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Explore the people, places, events, achievements, struggles and stories that shaped our journey.
Movements, leaders, victories and the continuing fight for equality.
Innovation, patents, science, technology and world-changing contributions.
Pioneers, champions, Negro Leagues, records, activism and excellence.
Meet the people whose lives, choices and achievements shaped the journey.
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Mansa Musa was the ruler of the Mali Empire in West Africa. Details recorded here should be sourced; unknown information is left blank.
MORE →Reflects the personal views, recollections, and perspective of the author, Mike Davis.
This is a personal recollection on the Move fire on May 13, 1985
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| Identifiers | |||||||||||||||||||||||||||||||
| Aliases | RUNX1T1, AML1T1, CBFA2T1, CDR, ETO, MTG8, ZMYND2, AML1-MTG8, t(8;21)(q22;q22), RUNX1 translocation partner 1, RUNX1 partner transcriptional co-repressor 1 | ||||||||||||||||||||||||||||||
| External IDs | OMIM: 133435; MGI: 104793; GeneCards: RUNX1T1 | ||||||||||||||||||||||||||||||
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Protein CBFA2T1 is a protein that in humans is encoded by the RUNX1T1 gene.[5][6][7]
The protein encoded by this gene is a putative zinc finger transcription factor and oncoprotein. In acute myeloid leukemia, especially in the M2 subtype, the t(8;21)(q22;q22) translocation is one of the most frequent karyotypic abnormalities. The translocation produces a chimeric gene made up of the 5′-region of the RUNX1 gene fused to the 3′-region of this gene. The chimeric protein is thought to associate with the nuclear corepressor/histone deacetylase complex to block hematopoietic differentiation. Several transcript variants encoding multiple isoforms have been found for this gene.[7]
RUNX1T1 has been shown to interact with:
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Source: Wikipedia. Article content is retrieved live through the MediaWiki API.
Protein CBFA2T1 is a protein that in humans is encoded by the RUNX1T1 gene.
Acute myeloblastic leukemia with maturation (M2) is a subtype of acute myeloid leukemia (AML). Acute myeloid leukemia (AML) is a type of cancer affecting blood cells that eventually develop into non-lymphocyte white blood cells. The disease originates from the bone marrow, the soft inner portion of select bones where blood stem cells develop into either lymphocyte or in this particular condition, myeloid cells. This acute disease prevents bone marrow cells from properly maturing, thus causing an accumulation of immature myeloblast cells in the bone marrow. Acute myeloid leukemia is more lethal than chronic myeloid leukemia, a disease that affects the same myeloid cells, but at a different pace. Many of the immature blast cells in acute myeloid leukemia have a higher loss of function and thus, a higher inability to carry out normal functions than those more developed immature myeloblast cells in chronic myeloid leukemia (O’Donnell et al. 2012). Acute in acute myeloid leukemia means that the amounts of blast cells are increasing at a very high rate. Myeloid refers to the type of white blood cells that are affected by the condition. Acute myeloid leukemia is the most common acute leukemia that is affecting the adult population. The 5-year survival rate for the cancer stands at around 26% (ACS, 2016). M2 acute myeloblastic leukemia with maturation refers to the subtype of acute myeloid leukemia characterized by the maturation stages of the myeloid cell development and the location of the AML1 gene. One of the hallmarks of M2 subtype acute myeloid leukemia is the formation of a fusion protein, AML1-ETO or RUNX1-RUNX1T1, due to a translocation of chromosome 8 to chromosome 21 or t(8;21) (Miyoshi et al., 1991, Andrieu et al., 1996). This cytogenetic abnormality has been found in 90% of M2 acute myeloblastic leukemia; while the other 10% constitutes a mix of M1 and M4 acute myeloid leukemia (GFHC, 1990). Another translocation between chromosome 6p23 and chromosome 9q34 is also associated with the M2 subtype. The t(6;9) causes the formation of a fusion oncogene made of DEK (6p23) and CAN/NUP214 (9q34). This rare translocation has a poor prognosis compared to the t(8;21) because 70% of t(6;9) acute myeloid leukemia patients have the FLT3-ITD mutation (Schwartz et al., 1983, Kottaridis, 2001). The FLT-ITD mutation is one of the most lethal mutations in acute myeloid leukemia (Chi et al., 2008). M2 acute myeloblastic leukemia with maturation, as classified by the FAB system, constitutes 25% of adult AML.
A homeobox is a DNA sequence, around 180 base pairs long, that regulates large-scale anatomical features in the early stages of embryonic development. Mutations in a homeobox may change large-scale anatomical features of the full-grown organism. Homeoboxes are found within genes that are involved in the regulation of patterns of anatomical development (morphogenesis) in animals, fungi, plants, and numerous single cell eukaryotes. Homeobox genes encode homeodomain protein products that are transcription factors sharing a characteristic protein fold structure that binds DNA to regulate expression of target genes. Homeodomain proteins regulate gene expression and cell differentiation during early embryonic development, thus mutations in homeobox genes can cause developmental disorders. Homeosis is a term coined by William Bateson to describe the outright replacement of a discrete body part with another body part, e.g. antennapedia—replacement of the antenna on the head of a fruit fly with legs. The "homeo-" prefix in the words "homeobox" and "homeodomain" stems from this mutational phenotype, which is observed when some of these genes are mutated in animals. The homeobox domain was first identified in a number of Drosophila homeotic and segmentation proteins, but is now known to be well-conserved in many other animals, including vertebrates.
Forkhead box protein P2 (FOXP2) is a protein that, in humans, is encoded by the FOXP2 gene. FOXP2 is a member of the forkhead box family of transcription factors, proteins that regulate gene expression by binding to DNA. It is expressed in the brain, heart, lungs and digestive system. FOXP2 is found in many vertebrates, where it plays an important role in mimicry in birds (such as birdsong) and echolocation in bats. FOXP2 is also required for the proper development of speech and language in humans. In humans, mutations in FOXP2 cause the severe speech and language disorder developmental verbal dyspraxia. Studies of the gene in mice and songbirds indicate that it is necessary for vocal imitation and the related motor learning. Outside the brain, FOXP2 has also been implicated in development of other tissues such as the lung and digestive system. Initially identified in 1998 as the genetic cause of a speech disorder in a British family designated the KE family, FOXP2 was the first gene discovered to be associated with speech and language and was subsequently dubbed "the language gene". However, other genes are necessary for human language development, and a 2018 analysis confirmed that there was no evidence of recent positive evolutionary selection of FOXP2 in humans.
Before the 1921 destruction of Tulsa’s Greenwood District, Black residents had created a remarkable center of business and community life. The district included stores, professional offices, entertainment venues and homes owned by Black citizens. Understanding Greenwood means learning what was built—not only what was burned.
MORE →The Greenwood District.
