This document summarizes a lecture on cell physiology, specifically cell signaling. It discusses the main types of cell signaling including autocrine, paracrine, and endocrine signaling. It also describes the basic process of cell signaling, including ligand binding to a receptor which causes a conformational change and activation of the receptor, leading to a response in the target cell. Finally, it discusses the main classes of receptors, including intracellular receptors and cell surface receptors, providing examples of each type.

1. BASIM ZWAIN LECTURES
MEDICAL PHYSIOLOGY
CELL PHYSIOLOGY - 2
Professor Dr. Basim Zwain
Faculty of Medicine
Jabir ibn Hayyan Medical University
basimzwain@jmu.edu.iq

2. CELL PHYSIOLOGY
Types of Cell Signaling
1. Autocrine signaling – e.g. cytokine
interleukin-1 in monocytes
2. Paracrine and juxtacrine signaling- e.g
fibroblast growth factors
3. Endocrine signaling (various hormones)

3. CELL PHYSIOLOGY

4. CELL PHYSIOLOGY
Cell Signaling Events
A ligand or primary messenger binds a
receptor associated with a target cell.
Ligand binding results in conformational
change and activation of the receptor.
The activated receptor elicits a response in
target cell, either directly or indirectly through
production of second messenger.
Target cell responses include alterations in
cellular metabolism and in gene transcription.

5. CELL PHYSIOLOGY
Types of Receptor Classes
1. Intracellular receptors located in the
cytoplasm or nucleus of the target cell
1. Cell surface receptors

6. CELL PHYSIOLOGY
Intracellular receptors are bound by lipophilic
ligands, which diffuse through plasma membrane.
Ligand binding alters the receptor’s conformation,
exposing the receptor’s DNA-binding domain.
Receptors bind specific gene promoter elements and
activate transcription of specific genes that results in
the synthesis of specific proteins.
An example is estrogen receptor in uterine smooth
muscle cells.

7. CELL PHYSIOLOGY
There are four types of cell surface receptors:
a. Nicotinic cholinergic receptors are linked to ligand-gated
ion channels (eg, nicotinic AchRs).
b. Catalytic receptors are transmembrane proteins
that have intrinsic enzymatic (eg, serine or tyrosine
kinase) activity.
c. Other receptors are linked to proteins with
enzymatic activity. (eg, cytokine receptor signaling
through cytoplasmic tyrosine kinase).
d. G-protein-linked receptors

8. CELL PHYSIOLOGY
G-protein-linked receptors have an extracellular
ligand-binding domain and an intracellular domain
that binds G-proteins. After ligand binding, receptors
interact with G-proteins which are heterodimeric
consist of α, β, and γ subunits that dissociate. G-proteins
α-subunits bound to GTP interact with and
activate specific membrane-bound enzymes, result in
production of 2nd messengers that elicit responses
in target cells. Adenylate cyclase & phospholipase
systems are examples.

9. CELL PHYSIOLOGY
CLINICAL CONSIDERATIONS
–Cholera toxin alters G-protein so that guanosine
triphosphatase (GTPase) is unable to hydrolyze GTP,
resulting in increased production of cAMP. Elevated
cAMP in intestinal epithelial cells results in massive
gut secretion of water and electrolytes, resulting in
severe diarrhea and dehydration.
–Pseudohypoparathyroidism results from a defective
G-protein causes decreased cAMP levels with
symptoms of hypoparathyroidism with normal or
slightly elevated parathyroid hormone levels.

10. CELL PHYSIOLOGY
CLINICAL CONSIDERATIONS
–Pertussis toxin blocks the activity of G1,
allowing adenylate cyclase to stay active
and increase cAMP.