Dua protein bekerja sama untuk membantu sel-sel menghilangkan sampah ; dapat mengakibatkan Parkinson --t-REC-komunitas reptil-semarang--KSE-komunitas satwa eksotik

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Dua protein bekerja sama untuk membantu sel-sel menghilangkan sampah ; dapat mengakibatkan Parkinson 

Date:

August 20, 2015

Source:

Medical College of Georgia at Georgia Regents University

Summary:

Dua protein yang berbagi kemampuan untuk membantu sel-sel menangani sampah mereka tampak saling membutuhkan untuk melakukan pekerjaan mereka dan ketika mereka tidak terhubung , tampaknya berkontribusi pada pengembangan penyakit Parkinson , para ilmuwan melaporkan .

............ Sama seperti jaringan masyarakat untuk penanganan sampah , sel juga memiliki  situs sampah yang disebut lisosom , di mana protein , yang berfungsi buruk karena usia atau alasan lain , menuju  untuk degradasi dan potensi daur ulang , kata Dr Wen - Cheng Xiong , neurobiologi perkembangan dan Weiss Profesor Riset di Medical College of Georgia di Georgia Regents University..........more

Two proteins work together to help cells eliminate
trash; Parkinson's may result

Date:

August 20, 2015

Source:

Medical College of Georgia at Georgia
Regents University

Summary:

Two proteins that share the ability to
help cells deal with their trash appear to need each other to do their jobs and
when they don't connect, it appears to contribute to development of Parkinson's
disease, scientists report.

.................

Two proteins that share the ability to
help cells deal with their trash appear to need each other to do their jobs and
when they don't connect, it appears to contribute to development of Parkinson's
disease, scientists report.

Much like a community's network for
garbage handling, cells also have garbage sites called lysosomes, where
proteins, which are functioning badly because of age or other reasons, go for
degradation and potential recycling, said Dr. Wen-Cheng Xiong, developmental
neurobiologist and Weiss Research Professor at the Medical College of Georgia
at Georgia Regents University.

Inside lysosomes, other proteins, called
proteases, help cut up proteins that can no longer do their job and enable
salvaging of things like precious amino acids. It's a normal cell degradation
process called autophagy that actually helps cells survive and is particularly
important in cells such as neurons, which regenerate extremely slowly, said
Xiong, corresponding author of the study in The Journal of Neuroscience.

Key to the process -- and as scientists
have shown, to each other -- are two more proteins, VPS35 and Lamp2a. VPS35 is
essential for retrieving membrane proteins vital to cell function. Levels
naturally decrease with age, and mutations in the VPS35 gene have been found in
patients with a rare form of Parkinson's. VPS35 also is a critical part of a
protein complex called a retromer, which has a major role in recycling inside
cells. Lamp2a enables unfit proteins to be chewed up and degraded inside
lysosomes.

If the two sound like a natural couple,
scientists now have more evidence that they are. They have shown that without
VPS35 to retrieve Lamp2a from the trash site for reuse, Lamp2a, or
lysosomal-associated membrane protein 2, will be degraded and its vital
function lost.

When the scientists generated
VPS35-deficient mice, the mice exhibited Parkinson's-like deficits, including
impaired motor control. When they looked further, they found the lysosomes
inside dopamine neurons, which are targets in Parkinson's, didn't function
properly in the mice. In fact, without VPS35, the degradation of Lamp2a itself
is accelerated. Consequently, yet another protein, alpha-synuclein, which is
normally destroyed by Lamp2a, is increased. Alpha-synuclein is a major
component of abnormal protein clumps, called Lewy bodies, found in the brains
of patients with Parkinson's.

"If alpha-synuclein is not
degraded, it just accumulates. If VPS35 function is normal, we won't see its
accumulation," Xiong said.

Conversely, when MCG scientists
increased expression of Lamp2a in the dopamine neurons of the VPS35-deficient
mice, alpha-synuclein levels were reduced, a finding that further supports the
linkage of the three proteins in the essential ability of the neurons to deal
with undesirables in their lysosomes.

Without lamp2a, dopamine neurons
essentially start producing more garbage rather than eliminating it. Recycling
of valuables such as amino acids basically stops, and alpha-synuclein is free
to roam to other places in the cell or other brain regions where it can damage
still viable proteins.

The bottom line is dopamine neurons are
lost instead of preserved. Brain scans document the empty spaces where neurons
used to be in patients with neurodegenerative diseases such as Parkinson's and
Alzheimer's. One of the many problems with treatment of these diseases is that
by the time the empty spaces and sometimes the associated symptoms are
apparent, much damage has occurred, Xiong said.

Putting these pieces together provides
several new, early targets for disease intervention. "Everything is
linked," Xiong said.

Dopamine is a brain chemical with many
roles, including motor control, and patients with Parkinson's have a loss of
the neurons that secrete this neurotransmitter. At least in mice, VPS35 is
naturally expressed in dopamine neurons in areas of the brain affected by
Parkinson's.

Xiong and her colleagues reported in
2011 that reduced expression of VPS35 enables activity of the
dormant-in-healthy-adults protein BACE1 to increase along with accumulation of
the brain plaque that is a hallmark of Alzheimer's. Xiong said then that impaired
VPS35 function likely also was a factor in Parkinson's.

In a definite vicious circle, trash
starts overwhelming the brain cell's natural garbage disposal system. Proteins
start getting misfolded and dysfunctional, potentially destructive proteins such
as BACE1 and Lamp2a end up in the wrong place and get activated/inactivated,
while good proteins get chopped up and/or bad proteins accumulate.

Parkinson's disease is characterized by
uncontrolled shaking, an unstable gait and cognitive loss.







Story Source:

The above post is reprinted from materials provided by Medical College of Georgia at Georgia
Regents University. Note:
Materials may be edited for content and length.







Journal Reference:

1.   
F.-L. Tang, J. R. Erion, Y. Tian, W.
Liu, D.-M. Yin, J. Ye, B. Tang, L. Mei, W.-C. Xiong. VPS35 in Dopamine
Neurons Is Required for Endosome-to-Golgi Retrieval of Lamp2a, a Receptor of
Chaperone-Mediated Autophagy That Is Critical for  -Synuclein Degradation
and Prevention of Pathogenesis of Parkinson's Disease. Journal of
Neuroscience, 2015; 35 (29): 10613 DOI: 10.1523/JNEUROSCI.0042-15.2015

http://www.sciencedaily.com/releases/2015/08/150820144850.htm

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