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MY'STORY

The MOVE Fire

This is a personal recollection on the Move fire on May 13, 1985 Philadelphia police fired thousands of rounds at the MOVE house, city officials approved dropping an explosive device on the roof, the resulting fire was allowed to burn, 11 people—including five children—died, and 61 homes were destroyed. Philadelphia City Council later called it a “brutal attack carried out by the City of Philadelphia on its own citizens” and acknowledged that no individual faced criminal consequences for the bombing. One timeline correction worth preserving for the BHP record: the major previous MOVE-police confrontation was August 8, 1978, about seven years before the bombing, not a year or two earlier. Officer James Ramp was killed, other police and firefighters were wounded, nine MOVE members were later convicted, and television cameras recorded police beating Delbert Africa during his arrest. The 1985 MOVE Commission later specifically criticized city planners for failing to adequately use lessons from that 1978 confrontation. And that actually strengthens the point you’re making: 1985 did not happen without precedent or institutional memory. There had already been a deadly confrontation with MOVE, years of conflict, negotiations and police involvement before Osage Avenue.

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BLACK FACTS
The Truths They Never Taught You...

Katherine Johnson — Mathematics to the Moon

Katherine Johnson’s mathematical calculations helped guide some of America’s most important early space missions while she confronted the racial and gender barriers faced by Black women in twentieth-century America.

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Wikipedia

BIN1

BIN1
Identifiers
AliasesBIN1, AMPH2, AMPHL, SH3P9, bridging integrator 1, CNM2
External IDsOMIM: 601248; MGI: 108092; GeneCards: BIN1
Available structures
PDBOrtholog search: PDBe RCSB
Orthologs
DatabasesNCBI: entry; OMA: entry
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001083334
NM_009668
NM_001360876

RefSeq (protein)

NP_001076803
NP_033798
NP_001347805

Location (UCSC)Chr 2: 127.05 – 127.11 MbChr 18: 32.51 – 32.57 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Myc box‑dependent‑interacting protein 1 (BIN1), also known as bridging integrator 1 and amphiphysin‑2, is a protein that in humans is encoded by the BIN1 gene.[5][6][7]

Function

[edit]

This gene encodes multiple isoforms of a membrane‑associated adaptor protein that can localize to the cytoplasm and, in some contexts, the nucleus. One isoform was originally identified as a MYC-interacting protein with characteristics of a tumor suppressor.[6] BIN1 plays important roles in membrane curvature, endocytosis, and organization of specialized membrane structures such as transverse (T)‑tubules in striated muscle.[8]

Nervous system

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Isoforms expressed in the central nervous system participate in synaptic vesicle endocytosis and membrane trafficking through interactions with dynamin, endophilin, synaptojanin, and clathrin.[9] Genetic variation at the BIN1 locus has been associated with risk of late‑onset Alzheimer's disease, and neuronal BIN1 isoforms interact with the microtubule‑associated protein tau.[10][11]

Muscle and cellular functions

[edit]

Muscle-specific and ubiquitously expressed isoforms are essential for the formation and maintenance of T-tubules and excitation–contraction coupling in skeletal and cardiac muscle.[7][8] Certain nuclear-localized isoforms have been reported to modulate cell cycle progression and to induce an apoptotic or growth‑suppressive response independent of caspase activation in tumor cells.[12]

Development and splicing

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Studies in mice suggest that this gene plays an important role in cardiac muscle development and postnatal maturation of T-tubules.[13] Alternative splicing of BIN1 generates numerous transcript variants encoding distinct isoforms with tissue‑specific expression patterns, and aberrant splice variants that attenuate BIN1 tumor-suppressor activity have been identified in several tumor cell lines and cancers.[14][15]

Clinical significance

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In humans, mutations in BIN1 have been associated with skeletal myopathies including centronuclear myopathy causing muscle weakness[7] and myotonic dystrophy causing progressive muscle wasting, myotonia, cataracts, and heart conduction defects.[9] An association has also been found between BIN1 mutations and Alzheimer's disease.[9] Knockdown of BIN1 produces a cardiomyopathy phenotype in zebrafish,[16] and in sheep BIN1 may be responsible for the loss of T-tubules seen in heart failure.[17]

