Results 101 to 110 of about 4,387,093 (287)

Hipocomplementemia en pacientes con enfermedad de Hodgkin Hypocomplementaemia in patients with Hodgkin disease

open access: yesRevista Cubana de Hematología, Inmunología y Hemoterapia, 2003
The haemolytic activity of the classical and alternative pathways, of factors B and D, as well as of the levels of C1q, C3 and C4 was determined in the serum of 24 adult patients with Hodgkin disease at different clinical stages.
doaj  

Kidney Diseases Caused by Complement Dysregulation: Acquired, Inherited, and Still More to Come

open access: yesClinical and Developmental Immunology, 2012
Inherited and acquired dysregulation of the complement alternative pathway plays an important role in multiple renal diseases. In recent years, the identification of disease-causing mutations and genetic variants in complement regulatory proteins has ...
Saskia F. Heeringa, Clemens D. Cohen
doaj   +1 more source

Properdin: A Novel Target for Neuroprotection in Neonatal Hypoxic-Ischemic Brain Injury

open access: yesFrontiers in Immunology, 2019
Background: Hypoxic-ischemic (HI) encephalopathy is a major cause of neonatal mortality and morbidity, with a global incidence of 3 per 1,000 live births.
Claudia Sisa   +5 more
doaj   +1 more source

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis   +3 more
wiley   +1 more source

Finding novel vulnerabilities of hypomorphic BRCA1 alleles

open access: yesMolecular Oncology, EarlyView.
Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder   +10 more
wiley   +1 more source

Activation of the alternative pathway of complement by apoptotic Jurkat cells [PDF]

open access: yes, 1994
Jurkat T cells die of apoptosis upon exposure to anti-Fas mAb. Here we show that although the alternative complement pathway generally does not attack homologous cells, anti-Fas-induced apoptotic Jurkat T cells were attacked antibody-independently by the
Hitosi Nishimura   +7 more
core   +1 more source

A novel quinazolinone insulin receptor inhibitor and its synergy with an EGFR inhibitor in glucose‐driven glioblastoma

open access: yesMolecular Oncology, EarlyView.
The novel styrylquinazolinone‐based molecule W1B effectively suppresses glioblastoma by inhibiting IGF1R and EGFR. In high‐glucose microenvironments driving tumor resistance, W1B acts synergistically with the EGFR inhibitor dacomitinib. This combination safely blocks compensatory survival signaling in zebrafish xenograft models. Showcasing promising in
Patryk Rurka   +9 more
wiley   +1 more source

Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization

open access: yesMolecular Oncology, EarlyView.
In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu   +13 more
wiley   +1 more source

Exploring the involvement of the alternative complement pathway in non-infectious uveitis pathogenesis. [PDF]

open access: yesFront Immunol, 2023
Kulshrestha P   +6 more
europepmc   +1 more source

Loss of proton‐sensing TDAG8 increases tumor progression in mouse models of colon cancer

open access: yesMolecular Oncology, EarlyView.
Loss of the pH‐sensing receptor TDAG8 accelerates colorectal cancer progression in mice. Animals lacking TDAG8 expression had increased tumor growth, DNA damage, and recruitment of tumor‐associated immune cells, including macrophages, neutrophils, and monocytes.
Ermanno Malagola   +11 more
wiley   +1 more source

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