Hello and welcome to my sandbox!
A definition and general explanation of missense mutation.
Examples of possible mutations that are caused by altering the genetic code:
Relationships with suppressors and other mutations:
Missense mutation with a related genetic code table (the focused is on mammals).
Examples of genetic diseases resulting from missense mutations (and perhaps possible therapies):
References/See Also
/ Mhk5600 ( talk) 20:47, 13 March 2013 (UTC)
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/ Mhk5600 ( talk) 16:28, 12 March 2013 (UTC)
Amino-acid biochemical properties | Nonpolar | Polar | Basic | Acidic | Termination: stop codon |
1st base |
2nd base | 3rd base | |||||||
---|---|---|---|---|---|---|---|---|---|
U | C | A | G | ||||||
U | UUU | (Phe/F) Phenylalanine | UCU | (Ser/S) Serine | UAU | (Tyr/Y) Tyrosine | UGU | (Cys/C) Cysteine | U |
UUC | UCC | UAC | UGC | C | |||||
UUA | (Leu/L) Leucine | UCA | UAA | Stop (Ochre) [B] | UGA | Stop (Opal) [B] | A | ||
UUG [A] | UCG | UAG | Stop (Amber) [B] | UGG | (Trp/W) Tryptophan | G | |||
C | CUU | CCU | (Pro/P) Proline | CAU | (His/H) Histidine | CGU | (Arg/R) Arginine | U | |
CUC | CCC | CAC | CGC | C | |||||
CUA | CCA | CAA | (Gln/Q) Glutamine | CGA | A | ||||
CUG | CCG | CAG | CGG | G | |||||
A | AUU | (Ile/I) Isoleucine | ACU | (Thr/T) Threonine | AAU | (Asn/N) Asparagine | AGU | (Ser/S) Serine | U |
AUC | ACC | AAC | AGC | C | |||||
AUA | ACA | AAA | (Lys/K) Lysine | AGA | (Arg/R) Arginine | A | |||
AUG [A] | (Met/M) Methionine | ACG | AAG | AGG | G | ||||
G | GUU | (Val/V) Valine | GCU | (Ala/A) Alanine | GAU | (Asp/D) Aspartic acid | GGU | (Gly/G) Glycine | U |
GUC | GCC | GAC | GGC | C | |||||
GUA | GCA | GAA | (Glu/E) Glutamic acid | GGA | A | ||||
GUG [A] | GCG | GAG | GGG | G |
Amino acid | DNA codons | Compressed | Amino acid | DNA codons | Compressed | |
---|---|---|---|---|---|---|
Ala, A | GCU, GCC, GCA, GCG | GCN | Ile, I | AUU, AUC, AUA | AUH | |
Arg, R | CGU, CGC, CGA, CGG; AGA, AGG | CGN, AGR; or CGY, MGR |
Leu, L | CUU, CUC, CUA, CUG; UUA, UUG | CUN, UUR; or CUY, YUR | |
Asn, N | AAU, AAC | AAY | Lys, K | AAA, AAG | AAR | |
Asp, D | GAU, GAC | GAY | Met, M | AUG | ||
Asn or Asp, B | AAU, AAC; GAU, GAC | RAY | Phe, F | UUU, UUC | UUY | |
Cys, C | UGU, UGC | UGY | Pro, P | CCU, CCC, CCA, CCG | CCN | |
Gln, Q | CAA, CAG | CAR | Ser, S | UCU, UCC, UCA, UCG; AGU, AGC | UCN, AGY | |
Glu, E | GAA, GAG | GAR | Thr, T | ACU, ACC, ACA, ACG | ACN | |
Gln or Glu, Z | CAA, CAG; GAA, GAG | SAR | Trp, W | UGG | ||
Gly, G | GGU, GGC, GGA, GGG | GGN | Tyr, Y | UAU, UAC | UAY | |
His, H | CAU, CAC | CAY | Val, V | GUU, GUC, GUA, GUG | GUN | |
START | AUG, CUG, UUG | HUG | STOP | UAA, UGA, UAG | URA, UAR |
The title of my first PubMed article is: Acute depletion of plasma membrane phosphatidylinositol 4,5-bisphosphate impairs specific steps in endocytosis of the G-protein-coupled receptor. [6]
The primary goals were to investigate the role and importance of Phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P(2)] in the plasma membrane on the endocytic process of GPCRs and to determine whether depleting PtdIns(4,5)P(2) would disrupt this process. [6] Three different GPCRs were studied including: luciferase-labeled type 1 angiotensin II (AT1R), type 2C serotonin (5HT2CR) and β(2) adrenergic (β2AR) receptors. The authors found that when they depleted PtdIns(4,5)P(2), there was generally a significant inhibition in the number of GPCRs in early endosomes. [6] This study confirmed that GPCRs rely on PtdIns(4,5)P(2) in their endocytic pathways. Delivery of one of the GPCRs to early endosomes for example was completely stopped when PtdIns(4,5)P(2) was depleted. [6]
