Search results
Results from the WOW.Com Content Network
Hematopoietic stem cells (HSCs) are the stem cells [1] that give rise to other blood cells.This process is called haematopoiesis. [2] In vertebrates, the first definitive HSCs arise from the ventral endothelial wall of the embryonic aorta within the (midgestational) aorta-gonad-mesonephros region, through a process known as endothelial-to-hematopoietic transition.
Diagram showing the development of different blood cells from haematopoietic stem cell to mature cells. Haematopoiesis (/ h ɪ ˌ m æ t ə p ɔɪ ˈ iː s ɪ s, ˌ h iː m ə t oʊ-, ˌ h ɛ m ə-/; [1] [2] from Ancient Greek αἷμα (haîma) 'blood' and ποιεῖν (poieîn) 'to make'; also hematopoiesis in American English, sometimes h(a)emopoiesis) is the formation of blood cellular ...
Types of mutations that can be introduced by random, site-directed, combinatorial, or insertional mutagenesis. In molecular biology, mutagenesis is an important laboratory technique whereby DNA mutations are deliberately engineered to produce libraries of mutant genes, proteins, strains of bacteria, or other genetically modified organisms.
Albinism is the mutation of the TYR gene, also termed tyrosinase. This mutation causes the most common form of albinism. The mutation alters the production of melanin, thereby affecting melanin-related and other dependent traits throughout the organism. Melanin is a substance made by the body that is used to absorb light and provides coloration ...
In genetics, a deletion (also called gene deletion, deficiency, or deletion mutation) (sign: Δ) is a mutation (a genetic aberration) in which a part of a chromosome or a sequence of DNA is left out during DNA replication.
Angiogenesis is the physiological process through which new blood vessels form from pre-existing vessels, [1] [2] [3] formed in the earlier stage of vasculogenesis. Angiogenesis continues the growth of the vasculature mainly by processes of sprouting and splitting, but processes such as coalescent angiogenesis , [ 4 ] vessel elongation and ...
DiGeorge syndrome is caused by a heterozygous deletion of part of the long arm (q) of chromosome 22, region 1, band 1, sub-band 2 (22q11.2). Approximately 80-90% of patients have a deletion of 3 Mb and 8% have a deletion of 1.5Mb. [31] [32] The number of genes affected by the deletion has been cited as approximately 30 to 50.
Most people never develop a blood clot in their lifetimes. [1] It is due to a specific gene mutation in which a guanine is changed to an adenine at position 20210 of the DNA of the prothrombin gene. Other blood clotting pathway mutations that increase the risk of clots include factor V Leiden. Prothrombin G20210A was identified in the 1990s. [2]