin

+ Papain Fragmen S1 dan S2

not ATPase activity
not binding at F-aktin

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Hydrolysis ATP movement
Cycle of Muscle contrction

H2O
Aktin ATP - Miosin
5 1
Aktin Miosin
ADP – Pi - Miosin
ATP
ATP 4 2 Aktin

Aktin - Miosin 3
Aktin-Miosin
ADP-Pi
ADP
+
P1 83
Muscle Contraction

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 Pathway of ATP Resynthesis
• Resyntesis ATP 4 methods:
1. Gliycoliysis :results piruvat and
laktat
2. Oxidative Fosforilation
3. Creatin phosphate
4. Adenilat Kinase System

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 OXIDATIVE FOSFORILATION
• Needs O2 suplay
• O2 binding by myoglobin
• Myoglobin >> red muscle
<< white muscle
• Glucosa Blood glucosa
Gliykogen endogen
Fatty Acid Tg (Adiposa)
Major substantion for aerob metabolism of
muscle 87
 Creatin Phosphat
Major Storage energy at muscle
Creatinphosphat
ATP + Creatin
(Muscle Relaksation)

Creatinkinase

Avoid faster depletion of ATP

with source to result
ATP from ADP

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 Adenilatkinase interkonvertion AMP,
ADP, ATP
Adenilatkinase katalizated 1 mol ATP & 1 mol
AMP forming from 2 mol ADP
ADP + ADP ATP + AMP
AMP + H2O IMP + NH3
IMP + H2O Adenosin + Pi
Adenosin + H2O Miosin + NH3
AMP, Pi, NH3 activated Fosfofruktokinase
(PFK-1)
Induced muscle glycolysis at sprinter. 89
Sprinter used creatin phosphate (4 – 5
second at the first) + glylcolysis anaerob
from muscle glikogen source glucosa
Marathon runner used fosforilase oksidatif
with aerob metabolism as source ATP and
Blood Glucosa and Free Fatty acid dari
trigliserida (Adiposa)

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 TUBULIN DAN DIENEIN
• Sel bukan otot : sperma Flagel/silia
bergerak sistem mikrotubulus
tubulus tubulin
• Tubulin : Protein dimer yang berbentuk tabung
berongga yang kaku.
• Dienein : Protein berupa sepasang lengan yang
terletak sepanjang mikrotubulus
• Neksin : Protein berupa pita yang elastis yang
menghubungkan tubulus ganda bagian luar

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 PERGERAKAN BIOLOGIK

Aktin – Miosin Tubulin – Dienein

- Kontraksi Otot - Debaran sillia dan
- Pergerakan amuboid flagella eukariotik
- Aliran Sitoplasma - Pergerakan kromoson
- Debar mikrovilli usus pada mitosis
- Pembelahan sel pada - Pergerakan vesikel
mitosis sekretonik

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 SPEKTRIN DAN ANKIRIN
• Keduanya membantu menentukan bentuk serta
fleksibilitas sel darah merah
• Spektrin : protein utama pada sitoskleton terdiri atas
2 polipeptida (rantai α dan β) tersusun anti paralel,
terjalin longgar berbentuk dimer dg 106 asam amino
• Ankirin : protein berbentuk piramid yang mengikat
spektrin sensitif terhadap proteolitik
• Abnormalitas spektrin eliptositosis herediter
• Abnormalitas ankirin sperositosis herediter
• Abnormalitas spektrin dan ankirin menyebabkan
anemia hemolitik
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 REFERENCES
• Harper Biochemistry
• Medical Biochemistry
• Skletal Muscle from Molecules to
Movement
• Color atlas of Biochemistry
• Biochemistry illustrated

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