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Flashcards in Membranes and Transport Deck (26):


Glycerol backbone with a phosphate group and two fatty acids esterified to backbone.

E.g. Phosphatidylcholine (outer), phosphatidylserine (inner), phosphatidylinositol (inner)



Sphingosine backbone, with a long chain fatty acid and phosphorylcholine.

E.g. Sphingomyelin - most common SL present in OUTER leaflet



Sphingosine backbone with carbohydrate residue (instead of phosphorylcholine like on sphingomyelin).

Found in OUTER leaflet of the lipid bilayer.



Embedded in lipid bilayer. Steroid nucleus with:
(1) hydroxyl group and
(2) hydrocarbon side-chain - interacts with hydrophobic tails of membrane


Phosphotidylserine (PS)

Glycerophospholipid on INNER leaflet.

Used as a marker for cell apoptosis.
-healthy cells have PS on inner leaflet
-apoptotic cells display PS on outer leaflet
-Serves as tag/label for apoptotic cells
-Dying cells recognized and phagocytically removed


Niemann-Pick Disease

Deficiency: Defective Acid Sphingomyelinase enzyme (A-SMase)

A-SMase: lysosomal enzyme that breaks down sphingomyelin (SM)
-SM accumulates in lysosomes of liver, spleen, CNS, bone marrow
-Hepatomegaly, splenomegaly and Neuro damage


Integral membrane proteins

Firmly EMBEDDED in the membrane, stabilized by hydrophobic interactions with lipids.

-Polytopic Transmembrane proteins
>Integral mem proteins spanning entire lipid bilayer, contact both internal/external environment several times
>Transporters, ion channels and receptors


Peripheral Proteins

LOOSELY BOUND to membrane via electrostatic interactions with lipids or proteins.


Lipid-anchored proteins

TETHERED to membranes via covalent attachment to a lipid



Carbohydrate shell on outer-membrane of cell due to presence of glycolipids and glycosylated proteins.
-Protects membrane from injury/degradation
-enables better contact with other cells (good in tissue formation)
-Allows body to differentiate healthy cells from foreign/diseased cells.


ABO Blood system

RBCs have carbohydrate antigens on surface. Blood transfer must be compatible: cross match ABO type.

Incompatible transfusion: acute hemolysis, renal failure, shock

Type A —> Contains Anti-B
Type B —> Contains Anti-A
Type A/B —> No antibodies in plasma (Universal acceptor)
Type O —> Contains Anti-A and Anti-B (Universal donor)


Rh antigen

Protein antigen on RBCs. Must be cross matched for compatibility in transfusion.

“D antigen” known as Rh factor - inherited in autosomal dominant fashion.

Rh+ individuals express D antigen. Rh- do not.


Erythroblastosis fetalis

Disease in which blood of mother and fetus is incompatible because mother is Rh- and fetus is Rh+.

Mother produces antibodies to the Rh factor of the fetus during pregnancy. Antibodies can cross placenta and attack fetus - risk greater in subsequent pregnancies.


Factors that influence membrane fluidity

(1) Temperature
-Tm = Temp which membrane switch from fluid to rigid
-TTm, optimal fluidity
-T>>>Tm, membrane too fluid

(2) Lipid composition
-Saturated v unsaturated Fatty acids
-Higher saturated fatty acids = tighter packing = reduced mobility
-Higher unsaturated FA = kinks, loose packing = increased fluidity

(3) Cholesterol
-cholesterol in rigid membrane = increases fluidity (intercalates in FAs preventing close packing)
-cholesterol in fluid membrane = reduces fluidity (fills in gaps from kinks)


Spur Cell Anemia

Condition of elevated cholesterol. Too much cholesterol in the RBC membranes makes them rigid, reduced fluidity/flexibility. When trying to squeeze past small capillaries, their membranes lyes.


Intracellular and Extracellular Ions

Intracellular: K+

Extracellular: Na+ , Cl- , Ca2+


Simple Diffusion vs Facilitated Diffusion

Simple Diffusion:
-small, non-polar and uncharged polar molecules diffuse across membrane (O2, N2, benzene, etc.)

Facilitated Diffusion:
-Needs transmembrane protein assistance
-Large and charged molecules (unable to cross membrane alone - Na+, Cl- , Glucose, etc.)
-Protein: ion channel or transporter



Increase in membrane potential due to influx of positively charged ions - triggers opening of voltage-gated ion channels.

E.g Sodium channel



Toxin that can block ion channels (Na+/K+ ATPase)

Used by puffer fish for defense


Primary vs Secondary Active Transport

Primary: Uses ATP directly
- P type ATPases: ATP is hydrolyzed and protein gets phosphorylated on a conserved aspartate residue (Na+/K+ ATPase)
-ABC transporters: ATP is hydrolyzed, but does NOT phosphorylation transporter (P glycoproteins)

Secondary: Use energy stored. In concentration gradient to move another molecule against its concentration gradient (E.g. SGLT, NCX)


Sodium-Glucose Transporter 1

Secondary active transporter in epithelial cells of small intestine and renal tubules.

Moves Na+ and glucose unilaterally from intestinal lumen to blood
Or from blood/urine to renal tubule.

Na+ moves downhill, providing energy for glucose to move uphill.
Na+ gradient resent by Na+/K+ ATPase

Inhibit SGLT and more glucose will be lost through urine - blood sugar goes down and increased urine output lowers blood pressure



Na+/Ca2+ Exchanger.

Antiporter maintaining low levels of intracellular calcium.
Imports 3 Na+ down concentration gradient and 1 Ca2+ uphill.


Cystic Fibrosis

Deficiency: Mutation in CFTR gene (cystic fibrosis transmembrane conductance regulator). Autosomal recessive disorder.

In the airway, Cl- cannot EXIT the cells and builds up intracellularly. Na+ enters to offset negative charge build up. Water then follows for osmotic compensation, thus dehydrating the surface mucous in the airway. Mucous becomes thick, breathing becomes difficult and leaves airways susceptible to bacterial infection.

In sweat glands, Cl- cannot ENTER the cell.



Defect in the TRANSPORT responsible for uptake of dimeric AA Cystine, and other dibasic AAs Arg, Lys and Ornithine. Autosomal Recessive disorder.

Cystine, which forms a dimmer with disulfide bonds, is not absorbed and thus builds up in the kidneys, forming Cystine crystals (kidney stones).

Manifests as “renal cholic” = abdominal pain that comes in waves and linked to kidney stones


Hartnup Disease

Defect in TRANSPORT of non-polar/neutral AAs: Ala, Val, Thr, Leu and most importantly, Tryptophan.

Transporter primarily in kidneys and intestine.

Trp is a precursor for serotonin, melatonin and niacin (vitamin precursor for NAD+).

Manifests in infancy as failure to thrive. Clinical findings: ataxia, nystagmus, tremor, photodermatitis and photosensitivity.


Cardiotonic Drugs

Cardiac glycosides ouabain and digoxin are contraction-inducing drugs. Used in congestive heart failure.

They inhibit Na+/K+ ATPase on cardiac myocytes (heart muscle cells). Leads to increase in intracellular Na+ —> leads to increase of Ca2+ due to NCX slowing down. Increased sarcoplasmic Ca2+ = stronger contraction of heart muscle per action potential.