Answer: Sex cell is the correct answer.
Answer:
Signal transduction is what allows cells to respond to the influences of the environment around them, providing cells with proper growth and normal cell function.
Explanation:
Living organisms have developed a wide variety of complex processes to transmit signals from the outside to the inside to elicit an adequate cellular response. Defects in these molecular pathways can lead to very different disorders, such as diabetes, cancer, and psychotic illnesses. Signal transduction is the process by which a cell converts a certain signal or external stimulus into another signal or specific response, that is, it is the mechanism by which a cell responds to the stimuli it receives from the environment through diffusion. of those signals to its internal compartments. First, a signaling molecule (also called a ligand) needs to activate a specific receptor on the cell's membrane or cytoplasm. Ligand-receptor binding is very specific; they are recognized as a key and a lock. Second messengers are molecules that allow the received signal to be amplified at the intracellular level. The binding of a ligand to the receptor can generate hundreds of second messenger molecules that, in turn, can modify thousands of effector molecules and give rise to different responses. Cells recognize, integrate, and respond to multiple signals from their environment due to signal transduction, providing cells with a normal cell function.
<em>sieve tube elements are the cells of phloem which allow transportation of photosynthates through phloem...
<u>
how sieve tube elements form sieve tubes:
</u>sieve tube elements are connected end to end and form a long chain which is called sieve tube,,,,
sieve tube elements are connected with the help of a side chain with the help of peptide bond...also one element has tapering end which easily overlaps with other end of next element to form sieve tube,,,,</em>
Answer:
One of the common genetic disorders is sickle cell anemia, in which 2 recessive alleles must meet to allow for destruction and alteration in the morphology of red blood cells. This usually leads to loss of proper binding of oxygen to hemoglobin and curved, sickle-shaped erythrocytes. The mutation causing this disease occurs in the 6th codon of the HBB gene encoding the hemoglobin subunit β (β-globin), a protein, serving as an integral part of the adult hemoglobin A (HbA), which is a heterotetramer of 2 α chains and 2 β chains that is responsible for binding to the oxygen in the blood. This mutation changes a charged glutamic acid to a hydrophobic valine residue and disrupts the tertiary structure and stability of the hemoglobin molecule. Since in the field of protein intrinsic disorder, charged and polar residues are typically considered as disorder promoting, in opposite to the order-promoting non-polar hydrophobic residues, in this study we attempted to answer a question if intrinsic disorder might have a role in the pathogenesis of sickle cell anemia. To this end, several disorder predictors were utilized to evaluate the presence of intrinsically disordered regions in all subunits of human hemoglobin: α, β, δ, ε, ζ, γ1, and γ2. Then, structural analysis was completed by using the SWISS-MODEL Repository to visualize the outputs of the disorder predictors. Finally, Uniprot STRING and D2P2 were used to determine biochemical interactome and protein partners for each hemoglobin subunit along with analyzing their posttranslational modifications. All these properties were used to determine any differences between the 6 different types of subunits of hemoglobin and to correlate the mutation leading to sickle cell anemia with intrinsic disorder propensity.
Explanation:
