By
KAUSHAL KUMAR SAHU
Assistant Professor (Ad Hoc)
Department of Biotechnology
Govt. Digvijay Autonomous P. G. College
Raj-Nandgaon ( C. G. )
Synopsis
1. Introduction
2. History
3. Endocytosis Pathways
 Clathrin mediated endocytosis
 Caveolae
 Pinocytosis
 Phagocytosis
4. RECEPTOR mediated endocytosis
i. Types of ligands
ii. Types of receptor
iii. Formation of clathrin coated vesicle
iv. Early endosome
v. Late endosome
vi. Lysosomes
5. Genetic disease
 LDL Receptor
6. Conclusion
7. References
1. Introduction
Receptor mediated endocytosis(RME)
also called clathrin dependent
endocytosis, is a process by which cells
internalize molecules(endocytosis) by the
inward budding of plasma membrane
vesicles containing protein with receptor
sites specific to the molecules being
internalized
2.History
1972- Micheal S.
Brown & Joseph L.
Goldstein delineated
the pathway of receptor
mediated endocytosis.
Endocytosis pathways
Endocytosis pathways could be subdivided into 4
catagories:
I. Clathrin mediated endocytosis
II. Caveolae
III.Pinocytosis
IV.Phagocytosis
I. Clathrin mediated endocytosis Clathrin mediated endocytosis
is mediated by small( approx. 100
nm in diameter) vesicles that have
a morphologically characteristic
crystalline coat made up of a
complex of protein.
Eg. Low density lipoprotein(LDL)
Growth factors
Antibodies
II. Caveolae
Caveolae are the most common reported non-
clathrin coated plasma membrane buds which exist
on the surface of many but not all cell types.
Caveolae are small (approx. 50 nm in diameter)
flask shape of a cave hance the name caveolae.
Eg. Adipocytes.
III. Pinocytosis:
Pinocytosis, which usually occurs from
highly ruffled region of the plasma
membrane is the invagination of the cell
membrane to form a pocket.
Size of vesicle(0.5-5 micro meter in
diameter)
IV. Phagocytosis
Phagocytosis is the process by which cells bind &
internalize particulate matter layer than around 0.75
micro meter in diameter.
Such as small sized dust particles, cell dabris,
microorganism & even apoptosis cells.
Receptor mediated endocytosis
i. Types of ligands
ii. Types of receptor
iii. Formation of clathrin coated vesicle
iv. Early endosome
v. Late endosome
vi. Lysosomes
I. Types of ligands:
 Biological molecules(Proteins, Corbohydrates,
lipids)
 Ions
 Microoganisms(Viruses, Bacteria)
Types of Receptor:
More than 20 different types of receptor
 LDL Receptor
Formation of clathrin coated vesicle:
 Clathrin is a protein plays a major role in the formation
of coated vesicles.
 Clathrin was 1st isolated & named by Barbara Pearse in
1975.
Early Endosomes:
Early endosomes are the 1st station of the
endocytic pathway.
 Vesicles up to 1 micro meter in diameter with
connected tubules of approx. 50 nm in diameter.
 Acidic pH (6.0-6.5)
Late Endosomes:
Late endosomes resive internalized material to
lysosomes, usually from early endosome in the
endocytic pathway, from the trans- Golgi
network(TGN) in the biosynthesis pathway &
from phagosomes in the phagocytic pathway.
They are acidic (Approx.pH 5.5)
Lysosomes:
Lysosomes are the last compartment of
the endocytic pathway.
They are acidic pH 4.8-5.0
They have a high content of lysosomal
membrane protein & active lysosomal
hydrolases.
Genetic disease
The Low – density of
lipoprotein or LDL
Receptor:
Cholesterol is
transpoted through the
blood stream in the
form of lipoprotein
particles, the most
common of which is
LDL.
In 1972 Michael Brown
Structure of LDL
Familial Hypercholesterolemia(FH)
FH is a genetic disease in which patients
have greatly elevated level of serum
cholesterol and suffer from heart attacks
early in life.
Michael Brown and Goldstein in1972
The Experiments:
In 1974 Brown and Goldstein
They investigated the binding of radio labeled
LDL to fibroblast from either normal individuals or
FH patients.
Increasing amount of radio active LDL bound to
normal cell as a function of incubation time.
Results:
 The cells of FH patients, failed to specifically bind radio
active LDL.
Accounting for the inability of LDL to inhibit HMG-coA
reductase (3-hydroxy-3-methyglutaryl coenzyme A
reductase)and the resultant over production of cholesterol.
Conclusion
The human spleen & liver which are
responsible for the disposal of more than
1011 aged blood cells on a daily basis.
Approx. 50% of the plasma membrane
is internalized receptor mediated
endocytosis every hour.
References :
THE CELL { A Molecular Approach, Fourth
Edition}
Geoffrey M. Copper
Robert E. Hausman
 www.ncbi.com
 www.cytochemistry.net/cellbiology

Receptor mediated endocytosis by kk

  • 1.
