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Function Of Human Body > Ahmad Lectures > Flashcards

Ahmad Lectures Flashcards

0
Q

Emx2

A

Open-lip Schizencephaly (cleft-lined with gray matter, connecting subarachnoid space with the ventricular system)

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1
Q

Otx2

A

Mutation causes microophthalmia or aniridia

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2
Q

Wnt

A

Presence of Wnt allow for target genes to be activated and B-catenine to be produced

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3
Q

Wnt1 & FGF8

A

Secreted by the isthmus and cause activation of engrailed (En) transciption factors

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4
Q

Engrailed Genes

A

Activated via Wnt1 and FGF8; cause differentitation of mid brain stem cells

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5
Q

Hox Genes

A
  1. Are regulated by concentration of retinoic acid (increases concentration in posterior end
  2. They regulate the motor neuron identity in the hindbrain
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6
Q

SHH (sonic hedgehog) Genes

A
  1. SHH (released from the notochord and floor plate) binds to Patched (PTC) which causes it to be inhibited so Smoothened (SMO) can activate Gli to activate gene expression
  2. Mainly turns stem cells of the ventral surface into motor neurons
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7
Q

BMP

A
  1. Released by surface ectoderm and the roof plate

2. Turns stem cells of the dorsal surface into sensory neurons

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8
Q

RA/FGF Factors

A

Required to help motor and interneuron differentiation

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9
Q

Chordin/Nogin

A

Needed to suppress the dorsalizing effects of BMP in the ventral part of the neural tube

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10
Q

Notch Receptor

A

Causes Gene Repression - heterodimeric receptor in the plasma membrane (are 4 types; Neurogenesis uses Notch 1)

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11
Q

Delta & Serrate (Jagged)

A

Ligands that bind to the Notch receptor, causes the cells to remain uncommitted due to inhibition of proneural genes

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12
Q

Proneural Genes

A
  1. Helps the cell differentiate into a different cell

2. Inhibited by Notch receptor binding to Delta and Serrate (Jagged)

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13
Q

Retinal Ganglion Cells

A

Take visual field information out of the eye to the brain

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14
Q

PDGF

A
  1. Platelet derived growth factor produce in utero that differentiates Type 1 Astrocytes into O2A Progenitor cells
  2. Cells lose the response to PDGF after birth
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15
Q

CNTF

A
  1. Produced by Type 1 Astrocytes after birth, help differentiate O2A progenitor cells into Type 2 Astrocytes with the help of ECM factors from mesodermal cells
  2. Also can be used to rescue neurons from death/is an important neurotrphic factor
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16
Q

Oligodendrocyte Development

A

Type 1 Astrocyte > PDGF > O2A Progenitor > No CNFT > Oligodendrocytes

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17
Q

Type 2 Astrocyte Development

A

Type 1 Astrocyte > PDGF > O2A Progenitor > CNTF & ECM factor > Type 2 Astrocyte

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18
Q

Filopodia

A

Slender motile extensions that sample the environment and then either extend or retract

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19
Q

Lamellipodia

A

Spaces between the filopodia

20
Q

Laminin

A

Major component of the basal lamina and are responsible for the growth promoting ability of the ECM…will bind to integrin

21
Q

Integrin

A

Are receptors on growth cones that will bind to laminin and cause cytoskeletal rearrangement that propel the filopodia

22
Q

Cadherin

A
  1. A group of cell adhesion molecules that promote calcium dependent cell adhesion
  2. Mediates stronger cell adhesion needed for tissue histogenesis and integrity…without it, fetuses will die
23
Q

Catenin

A

Link cadherin molecules to the cytoplasm

24
Q

IgG-Like Adhesion molecules

A
  1. A group of cell adhesion molecules that promote calcium independent cell adhesion.
  2. Important in fine tuning the adhesion and growth processes…loss is a mild phenotype
25
Q

Slit Genes

A

Expressed on midline cells in the brain and repel any axons possessing the Robo receptor

26
Q

Robo (roundabout) Receptors

A

Axons with these receptors will not be able to cross the midline because they are repelling by the Slit ligands on the midline cells

