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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...

Wilmington 1898 — An American Coup

Wilmington, North Carolina once had a thriving Black middle class and an elected interracial government. In 1898 white supremacists used violence to overthrow that government, kill Black residents and drive many others from the city.

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Wikipedia

FOXG1

FOXG1
Identifiers
AliasesFOXG1, BF1, BF2, FHKL3, FKH2, FKHL1, FKHL2, FKHL3, FKHL4, FOXG1A, FOXG1B, FOXG1C, HBF-1, HBF-2, HBF-3, HBF-G2, HBF2, HFK1, HFK2, HFK3, KHL2, QIN, forkhead box G1
External IDsOMIM: 164874; MGI: 1347464; GeneCards: FOXG1
Orthologs
DatabasesNCBI: entry; OMA: entry
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_005249

NM_001160112
NM_008241

RefSeq (protein)

NP_005240

NP_001153584
NP_032267

Location (UCSC)Chr 14: 28.77 – 28.77 MbChr 12: 49.43 – 49.43 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Forkhead box protein G1 is a protein that in humans is encoded by the FOXG1 gene.[5][6][7]

Function

[edit]

This gene belongs to the forkhead family of transcription factors that is characterized by a distinct forkhead domain. The complete function of this gene has not yet been determined; however, it has been shown to play a role in the development of the brain and telencephalon. Mutations of FOXG1 are the cause of FoxG1 syndrome.[8]

Associated disorders

[edit]

FOXG1 syndrome is characterized by microcephaly and brain malformations. It affects most aspects of development and can cause seizures. FOXG1 syndrome is classified as an autism spectrum disorder and was previously considered a variant of Rett syndrome.[9][10]

Interactions

[edit]

FOXG1 has been shown to interact with JARID1B.[11]

See also

[edit]

References

[edit]
  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000176165 – Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000020950 – 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. ^ Murphy DB, Wiese S, Burfeind P, Schmundt D, Mattei MG, Schulz-Schaeffer W, Thies U (Nov 1994). "Human brain factor 1, a new member of the fork head gene family". Genomics. 21 (3): 551–7. doi:10.1006/geno.1994.1313. PMID 7959731.
  6. ^ Bredenkamp N, Seoighe C, Illing N (Feb 2007). "Comparative evolutionary analysis of the FoxG1 transcription factor from diverse vertebrates identifies conserved recognition sites for microRNA regulation". Dev Genes Evol. 217 (3): 227–33. doi:10.1007/s00427-006-0128-x. PMID 17260156. S2CID 20867411.
  7. ^ "Entrez Gene: FOXG1B forkhead box G1B".
  8. ^ Ariani F, Hayek G, Rondinella D, Artuso R, Mencarelli MA, Spanhol-Rosseto A, Pollazzon M, Buoni S, Spiga O, Ricciardi S, Meloni I, Longo I, Mari F, Broccoli V, Zappella M, Renieri A (2008). "FOXG1 is responsible for the congenital variant of Rett syndrome". Am. J. Hum. Genet. 83 (1): 89–93. doi:10.1016/j.ajhg.2008.05.015. PMC 2443837. PMID 18571142.
  9. ^ "FOXG1 syndrome".
  10. ^ "FOXG1 Syndrome: More than a congenital variant of Rett Syndrome? | the University of Chicago Genetic Services".
  11. ^ Tan K, Shaw AL, Madsen B, Jensen K, Taylor-Papadimitriou J, Freemont PS (Jun 2003). "Human PLU-1 Has transcriptional repression properties and interacts with the developmental transcription factors BF-1 and PAX9". J. Biol. Chem. 278 (23): 20507–13. doi:10.1074/jbc.M301994200. PMID 12657635.

Further reading

[edit]
[edit]

This article incorporates text from the United States National Library of Medicine, which is in the public domain.


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

Wikipedia

FOXG1

Forkhead box protein G1 is a protein that in humans is encoded by the FOXG1 gene.

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Wikipedia

FOXG1 syndrome

FOXG1 syndrome (sometimes FOXG1-related disorder) is a rare genetic disorder caused by mutation in the gene FOXG1. The main signs of this disease are: severe intellectual disability, microcephaly, epilepsy, and hyperkinetic-dyskinetic movement disorder and hypotonia with brain structure anomalies. FOXG1 syndrome is inherited in autosomal dominant fashion. The syndrome affects about 1/30 000 births, with about 1200 cases having been reported as of January 1, 2025.

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Wikipedia

Retina

The retina (from Latin rete 'net'; pl. retinae or retinas) is the innermost, light-sensitive layer of tissue of the eye. The optics of the eye create a focused two-dimensional image of the visual world on the retina, which then processes that image within the retina and sends nerve impulses along the optic nerve to the visual cortex to create visual perception. The retina serves a function that is in many ways analogous to that of the film or image sensor in a camera. The neural retina consists of several layers of neurons interconnected by synapses and is supported by an outer layer of pigmented epithelial cells. The primary light-sensing cells in the retina are the photoreceptor cells, which are of two types: rods and cones. Rods function mainly in dim light and provide monochromatic vision. Cones function in well-lit conditions and are responsible for the perception of colour through the use of a range of opsins, as well as high-acuity vision used for tasks such as reading. A third type of light-sensing cell, the photosensitive ganglion cell, is important for entrainment of circadian rhythms and reflexive responses such as the pupillary light reflex. Light striking the retina initiates a cascade of chemical and electrical events that ultimately trigger nerve impulses that are sent to various visual centres of the brain through the fibres of the optic nerve. Neural signals from the rods and cones undergo processing by other neurons, whose output takes the form of action potentials in retinal ganglion cells whose axons form the optic nerve. In vertebrate embryonic development, the retina and the optic nerve originate as outgrowths of the developing brain, specifically the embryonic diencephalon; thus, the retina is considered part of the central nervous system (CNS) and is actually brain tissue. It is the only part of the nervous system that can be visualized noninvasively. Like most of the brain, the retina is isolated from the vascular system by the blood–brain barrier. The retina is the part of the body with the greatest continuous energy demand.

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Wikipedia

Rett syndrome

Rett syndrome (RTT) is a genetic disorder that typically becomes apparent after 6–18 months of age and almost exclusively in girls. Symptoms include impairments in language and coordination, and repetitive movements. Those affected often have slower growth, difficulty walking, and a smaller head size. Complications of Rett syndrome can include seizures, scoliosis, and sleeping problems. The severity of the condition is variable. Rett syndrome is due to a genetic mutation, usually in the MECP2 gene, on the X chromosome. It almost always occurs as a new mutation, with less than one percent of cases being inherited. It occurs almost exclusively in girls; boys who have a similar mutation typically die shortly after birth. Diagnosis is based on the symptoms and can be confirmed with genetic testing. There is no known cure for Rett syndrome. Treatment is directed at improving symptoms. Anticonvulsants may be used to help with seizures. Special education, physiotherapy, and leg braces may also be useful depending on the needs of the child. Many of those with the condition live into middle age. The condition affects about 1 in 8,500 females. In 1999, Lebanese-American physician Huda Zoghbi discovered the mutation that causes the condition.

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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 became the first Black woman to travel into space?

Mae Jemison, aboard Space Shuttle Endeavour in 1992.