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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
| MID1 | |||||||||||||||||||||||||||||||
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| Identifiers | |||||||||||||||||||||||||||||||
| Aliases | MID1, BBBG1, FXY, GBBB1, MIDIN, OGS1, OS, OSX, RNF59, TRIM18, XPRF, ZNFXY, midline 1, GBBB | ||||||||||||||||||||||||||||||
| External IDs | OMIM: 300552; MGI: 1100537; GeneCards: MID1 | ||||||||||||||||||||||||||||||
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MID1 is a protein that belongs to the Tripartite motif family (TRIM) and is also known as TRIM18.[5][6] The MID1 gene is located on the short arm of the X chromosome and loss-of-function mutations in this gene are causative of the X-linked form of a rare developmental disease, Opitz G/BBB Syndrome.[5][7]
The human MID1 gene is located on the short arm of the X chromosome (Xp22.2) and includes 9 coding exons, spanning approximately 400 kb of the genome.[5][8] Upstream to the first coding exon, the MID1 gene employs alternative 5' untranslated exons and at least five alternative promoters that drive the transcription of the gene, resulting in several MID1 transcript isoforms.[9] The MID1 gene encodes a 667 amino acid protein that belongs to the TRIM family. MID1 protein consists of a conserved N-terminal tripartite module composed of a RING domain, 2 B-Box domains (B-box 1 and B-box 2) and a coiled-coil region.[5][6] Within the TRIM family, MID1 belongs to the C-I subgroup characterised by the presence, downstream to the tripartite motif, of a COS domain, a Fibronectin type III (FN3) repeat and a PRY-SPRY domain.[10]
MID1 is a microtubular protein[11][12] that acts as an ubiquitin E3 ligase in vitro and in cells. Ubiquitination is a type of post-translational modification in which the transfer of one or several ubiquitin peptide molecules to substrates determines their stability and/or activity.[13] The MID1 E3 ubiquitin ligase activity is catalysed by the RING domain, a hallmark of one of the main classes of E3 ubiquitin ligases that, within the ubiquitination cascade, facilitate the transfer of the ubiquitin peptide to specific substrates.[14][15][16] Several MID1 E3 ubiquitin ligase targets have been reported: Alpha4 (α4) and its associated phosphatase, PP2A,[14] Fu,[17] Pax6[18] and BRAF35.[19]
Together with α4 and PP2A, MID1 can form a ternary complex in which α4 acts as an adaptor protein.[14] The data so far indicate that MID1 promotes α4 mono-ubiquitination, leading to its calpain-dependent cleavage[20] that in turn causes PP2A catalytic subunit (PP2Ac) polyubiquitination and proteasomal degradation.[14] Since PP2A is involved in many cellular processes,[21] the MID1-α4-PP2A ternary complex may be involved in the regulation of several of them, mainly on microtubules. The complex can modulate mTORC1 signalling; indeed PP2A attenuates mTORC1 activity through dephosphorylation. By lowering PP2Ac levels, MID1 leads to increase mTORC1 signalling.[22] Conversely, the lack or loss-of-function mutations of MID1 lead to increased levels of PP2A and, as a consequence, to a general hypo-phosphorylation of PP2A targets, included mTORC1. The signalling of mTORC1 is implicated in cytoskeletal dynamics, intracellular transport, cell migration, autophagy, protein synthesis, cell metabolism, so it is possible that MID1, by controlling PP2Ac, is ultimately implicated in some of these cellular processes.
MID1 is also involved is the Sonic Hedgehog (Shh) pathway.[23] MID1 catalyses the ubiquitination and proteasomal-dependent cleavage of Fu, a kinase involved in Hedgehog signalling pathway.[17] The cleavage of the kinase domain of Fu favours the translocation of the transcription factor GLI3A (activator form) in the nucleus.[17][24] In this way, GLI3A activates the expression of Shh target genes, leading to an increase of Shh signalling. The cross talk between MID1 and the Shh pathway is also supported by experimental evidence in model organisms.[18][25]
MID1 is nearly ubiquitously expressed in all embryonic tissues, having an important function during development. Several model organisms have been used to study the expression pattern of MID1 transcript at different times of gestation: mouse,[26][27] chicken,[28][29] xenopus[18][30] and also human embryos.[31] At the very early stage of embryonic development, MID1 is expressed in the primitive node where MID1 plays a pivotal role in establishing the molecular asymmetry at the node, which is crucial for the early definition of the laterality as embryonic development progresses. Later in embryogenesis, at the neurulation stage, MID1 transcript is mainly observed in the cranial region of the developing neural folds. Starting from midgestation, the highest levels of MID1 transcript are observed in the proliferating compartments of the central nervous system and in the epithelia of the developing branchial arches, craniofacial processes, optic vesicle, in the heart and in the gastrointestinal and urogenital system.