The title of my second PubMed article is: MCAK activity at microtubule tips regulates spindle microtubule length to promote robust kinetochore attachment. [7]
The main goal of this study was to see if MCAK’s (mitotic centromere-associated kinesin) effect on dynamic microtubule plus ends is the reason shorter spindles are observed during meiotic spindle assembly when MCAK levels are raised. The authors tested this in human mitotic cells by depleting MCAK levels using siRNA and then observing the spindle assembly in the cells. [7] The authors found that the tip-tracking activity for MCAK was played an important role in stopping the centrosomes from separating when bipolar spindles were being assembled. The significance of this was clarified when the authors also monitored kinetochore attachment. [7] It turned out that when cells were lacking MCAK, the spindle fibers that were made had “excessively” long microtubules that were not kinetochore related. [7]
{{
cite journal}}
: Explicit use of et al. in: |author=
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help)CS1 maint: date and year (
link) CS1 maint: multiple names: authors list (
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{{
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: CS1 maint: date and year (
link) CS1 maint: multiple names: authors list (
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Hello and welcome to my sandbox!
A definition and general explanation of missense mutation.
Examples of possible mutations that are caused by altering the genetic code:
Relationships with suppressors and other mutations:
Missense mutation with a related genetic code table (the focused is on mammals).
Examples of genetic diseases resulting from missense mutations (and perhaps possible therapies):
References/See Also
/ Mhk5600 ( talk) 20:47, 13 March 2013 (UTC)
{{
cite journal}}
: Explicit use of et al. in: |author=
(
help)CS1 maint: date and year (
link) CS1 maint: multiple names: authors list (
link){{
cite journal}}
: CS1 maint: date and year (
link){{
cite journal}}
: CS1 maint: date and year (
link)
{{
cite journal}}
: Explicit use of et al. in: |author=
(
help)CS1 maint: date and year (
link) CS1 maint: multiple names: authors list (
link)
{{
cite journal}}
: CS1 maint: date and year (
link)
{{
cite journal}}
: CS1 maint: date and year (
link)
{{
cite journal}}
: CS1 maint: date and year (
link)
{{
cite journal}}
: CS1 maint: multiple names: authors list (
link) CS1 maint: unflagged free DOI (
link)
{{
cite journal}}
: CS1 maint: multiple names: authors list (
link) CS1 maint: unflagged free DOI (
link)
/ Mhk5600 ( talk) 16:28, 12 March 2013 (UTC)
Amino-acid biochemical properties | Nonpolar | Polar | Basic | Acidic | Termination: stop codon |
1st base |
2nd base | 3rd base | |||||||
---|---|---|---|---|---|---|---|---|---|
U | C | A | G | ||||||
U | UUU | (Phe/F) Phenylalanine | UCU | (Ser/S) Serine | UAU | (Tyr/Y) Tyrosine | UGU | (Cys/C) Cysteine | U |
UUC | UCC | UAC | UGC | C | |||||
UUA | (Leu/L) Leucine | UCA | UAA | Stop (Ochre) [B] | UGA | Stop (Opal) [B] | A | ||
UUG [A] | UCG | UAG | Stop (Amber) [B] | UGG | (Trp/W) Tryptophan | G | |||
C | CUU | CCU | (Pro/P) Proline | CAU | (His/H) Histidine | CGU | (Arg/R) Arginine | U | |
CUC | CCC | CAC | CGC | C | |||||
CUA | CCA | CAA | (Gln/Q) Glutamine | CGA | A | ||||
CUG | CCG | CAG | CGG | G | |||||