    By KAUSHAL KUMAR SAHU AssistantProfessor (Ad Hoc) Department of Biotechnology Govt. Digvijay Autonomous P. G. College Raj-Nandgaon ( C. G. )
  • 2.
    Synopsis 1. Introduction 2. History 3.Endocytosis Pathways  Clathrin mediated endocytosis  Caveolae  Pinocytosis  Phagocytosis 4. RECEPTOR mediated endocytosis i. Types of ligands ii. Types of receptor iii. Formation of clathrin coated vesicle iv. Early endosome v. Late endosome vi. Lysosomes 5. Genetic disease  LDL Receptor 6. Conclusion 7. References
  • 3.
    1. Introduction Receptor mediatedendocytosis(RME) also called clathrin dependent endocytosis, is a process by which cells internalize molecules(endocytosis) by the inward budding of plasma membrane vesicles containing protein with receptor sites specific to the molecules being internalized
  • 4.
    2.History 1972- Micheal S. Brown& Joseph L. Goldstein delineated the pathway of receptor mediated endocytosis.
  • 5.
    Endocytosis pathways Endocytosis pathwayscould be subdivided into 4 catagories: I. Clathrin mediated endocytosis II. Caveolae III.Pinocytosis IV.Phagocytosis I. Clathrin mediated endocytosis Clathrin mediated endocytosis is mediated by small( approx. 100 nm in diameter) vesicles that have a morphologically characteristic crystalline coat made up of a complex of protein. Eg. Low density lipoprotein(LDL) Growth factors Antibodies
  • 6.
    II. Caveolae Caveolae arethe most common reported non- clathrin coated plasma membrane buds which exist on the surface of many but not all cell types. Caveolae are small (approx. 50 nm in diameter) flask shape of a cave hance the name caveolae. Eg. Adipocytes.
  • 7.
    III. Pinocytosis: Pinocytosis, whichusually occurs from highly ruffled region of the plasma membrane is the invagination of the cell membrane to form a pocket. Size of vesicle(0.5-5 micro meter in diameter)
  • 8.
    IV. Phagocytosis Phagocytosis isthe process by which cells bind & internalize particulate matter layer than around 0.75 micro meter in diameter. Such as small sized dust particles, cell dabris, microorganism & even apoptosis cells.
  • 9.
    Receptor mediated endocytosis i.Types of ligands ii. Types of receptor iii. Formation of clathrin coated vesicle iv. Early endosome v. Late endosome vi. Lysosomes I. Types of ligands:  Biological molecules(Proteins, Corbohydrates, lipids)  Ions  Microoganisms(Viruses, Bacteria)
  • 10.
    Types of Receptor: Morethan 20 different types of receptor  LDL Receptor Formation of clathrin coated vesicle:  Clathrin is a protein plays a major role in the formation of coated vesicles.  Clathrin was 1st isolated & named by Barbara Pearse in 1975.
  • 12.
    Early Endosomes: Early endosomesare the 1st station of the endocytic pathway.  Vesicles up to 1 micro meter in diameter with connected tubules of approx. 50 nm in diameter.  Acidic pH (6.0-6.5) Late Endosomes: Late endosomes resive internalized material to lysosomes, usually from early endosome in the endocytic pathway, from the trans- Golgi network(TGN) in the biosynthesis pathway & from phagosomes in the phagocytic pathway. They are acidic (Approx.pH 5.5)
  • 13.
    Lysosomes: Lysosomes are thelast compartment of the endocytic pathway. They are acidic pH 4.8-5.0 They have a high content of lysosomal membrane protein & active lysosomal hydrolases.
  • 14.
    Genetic disease The Low– density of lipoprotein or LDL Receptor: Cholesterol is transpoted through the blood stream in the form of lipoprotein particles, the most common of which is LDL. In 1972 Michael Brown Structure of LDL
  • 15.
    Familial Hypercholesterolemia(FH) FH isa genetic disease in which patients have greatly elevated level of serum cholesterol and suffer from heart attacks early in life. Michael Brown and Goldstein in1972 The Experiments: In 1974 Brown and Goldstein They investigated the binding of radio labeled LDL to fibroblast from either normal individuals or FH patients. Increasing amount of radio active LDL bound to normal cell as a function of incubation time.
  • 17.
    Results:  The cellsof FH patients, failed to specifically bind radio active LDL. Accounting for the inability of LDL to inhibit HMG-coA reductase (3-hydroxy-3-methyglutaryl coenzyme A reductase)and the resultant over production of cholesterol.
  • 18.
    Conclusion The human spleen& liver which are responsible for the disposal of more than 1011 aged blood cells on a daily basis. Approx. 50% of the plasma membrane is internalized receptor mediated endocytosis every hour.
  • 19.
    References : THE CELL{ A Molecular Approach, Fourth Edition} Geoffrey M. Copper Robert E. Hausman  www.ncbi.com  www.cytochemistry.net/cellbiology