Search results
Results From The WOW.Com Content Network
Cholera (/ ˈ k ɒ l ər ə /) is an infection of the small intestine by some strains of the bacterium Vibrio cholerae. [4] [3] Symptoms may range from none, to mild, to severe. [3]The classic symptom is large amounts of watery diarrhea lasting a few days. [2]
One of the most important aspects of cholera toxin is the retrograde traffic mechanism that transports the toxin from the cell membrane back to the trans-Golgi network and the endoplasmic reticulum. Since both cholera toxin and GM1 species can be tagged with a fluorescent tags, the mechanism of retrograde traffic can be monitored.
Cholera is a bacterial infection of the intestines that leads to severe diarrhea and rapid dehydration, "which can quickly become life-threatening without treatment," says Dr. Jason Nagata, a ...
The bacterium as the cause of cholera was discovered by Robert Koch in 1884. Sambhu Nath De isolated the cholera toxin and demonstrated the toxin as the cause of cholera in 1959. The bacterium has a flagellum (a tail like structure) at one pole and several pili throughout its cell surface. It undergoes respiratory and fermentative metabolism.
Quorum sensing is essentially the intercommunication between cells to interact and respond to its environment.V. cholerae uses two autoinducers: cholera autoinducer-1 (CAI-1) and autoinducer-2 (AI-2). CAI-1 is the major quorum-sensing signal. Quorum sensing is the cell to cell communication that allows organisms to share information.
Intestinal stem cell aging has been studied in Drosophila as a model for understanding the biology of stem cell/niche aging. [4] Using knockdown mutants defective in various genes that function in the DNA damage response in enterocytes, it was shown that deficiency in the DNA damage response accelerates intestinal stem cell aging, thus ...
Cholera toxin is an AB toxin that has five B subunints and one A subunit. The toxin acts by the following mechanism: First, the B subunit ring of the cholera toxin binds to GM1 gangliosides on the surface of target cells. If a cell lacks GM1 the toxin most likely binds to other types of glycans, such as Lewis Y and Lewis X, attached to proteins ...
The prokaryotic cell is shown with its DNA, in green. 2. The bacteriophage attaches and releases its DNA, shown in red, into the prokaryotic cell. 3. The phage DNA then moves through the cell to the host's DNA. 4. The phage DNA integrates itself into the host cell's DNA, creating prophage. 5. The prophage then remains dormant until the host ...