27
Q

Robo3

A

Anti-Robo that down-regulates Robo1/Robo2 which allows an axon to cross midline

28
Q

Netrin

A
  1. A glycoprotein that is drawn to a DCC receptor and attracts axons from dorsally located commissural neurons toward the midline in the floor plate
  2. Also can mediate repulsion if DCC and UNC-5 receptors are expressed at the same time on the same axon
29
Q

UNC-6

A
  1. A homologous gene to Netrin in c. elegans

2. A mutation in this gene causes uncoordination because it prevents axons from reaching and/or crossing midline

30
Q

Semaphorin

A

Are secreted (long-range) and membrane bound (short-range) ligands that cause the collapse of growth cones

31
Q

Ephrin A

A

Membrane-bound ligand tethered to glycosyl-phosphatidyl-inositol (GPI) and interacts with EphA causing a repulsion

32
Q

Ephrine B

A

Transmembrane ligand that interacts with EphB causing a repulsion

33
Q

Eph Receptors

A

A receptors that binds Ephrin…causes a repulsion and prevents midline crossing and helps determine where in the axons of the RGC terminate in teh tectum (superior colliculus)

34
Q

NGF or trkA

A

2 nerve growth factors in the Neurotrophin class that if absent would result in the absence of sympathetic ganglia

35
Q

NT3

A

A nerve growth factor in the Neurotrophin class that if absent would result in a reduced number of sympathetic ganglia

36
Q

Bcl-2 and Bcl-xl

A

Anti-apoptotic, found in mitochondria, ER, and perinuclear membrane, will promote the survival of sympathetic neurons in the absence of NGF and inhibit Bas and Bad

37
Q

Bax and Bad

A
  1. Pro-apoptotic factors, induced by withdrawal of NGF of injury
  2. Will cause the release of cytochromme C which will then go on to activate caspase 9
38
Q

DP5/Hrk

A
  1. Induced by NGF-deprivation, oxidative stress, or an increase in calcium
  2. Helps activate Bas by translocating Bas from the cytosol into the mitochondria where it can cause the release of cytochrome C which will activate caspase 9
39
Q

Cytochrome C

A

A soluble electron transport protein (a strong pro-apototic signal) that activates caspase 9 leading to PCD

40
Q

Par4

A
  1. An essential pro-apoptotic element in the developmental and pathological neural death, particularly in Alzheimer’s disease
  2. Activated by oxidative stress and an increase in calcium conceentration and induces mitochondrial dysfunction by inhibiting Bcl-2
41
Q

Apaf2

A
  1. Helps to transmit apoptotic signals (cytochrome C) from the dysfunctional mitochondria to activate caspases
  2. Forms a complex with cytochrome C and active Caspase 9 (this is an energy dependent step that requires ATP)
42
Q

Caspases

A
  1. Cysteine proteases that activate each other in a cascade in response to apoptotic signals
  2. They cause DNA damage by activating DNase and by cleaving poly-ADP-ribose-polymerase (PARP), a DNA repair enzyme
43
Q

IAPs

A

Critical regulator of PCD as they influence both extrinsic and intrinsic PCD pathways by inhibiting caspases

44
Q

X-IPA & Survivin

A

Best known IAPs

45
Q

Mn-SOD

A
  1. A key anti-oxidant enzyme that protects cells from apoptosis by inhibiting the formation of reactive oxygen species (= oxidative stress)
  2. Oxidative stress activates DP5/Hrk and Par4
46
Q

Telomerase

A
  1. An enzyme that adds 6-base DNA sequences to the ends of the chromosomes, preventing their shortening and protecting them during chromosomal segregation in mitotic cells (increased resistance of neurons to apoptosis)
47
Q

NF-kB

A
  1. A transcriptional factor that if we lost, would cause neuronal cell death
  2. Plays an important role in suppressing PCD by up-regulating the expression of anti-apoptotic proteins, Bcl-2, IAPs and Mn-SOD
48
Q

Phases of PCD:

A
  1. Survival Phase
  2. Initiation Phase
  3. Effector Phase
  4. Degradation Phase

Function Of Human Body (5 decks)

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