Final Bio 1A Lec 29

Front 1

[steroids] when receptor binds to DNA it's called a "___"

Back 1

sequence specific interaction

Front 2

the steroid binding site on the DNA is called ____

Back 2

Hormone Response Element (HRE)

Front 3

Glucocorticoid receptor react w/

Back 3

glucocorticoid response element (GRE)

**it has a speicific seq. on the DNA that it interact w/.

Front 4

Estrogen Receptor binds to

Back 4

Estrogen response element

Front 5

According to the Gel shift assay experiment for DNA binding the result shows that Progestones, androgens, mineralcorticoid, and glucocorticoid binds to the same DNA. So what detates specificity?

Back 5

**Even they bind to the same DNA, steroid binding is diff.

**protein interactions--- target gene is different---> each have a diff transcription factor and each receptors interact w/ diff. kind of trancription factor.

**thus can have commun featurs, but diff. specificity

Front 6

the 3 steroid receptor function domain are important and there are disease that relate to it. For example Androgen Insensitivity. what is that?

Back 6

Mutations in the androgen receptor (AR) or in the functional domains.

Front 7

what happen when the AR prevents expression or function?

Back 7

the XY individual can not properly respond to the testosterone, and locks female on the outside (still have male organs inside the body)

Front 8

So where does the mutations occure in Androgen insensitivity?

Back 8

**one is the promoter-- which alters the expression.
**Defects in any of the three domain (steroid, protien, and DNA binding) indicates how severe it its.

**point is structure function is important

Front 9

[GLUCOSE HOMEOSTASIS] give the pathway of high glucose level

Back 9

high glucose level---> stimulate Beta- Islet cells of the pancreas--->produce insulin--->binds to receptors in the liver--->response = store glucouse and transport glucouse ---> produce glycosidic--> result reduce blood glucouse

Front 10

[GLUCOSE HOMEOSTASIS] give the pathway for low blood glucouse

Back 10

low blood glucose---> stimulates the alpa-slet cells (pancreas)--> produce glucagon---> glucagon binds to receptors in liver--->produce glucose---> incr. blood glucose

Front 11

why is CAMP very important?

Back 11

b/c its a secondary messenger
1. mediates the response
2. timing occurs prior to the response itself

Front 12

where do you produce CAMP?

Back 12

Adenylate cyclase

Front 13

CAMP bindto PKA through and enzyme called ______

Back 13

phosphodiesterase

Front 14

phosphodiesterase brake CAMP to _____

Back 14

5'--AMP (not good inactive product)

Front 15

____ inhibits phosphodiesterase

Back 15

caffeine

Front 16

there are two types of phosphodiester? what are they?

Back 16

1. one know down CAMP
2. Knock down CGMP ---> to 5'GMP

Front 17

What patthway does viagra block?

Back 17

Know down CGMP to 5'GMP

GTC--> CGMP --> 5' GMP

**isntead of lowering blood pressure, viagra keeps erection on longer inhibitiong Phosphodiester from breaking down CGMP

Front 18

What happens if CGMP goes on for a long time?

Back 18

you get blindness b/c the pathway of CGMP is in the rod cone of your eyes

Front 19

[REPRODUCTION] reproductive glands/organ is called

Back 19

gonads

*testes and ovaries

Front 20

what is the roles of gonads

Back 20

**produce gametes
**produce the reproductive steroids hormones

Front 21

male produce what kind of reproductive steroids hormones?

Back 21

testosterone

Front 22

female produce what kind of reproductive steroids hormones?

Back 22

dihyrotestosterone (DHT), estrogen, and progesterone

Front 23

[MALE REPROD.] spermatogenesis occurs in the testes and this is called the ______

Back 23

seminiferous tubules

Front 24

in the seminiferous tubules there are many cell types. What are they?

Back 24

**spermatocenic cells
**accessory cells
--leydig cells
--sertoli cells

Front 25

leydig cells converts ____ to ____

Back 25

cholesterol to testosterone

Front 26

sertoli cells convert ___ to ____

Back 26

testosterone to DHT

Front 27

______ goes through the bridge

Back 27

1st spermatocytes

Front 28

On the other side of the bridge 1st spermatocyes undergoes _____

Back 28

mieotic division

Front 29

spermatogenesis is continous b/c of _____

Back 29

feedback negative (the ability to keep a process in a constant level)

Front 30

spermatozao get transported from the seminiferous and to to the ____ where it stays there for _____ days to mature

Back 30

epididymous
20 days (can move)

Front 31

Epididymous is a multple/single duct?

Back 31

single

Front 32

seminiferous tubules is a single/multiple duct?

Back 32

multiple

Front 33

In the ejaculatory duct there are several glands connected to it (seminal vessicle, prostate gland, bolbaurethral gland) together they help____

Back 33

provide enzymes for fertilization and movement

**PH, suger (energy), ect

Front 34

what is erection?

Back 34

a vascular process due to arterial dilation nerve input

Front 35

the erection process if controlled by Homone like _____

Back 35

gas nitric oxide (NO)

Front 36

NO regulates what

Back 36

regulates GTP (convert GTP to CGMP)

Front 37

Insulin and Glucagon are different. what is the differences?

Back 37

**Glucagon
-raise blood sugar

**Insulin
-reduce blood sugar

**both are the negative feedback regulators

Front 38

[More details of Insulin and Glugogen] Inulin is part of a _____ pathway and its receptor is called ____

Back 38

generalize pathwath

Single Pass Transmembrane Receptor

Front 39

How does insulin work?

Back 39

Receptors (inactive, sits on the PM) have an enzyme (tyrosine kinase) in the Enoplasmic domain---> Insuline Hormone (IS) comes in and bind to receptor---> dimerize--> causes a change in R (b/f R move "free lateral diffusion; after hormones bind R has affinity for each other)---> activates the Tyrosine Kinase (its substrate is the other dimerize R molecules)---> R becomes phosphoralated---> allows the binding of signaling molecules---> response

Front 40

Defects of tyrosin kinase or the insulin receptor can lead to

Back 40

diabetic states

Front 41

Insulin receptors also have substrates called IRS- 1. In this case IRS-1 get ______ and interact w/ _________ and lead to a response

Back 41

phosphoralated

cell signalling molecules

Front 42

What is the differences b/w IRS-1 and insulin receptors?

Back 42

the active tyrosin kinase phosphoralate itself across the receptors and phosphoralted IRS-1 cause a response---> becomes a platform for cell molecules signaling binding

**have differen site of phophorlation

Front 43

[study this right after Glucouse path way] Glucose on the other hand is different from insulin b/c _____

Back 43

it interacts w/ a G-protein (in GDP form). and upon binding there's a GDP to GTP exchange.

Front 44

The GTP move across and disociate from the recptor and binds to an enzyme called

Back 44

Adenylate cyclase

Front 45

Adenylate cyclase converts ATP to ____

Back 45

CAMP

Front 46

when you are hungry this pathway of CAMP (part of glucose pathway) is activated. CAMP is also involved in _____

Back 46

water retention

**Cholera toxins
*keeping G protein in the active form making a lot of CAMP---> threfore you can't retain water