<h2><u>
Heart and lungs:</u></h2>
The upper chamber of the heart is called atrium and lower chamber of the heart is called ventricles.
The blood circulation in the heart is basically under the functioning of three blood vessels namely:
<h3><u>Arteries:
</u></h3>
- They start with the aorta, the huge vein leaving the heart.
- Veins divert oxygen-rich blood from the heart to the majority of the body's tissues.
- They branch a few times, decreasing and littler as they convey blood more remote from the heart.
<h3><u>Capillaries:
</u></h3>
- These are little; flimsy blood vessels that associate the arteries and the veins.
- Their dainty dividers permit oxygen, supplements, carbon dioxide, and other waste items to go to and from our organ's cells.
<h3><u>Veins:
</u></h3>
- These are the blood vessels that return blood to the heart; this blood needs (oxygen-poor) and is wealthy in waste items that are to be discharged or expelled from the body.
- Veins become bigger and bigger as they draw nearer to the heart.
- The unrivaled vena cava is the huge vein that brings blood from the head and arms to the heart, and the second rate vena cava brings blood from the mid-region and legs into the heart.
I am mostly sure the answer is B. Good luck, and sorry if it's wrong! :(
Blood clots form when platelets and plasma proteins thicken to form a sort of solid mass. They can form from an injury, blood flowing slowly through your system, or even for no obvious reason.
Answer:
1. P120 is degraded in the 26S proteasome
2. The 26S proteasome has a major role in protein degradation and is critical for protein homeostasis
3. Cell cycle and DNA replication are cellular processes regulated by the Ras and NFkB pathways
Explanation:
The proliferation-associated nucleolar protein (p120) is a protein known to be expressed during the interphase of the cell cycle, specifically in G1 and early S phase, where any problem with DNA replication trigger a checkpoint, i.e., a molecular cascade of signaling events that suspend DNA replication until the problem is resolved. In mammalian cells, the 26S proteasome is responsible for catalyzing protein degradation of about 80% (or even more) of their proteins. The 26S proteasome acts to degrade rapidly misfolded and regulatory proteins involved in the cell cycle, thereby having a major role in protein homeostasis and in the control of cellular processes. It is for that reason that inhibitors that block 26S proteasome function have shown to be useful as therapeutic agents in diseases associated with the failure of protein degradation mechanisms (e.g., multiple myeloma). The NF-κB are highly conserved transcription factors capable of regulating different cellular processes including, among others, cellular growth, inflammatory responses and apoptosis. Moreover, the MAPK/ERK pathway is able to transduce different signals received on the cell surface to the nucleus. The MAPK/ERK pathway is activated when a singling molecule binds to a cell receptor which triggers a signaling cascade that ends when a transcription factor induces the expression of target genes, ultimately producing a response in the cell (for example, the progression through the cell cycle).