The MID1 gene was identified concomitantly with the discovery that it was causatively mutated in patients with a rare genetic disease, the X-linked form of Opitz G/BBB syndrome (XLOS) (OMIM #300000).[5] XLOS is a congenital malformative disorder characterised by defects in the embryonic development of midline structures. XLOS is characterised by high variability of the clinical signs and, being X-linked, males are generally affected. The most frequently observed signs are: dysmorphic features, mainly represented by hypertelorism often associated with cleft lip and palate, frontal bossing, large nasal bridge, and low-set ears. Laryngo-tracheo-esophageal abnormalities are also frequently observed in XLOS patients as well as external genitalia abnormalities that are predominantly represented by various-degree-hypospadias.[32] In addition, XLOS patients can present cardiac abnormalities and anal defects.[32] XLOS also shows a neurological component represented by cerebellar vermis hypoplasia and agenesis or hypoplasia of the corpus callosum accompanied by intellectual disabilities and developmental delays.[32] Since its discovery as the causative gene for XLOS, approximately one hundred different pathogenetic mutations have been described in the MID1 gene. Even though the type and the distribution of mutations suggested a loss-of-function mechanism in the pathogenesis of Opitz syndrome, the aetiology of the disease remains still unclear. Additional clinical conditions are described to be associated with alterations of MID1, given also its implication in a wide variety of cellular mechanisms. In fact, involvement of MID1 in asthma, cancer, and neurodegeneration relevant pathways has been reported.
 | The version of this article was updated by an external expert under a dual publication model. The corresponding academic peer reviewed article was published in Gene and can be cited as: Rossella Baldini, Martina Mascaro, Germana Meroni (2020). "The MID1 gene product in physiology and disease". Gene. Gene Wiki Review Series 144655. doi:10.1016/j.gene.2020.144655. PMC 8011326. PMID 32283114. Wikidata Q91863888. |
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Source: Wikipedia. Article content is retrieved live through the MediaWiki API.
MID1 is a protein that belongs to the Tripartite motif family (TRIM) and is also known as TRIM18. The MID1 gene is located on the short arm of the X chromosome and loss-of-function mutations in this gene are causative of the X-linked form of a rare developmental disease, Opitz G/BBB Syndrome.
Nuu-chah-nulth (nuučaan̓uɫ), a.k.a. Nootka (), is a Wakashan language in the Pacific Northwest of North America on the west coast of Vancouver Island, from Barkley Sound to Quatsino Sound in British Columbia by the Nuu-chah-nulth peoples. Nuu-chah-nulth is a Southern Wakashan language related to Nitinaht and Makah. It is the first language of the indigenous peoples of the Pacific Northwest Coast to have documentary written materials describing it. In the 1780s, Captains Vancouver, Quadra, and other European explorers and traders frequented Nootka Sound and the other Nuu-chah-nulth communities, making reports of their voyages. From 1803 to 1805 John R. Jewitt, an English blacksmith, was held captive by chief Maquinna at Nootka Sound. He made an effort to learn the language, and in 1815 published a memoir with a brief glossary of its terms.
Schizosaccharomyces pombe, also called "fission yeast", is a species of yeast used in traditional brewing and as a model organism in molecular and cell biology. It is a unicellular eukaryote, whose cells are rod-shaped. Cells typically measure 3 to 4 micrometres in diameter and 7 to 14 micrometres in length. Its genome, which is approximately 14.1 million base pairs, is estimated to contain 4,970 protein-coding genes and at least 450 non-coding RNAs. These cells maintain their shape by growing exclusively through the cell tips and divide by medial fission to produce two daughter cells of equal size, which makes them a powerful tool in cell cycle research. Fission yeast was isolated in 1893 by Paul Lindner from East African millet beer. The species name pombe is the Swahili word for beer. It was first developed as an experimental model in the 1950s: by Urs Leupold for studying genetics, and by Murdoch Mitchison for studying the cell cycle. Paul Nurse, a fission yeast researcher, successfully merged the independent schools of fission yeast genetics and cell cycle research. Together with Lee Hartwell and Tim Hunt, Nurse won the 2001 Nobel Prize in Physiology or Medicine for work on cell cycle regulation. The sequence of the S. pombe genome was published in 2002, by a consortium led by the Sanger Institute, becoming the sixth model eukaryotic organism whose genome has been fully sequenced. S. pombe researchers are supported by the PomBase MOD (model organism database). This has fully unlocked the power of this organism, with many genes orthologous to human genes identified — 70% to date, including many genes involved in human disease. In 2006, sub-cellular localization of almost all the proteins in S. pombe was published using green fluorescent protein as a molecular tag. Schizosaccharomyces pombe has also become an important organism in studying the cellular responses to DNA damage and the process of DNA replication. Approximately 160 natural strains of S. pombe have been isolated. These have been collected from a variety of locations including Europe, North and South America, and Asia. The majority of these strains have been collected from cultivated fruits such as apples and grapes, or from the various alcoholic beverages, such as Brazilian Cachaça. S. pombe is also known to be present in fermented tea, kombucha. It is not clear at present whether S. pombe is the major fermenter or a contaminant in such brews. The natural ecology of Schizosaccharomyces yeasts is not well-studied.
Thigmomorphogenesis involves plants altering their growth and development in response to mechanical stimuli, such as touch, wind, or rain. This process begins with the perception of mechanical forces by cellular mechanosensors, followed by their transduction into signal transduction pathways cascades, and culminating in changes in gene expression and hormone activity. The response integrates diverse molecular components, including mechanosensitive ion channels, receptor-like kinases, the cytoskeletal elements, phytohormones, and transcription factors, which collectively drive both immediate physiological and long-term morphological adaptations. Early observations noted that greenhouse-grown plants were often taller and more slender than stockier plants grown outdoors, where they were exposed to natural mechanical stresses. The term "thigmomorphogenesis" is derived from Ancient Greek θιγγάνω (thingánō, "to touch"), μορφή (morphê, "shape"), and γένεσις (génesis, "creation").
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 →Madam C.J. Walker