References

[edit]
  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000136717 – Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000024381 – Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ Negorev D, Riethman H, Wechsler-Reya R, Sakamuro D, Prendergast GC, Simon D (January 1997). "The Bin1 gene localizes to human chromosome 2q14 by PCR analysis of somatic cell hybrids and fluorescence in situ hybridization". Genomics. 33 (2): 329–331. doi:10.1006/geno.1996.0205. PMID 8725406.
  6. ^ a b Sakamuro D, Elliott KJ, Wechsler-Reya R, Prendergast GC (October 1996). "BIN1 is a novel MYC-interacting protein with features of a tumour suppressor". Nature Genetics. 14 (1): 69–77. doi:10.1038/ng0996-69. PMID 8782822. S2CID 21484402.
  7. ^ a b c Nicot AS, Toussaint A, Tosch V, Kretz C, Wallgren-Pettersson C, Iwarsson E, et al. (August 2007). "Mutations in amphiphysin 2 (BIN1) disrupt interaction with dynamin 2 and cause autosomal recessive centronuclear myopathy". Nature Genetics. 39 (9): 1134–1139. doi:10.1038/ng2086. PMID 17676042. S2CID 16861439.
  8. ^ a b Hong T, Smyth JW, Gao H, Chu KY, Vogan JM, Fong TS, et al. (January 2014). "BIN1 localizes the L-type calcium channel to cardiac T-tubules". PLOS Biology. 12 (2) e1001682. doi:10.1371/journal.pbio.1001682. PMC 3933470. PMID 24586119.
  9. ^ a b c Prokic I, Cowling BS, Laporte J (May 2014). "Amphiphysin 2 (BIN1) in physiology and diseases". Journal of Molecular Medicine. 92 (5). Berlin, Germany: 453–463. doi:10.1007/s00109-014-1138-1. PMID 24590001. S2CID 14038898.
  10. ^ Lambert JC, Ibrahim-Verbaas CA, Harold D, Naj AC, Sims R, Bellenguez C, et al. (December 2013). "Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer's disease". Nature Genetics. 45 (12): 1452–1458. doi:10.1038/ng.2802. PMC 3896259. PMID 24162737.
  11. ^ Ramijan K, Ultee E, Willemse J, Zhang Z, Wondergem JA, van der Meij A, et al. (2018). "Structural basis of tau interaction with BIN1 and regulation by tau phosphorylation". Frontiers in Molecular Neuroscience. 11 421. doi:10.3389/fnmol.2018.00421. PMC 6259631. PMID 30514921.
  12. ^ Elliott K, Sakamuro D, Basu A, Du W, Wunner W, Staller P, et al. (May 1999). "BIN1 functionally interacts with Myc and inhibits cell proliferation via multiple mechanisms". Oncogene. 18 (24): 3564–3573. doi:10.1038/sj.onc.1202707. PMID 10380881.
  13. ^ Hong T, Yang H, Zhang SS, Cho HC, Kalashnikova M, Sun B, et al. (December 2010). "Cardiac BIN1 folds T-tubule membrane, controlling ion flux and limiting arrhythmia". Nature Medicine. 16 (12): 1281–1286. doi:10.1038/nm.2250. PMC 3058211. PMID 21076393.
  14. ^ Ge K, Minhas F, Duhadaway JB, Mao NC, Wilson D, Buccafusca R, et al. (March 2000). "Loss of heterozygosity and tumor suppressor activity of BIN1 in prostate carcinoma". International Journal of Cancer. 87 (3): 241–245. doi:10.1002/1097-0215(20000801)87:3<241::AID-IJC1>3.0.CO;2-I. PMID 10861484.
  15. ^ Zhu J, Sanborn JZ, Benz S, Szeto C, Hsu F, Kuhn RM, et al. (February 2012). "The association of aberrant alternative splicing with tumor status in human cancer". Molecular Cancer. 11 13. doi:10.1186/1476-4598-11-13. PMC 3311074. PMID 22369237.
  16. ^ Hong TT, Smyth JW, Chu KY, Vogan JM, Fong TS, Jensen BC, et al. (May 2012). "BIN1 is reduced and Cav1.2 trafficking is impaired in human failing cardiomyocytes". Heart Rhythm. 9 (5): 812–820. doi:10.1016/j.hrthm.2011.11.055. PMC 3306544. PMID 22138472.
  17. ^ Caldwell JL, Smith CE, Taylor RF, Kitmitto A, Eisner DA, Dibb KM, et al. (December 2014). "Dependence of cardiac transverse tubules on the BAR domain protein amphiphysin II (BIN-1)". Circulation Research. 115 (12): 986–996. doi:10.1161/CIRCRESAHA.116.303448. PMC 4274343. PMID 25332206.

