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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

TICAM1

TICAM1
Identifiers
AliasesTICAM1, IIAE6, MyD88-3, PRVTIRB, TICAM-1, TRIF, toll like receptor adaptor molecule 1, TIR domain containing adaptor molecule 1
External IDsOMIM: 607601; MGI: 2147032; GeneCards: TICAM1
Available structures
PDBOrtholog search: PDBe RCSB
Orthologs
DatabasesNCBI: entry; OMA: entry
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_182919
NM_014261
NM_001385678
NM_001385679
NM_001385680

NM_174989

RefSeq (protein)

NP_891549

NP_778154

Location (UCSC)Chr 19: 4.82 – 4.83 MbChr 17: 56.58 – 56.58 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

TIR domain containing adaptor molecule 1 (TICAM1; formerly known as TIR-domain-containing adapter-inducing interferon-β or TRIF) is an adapter in responding to activation of toll-like receptors (TLRs). It mediates the rather delayed cascade of two TLR-associated signaling cascades, where the other one is dependent upon a MyD88 adapter.[5]

Toll-like receptors (TLRs) recognize specific components of microbial invaders and activate an immune response to these pathogens. After these receptors recognize highly conserved pathogenic patterns, a downstream signaling cascade is activated in order to stimulate the release of inflammatory cytokines and chemokines as well as to upregulate the expression of immune cells. All TLRs have a TIR domain that initiates the signaling cascade through TIR adapters. Adapters are platforms that organize downstream signaling cascades leading to a specific cellular response after exposure to a given pathogen.[6]

Structure

[edit]

TICAM1 is primarily active in the spleen and is often regulated when MyD88 is deficient in the liver, indicating organ-specific regulation of signaling pathways. Curiously, there is a lack of redundancy within the TLR4 signaling pathway that leads to microbial evasion of immune response in the host after mutations occur within intermediates of the pathway.[7] Three TRAF-binding motifs present in the amino terminal region of TICAM1 are necessary for association with TRAF6. Destruction of these motifs reduced the activation of NF-κB, a transcription factor that is also activated by the carboxy-terminal domain of TICAM1 in the upregulation of cytokines and co-stimulatory immune molecules. This domain recruits receptor-interacting protein (RIP1) and RIP3 through the RIP homotypic interaction motif. Cells deficient for RIP1 gene display attenuated TLR3 activation of NF-κB, indicating the use of the RIP1 gene in downstream TICAM1 activation, in contrast to other TLRs that use IRAK protein for the activation of NF-κB.[8]

Areas of research

[edit]

Investigations into the function of TICAM1 are of great significance to various fields of biomedical research. The pathogenesis of infectious disease, septic shock, tumor growth, and rheumatoid arthritis all have close ties with TLR signaling pathways, specifically to that of TICAM1 . Better understanding of the TICAM1 pathway will be therapeutically useful in the development of vaccines and treatments that can control associated inflammation and antiviral responses. Experiments involving wild-type and TICAM1-deficient mice are critical for understanding the coordinated responses of TLR pathways. It is necessary to study the coordinated effects of these pathways in order to understand the complex responses initiated by TICAM1.[9]

References

[edit]
  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000127666 – Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000047123 – 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. ^ Palsson-McDermott EM, O'Neill LA (October 2004). "Signal transduction by the lipopolysaccharide receptor, Toll-like receptor-4". Immunology. 113 (2): 153–162. doi:10.1111/j.1365-2567.2004.01976.x. PMC 1782563. PMID 15379975. Open access icon
  6. ^ Guo B, Cheng G (2007). "Modulation of the interferon antiviral response by the TBK1/IKKi adaptor protein TANK". The Journal of Biological Chemistry. 282 (16): 11817–11826. doi:10.1074/jbc.M700017200. PMID 17327220.
  7. ^ Palsson-McDermott, Eva and Luke A J O’Neill (2004) Immunology. 113(2) 153-162
  8. ^ Kawai, Taro and Shizuo Akira. (2004). Arthritis Res. Ter. 7(1) 12-19
  9. ^ Ouyang X, Negishi H, Takeda R, Fujita Y, Taniguchi T, Honda K (2007). "Cooperation between MyD88 and TICAM1 pathways in TLR synergy via IRF5 activation". Biochemical and Biophysical Research Communications. 354 (4): 1045–1051. doi:10.1016/j.bbrc.2007.01.090. PMID 17275788.
[edit]

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

Wikipedia

TICAM1

TIR domain containing adaptor molecule 1 (TICAM1; formerly known as TIR-domain-containing adapter-inducing interferon-β or TRIF) is an adapter in responding to activation of toll-like receptors (TLRs). It mediates the rather delayed cascade of two TLR-associated signaling cascades, where the other one is dependent upon a MyD88 adapter. Toll-like receptors (TLRs) recognize specific components of microbial invaders and activate an immune response to these pathogens. After these receptors recognize highly conserved pathogenic patterns, a downstream signaling cascade is activated in order to stimulate the release of inflammatory cytokines and chemokines as well as to upregulate the expression of immune cells. All TLRs have a TIR domain that initiates the signaling cascade through TIR adapters. Adapters are platforms that organize downstream signaling cascades leading to a specific cellular response after exposure to a given pathogen.

MORE →
Wikipedia

Neomycin

Neomycin, also known as framycetin, is an aminoglycoside antibiotic that displays bactericidal activity against Gram-negative aerobic bacilli and some anaerobic bacilli where resistance has not yet arisen. It is generally not effective against Gram-positive bacilli and anaerobic Gram-negative bacilli. Neomycin comes in oral and topical formulations, including creams, ointments, and eyedrops. Neomycin belongs to the aminoglycoside class of antibiotics that contain two or more amino sugars connected by glycosidic bonds. Neomycin was discovered in 1949 by microbiologist Selman Waksman and his student Hubert Lechevalier at Rutgers University. Neomycin received approval for medical use in 1952. Rutgers University was granted the patent for neomycin in 1957.

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Wikipedia

Bruce Beutler

Bruce Alan Beutler ( BOYT-lər; born December 29, 1957) is an American immunologist and geneticist. Together with Jules A. Hoffmann, he received one-half of the 2011 Nobel Prize in Physiology or Medicine, for "discoveries concerning the activation of innate immunity." Beutler discovered the long-elusive receptor for lipopolysaccharide (LPS; also known as endotoxin). He did so by identifying spontaneous mutations in the gene coding for mouse Toll-like receptor 4 (Tlr4) in two unrelated strains of LPS-refractory mice and proving they were responsible for that phenotype. Subsequently, and chiefly through the work of Shizuo Akira, other TLRs were shown to detect signature molecules of most infectious microbes, in each case triggering an innate immune response. The other half of the Nobel Prize went to Ralph M. Steinman for "his discovery of the dendritic cell and its role in adaptive immunity." Beutler is currently a Regental Professor and Director of the Center for the Genetics of Host Defense at the University of Texas Southwestern Medical Center in Dallas, Texas. In 2012, Beutler was appointed as an Honorary Professor in the School of Biochemistry and Immunology at Trinity College Dublin.

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Wikipedia

Outline of immunology

The following outline is provided as an overview of and topical guide to immunology: Immunology – study of all aspects of the immune system in all organisms. It deals with the physiological functioning of the immune system in states of both health and disease; malfunctions of the immune system in immunological disorders (autoimmune diseases, hypersensitivities, immune deficiency, transplant rejection); the physical, chemical and physiological characteristics of the components of the immune system in vitro, in situ, and in vivo.

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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

Which Black woman became the first elected to the United States Congress?

Shirley Chisholm, elected in 1968.