Answer:
D
Explanation:
Facilitated diffusion is a form of passive transport hence no energy is required by the cell. This means that while the molecules are moving down a concentration gradient – line normal diffusion – the movement of the molecules needs to be facilitated (in this case by a transmembrane protein) either because the molecule is polar and can't pass through the hydrophobic region of the cell membrane, or the molecule is too big to passively pass through the small natural pores of the cell membrane.
Answer:
Explanation:
The basis for the inverse relationship between number of matured HDL in circulation and and cardiovascular disease is that when new HDL entertainment circulation they mature by picking up extra cholesterol until they become mature and high cholesterol level is a major cause of cardiovascular disease and atherosclerosis. The implication of this is that the more the number of matured HDL in circulation, the lower the cholesterol level in the blood thus the lower the risk of cardiovascular disease and atherosclerosis.
...The origin of life on Earth is a set of paradoxes. In order for life to have gotten started, there must have been a genetic molecule.. something like DNA or RNA—capable of passing along blueprints for making proteins, the workhorse molecules of life.
Protein-protein interactions within the CARMA1-BCL10-MALT1 complex:
- The T-cell receptor and B-cell receptor-dependent NF-B induction and lymphocyte activation are mediated by the CBM complex, which is made up of the proteins CARMA1, BCL10, and MALT1.
- Each of the proto-oncoproteins CARMA1, BCL10, and MALT1 is a somatic gain-of-function mutation or chromosomal translocation, and dysregulation of CBM signaling is a characteristic of numerous lymphoid malignancies, including Activated B-cell Diffuse Large B-cell Lymphoma.
- Moreover, a number of immunological dysregulation diseases have been linked to both gain- and loss-of-function germline mutations in CBM complex proteins.
- Over the past ten years, careful examination of the interactions of CBM components has yielded a wealth of detailed structural knowledge.
- Here, we discuss important discoveries about the molecular nature of these protein-protein interactions that have helped the research develop a detailed understanding of how these proteins come together to form high-order filamentous CBM complexes.
- Approaches to therapeutic suppression of the CBM complex have thus far centered on obstructing MALT1 protease activity in order to treat lymphoid malignancy and/or autoimmunity.
- The structural effects of MALT1 protease inhibitors on significant protein-protein interactions are also reviewed in detail.
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