Further reading

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Source: Wikipedia. Article content is retrieved live through the MediaWiki API.

Wikipedia

BIN1

Myc box‑dependent‑interacting protein 1 (BIN1), also known as bridging integrator 1 and amphiphysin‑2, is a protein that in humans is encoded by the BIN1 gene.

MORE →
Wikipedia

Three-section staff

The three-section staff, three-part staff, triple staff, originally sanjiegun (Chinese: 三節棍; pinyin: sānjiégùn; Jyutping: saam1 zit3 gwan3) or sansetsukon (Japanese: さんせつこん), three-section whip, originally sanjiebian (Chinese: 三節鞭; pinyin: sānjiébiān; Jyutping: saam1 zit3 bin1), is a Chinese flail weapon that consists of three wooden or metal staves connected by metal rings or rope. The weapon is also known as the coiling dragon staff, originally panlong gun (Chinese: 蟠龍棍; pinyin: pánlónggùn; Jyutping: faan4 lung4 gwan3). A more complicated version of the two section staff, the staves can be spun to gather momentum resulting in a powerful strike, or their articulation can be used to strike over or around a shield or other defense.

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Wikipedia

Alzheimer's disease in the Hispanic/Latino population

Alzheimer's disease (AD) in the Hispanic/Latino population is becoming a topic of interest in AD research as Hispanics and Latinos are disproportionately affected by Alzheimer's Disease and underrepresented in clinical research. AD is a neurodegenerative disease, characterized by the presence of amyloid-beta plaques and neurofibrillary tangles, that causes memory loss and cognitive decline in its patients. However, pathology and symptoms have been shown to manifest differently in Hispanic/Latinos, as different neuroinflammatory markers are expressed and cognitive decline is more pronounced. Additionally, there is a large genetic component of AD, with mutations in the amyloid precursor protein (APP), apolipoprotein E APOE), presenilin 1 (PSEN1), bridging Integrator 1 (BIN1), SORL1, and clusterin (CLU) genes increasing one's risk to develop the condition. However, research has shown these high-risk genes have a different effect on Hispanics and Latinos then they do in other racial and ethnic groups. Additionally, this population experiences higher rates of comorbidities, that increase their risk of developing AD. Hispanics and Latinos also face socioeconomic and cultural factors, such as low income and a language barrier, that affect their ability to engage in clinical trials and receive proper care.

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Wikipedia

Sichuan

Sichuan is an inland province in Southwestern China. It is located in the Sichuan Basin and Tibetan Plateau—between the Jinsha River to the west, the Daba Mountains to the north, and the Yunnan–Guizhou Plateau to the south. Its capital city is Chengdu, and the province's population stands at 83 million. Sichuan neighbors Qinghai and Gansu to the north, Shaanxi and Chongqing to the east, Guizhou and Yunnan to the south, and Tibet to the west. During antiquity, Sichuan was home to the kingdoms of Ba and Shu until their incorporation by the Qin round 316 BC. During the Three Kingdoms era (220–280), Liu Bei's state of Shu was based in Sichuan. The area was devastated in the 17th century by Zhang Xianzhong's rebellion and the area's subsequent Manchu conquest. The area recovered to become one of China's most productive by the 19th century. During World War II, Chongqing served as the temporary capital of the Republic of China, and was heavily bombed. It was one of the last mainland areas captured by the People's Liberation Army during the Chinese Civil War, and was divided into four parts from 1949 to 1952, with Chongqing restored two years later. It suffered gravely during the Great Chinese Famine (1959–1961) but remained China's most-populous province until Chongqing was again separated from it in 1997. The Sichuanese people speak distinctive dialects of Mandarin Chinese. The Sichuan pepper, with its distinctive flavor and numbing effect, is prominent in modern Sichuan cuisine, featuring dishes, including Kung Pao chicken and mapo tofu, that have become staples of Chinese cuisine around the world. There are many panda stations in the province and large reserves for these creatures, such as the Chengdu Research Base of Giant Panda Breeding. Sichuan is the 5th-largest provincial economy of China, the largest in Western China, and the largest among inland provinces. As of 2021, its nominal GDP was CN¥5,385 billion (US$847.68 billion), ahead of that of Turkey ($815 billion). If it were its own country, Sichuan would be the 18th-largest economy and 19th-most populous as of 2021.

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TOPIC OF THE DAY

Greenwood / Black Wall Street

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.

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TRIVIA QUESTION OF THE DAY

Who was the first African-American woman millionaire in the United States?

Madam C.J. Walker