A | AUU | (Ile/I) Isoleucine | ACU | (Thr/T) Threonine | AAU | (Asn/N) Asparagine | AGU | (Ser/S) Serine | U |
AUC | ACC | AAC | AGC | C | |||||
AUA | ACA | AAA | (Lys/K) Lysine | AGA | (Arg/R) Arginine | A | |||
AUG [A] | (Met/M) Methionine | ACG | AAG | AGG | G | ||||
G | GUU | (Val/V) Valine | GCU | (Ala/A) Alanine | GAU | (Asp/D) Aspartic acid | GGU | (Gly/G) Glycine | U |
GUC | GCC | GAC | GGC | C | |||||
GUA | GCA | GAA | (Glu/E) Glutamic acid | GGA | A | ||||
GUG [A] | GCG | GAG | GGG | G |
Amino acid | DNA codons | Compressed | Amino acid | DNA codons | Compressed | |
---|---|---|---|---|---|---|
Ala, A | GCU, GCC, GCA, GCG | GCN | Ile, I | AUU, AUC, AUA | AUH | |
Arg, R | CGU, CGC, CGA, CGG; AGA, AGG | CGN, AGR; or CGY, MGR |
Leu, L | CUU, CUC, CUA, CUG; UUA, UUG | CUN, UUR; or CUY, YUR | |
Asn, N | AAU, AAC | AAY | Lys, K | AAA, AAG | AAR | |
Asp, D | GAU, GAC | GAY | Met, M | AUG | ||
Asn or Asp, B | AAU, AAC; GAU, GAC | RAY | Phe, F | UUU, UUC | UUY | |
Cys, C | UGU, UGC | UGY | Pro, P | CCU, CCC, CCA, CCG | CCN | |
Gln, Q | CAA, CAG | CAR | Ser, S | UCU, UCC, UCA, UCG; AGU, AGC | UCN, AGY | |
Glu, E | GAA, GAG | GAR | Thr, T | ACU, ACC, ACA, ACG | ACN | |
Gln or Glu, Z | CAA, CAG; GAA, GAG | SAR | Trp, W | UGG | ||
Gly, G | GGU, GGC, GGA, GGG | GGN | Tyr, Y | UAU, UAC | UAY | |
His, H | CAU, CAC | CAY | Val, V | GUU, GUC, GUA, GUG | GUN | |
START | AUG, CUG, UUG | HUG | STOP | UAA, UGA, UAG | URA, UAR |
The title of my first PubMed article is: Acute depletion of plasma membrane phosphatidylinositol 4,5-bisphosphate impairs specific steps in endocytosis of the G-protein-coupled receptor. [6]
The primary goals were to investigate the role and importance of Phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P(2)] in the plasma membrane on the endocytic process of GPCRs and to determine whether depleting PtdIns(4,5)P(2) would disrupt this process. [6] Three different GPCRs were studied including: luciferase-labeled type 1 angiotensin II (AT1R), type 2C serotonin (5HT2CR) and β(2) adrenergic (β2AR) receptors. The authors found that when they depleted PtdIns(4,5)P(2), there was generally a significant inhibition in the number of GPCRs in early endosomes. [6] This study confirmed that GPCRs rely on PtdIns(4,5)P(2) in their endocytic pathways. Delivery of one of the GPCRs to early endosomes for example was completely stopped when PtdIns(4,5)P(2) was depleted. [6]
The title of my second PubMed article is: MCAK activity at microtubule tips regulates spindle microtubule length to promote robust kinetochore attachment. [7]
The main goal of this study was to see if MCAK’s (mitotic centromere-associated kinesin) effect on dynamic microtubule plus ends is the reason shorter spindles are observed during meiotic spindle assembly when MCAK levels are raised. The authors tested this in human mitotic cells by depleting MCAK levels using siRNA and then observing the spindle assembly in the cells. [7] The authors found that the tip-tracking activity for MCAK was played an important role in stopping the centrosomes from separating when bipolar spindles were being assembled. The significance of this was clarified when the authors also monitored kinetochore attachment. [7] It turned out that when cells were lacking MCAK, the spindle fibers that were made had “excessively” long microtubules that were not kinetochore related. [7]
{{
cite journal}}
: Explicit use of et al. in: |author=
(
help)CS1 maint: date and year (
link) CS1 maint: multiple names: authors list (
link)
{{
cite journal}}
: CS1 maint: date and year (
link) CS1 maint: multiple names: authors list (
link)