Results 101 to 110 of about 1,688,140 (295)

Mutants used to define functional residues in SMIPP-S complement inhibition.

open access: yes, 2014
Mutants used to define functional residues in SMIPP-S complement inhibition.
Katja Fischer (152079)   +7 more
core   +1 more source

Modulator-induced conformational changes in complement C5, implications for function and drug design

open access: yesFrontiers in Immunology
BackgroundThe human complement system comprises proteolytic cascades that drive protective inflammatory and cytolytic responses, making it a crucial part of innate immunity.
Andrey Zhivnov   +7 more
doaj   +1 more source

Metastasis on pause: How dormant tumor cells stay hidden within the tumor microenvironment and evade immune surveillance

open access: yesMolecular Oncology, EarlyView.
Dormant cancer cells can hide in distant organs for years, evading treatment and the immune system. This review highlights how signals from the surrounding tissue and immune environment keep these cells inactive or trigger their reawakening. Understanding these mechanisms may help develop therapies to eliminate or control dormant cells and prevent ...
Kanishka Tiwary   +1 more
wiley   +1 more source

Complement C5 inhibitor as a rescue therapy for acute NMOSD attacks: a multicenter retrospective cohort study in China

open access: yesFrontiers in Immunology
BackgroundComplement activation plays a key role in the pathogenesis of neuromyelitis optica spectrum disorder (NMOSD). While eculizumab effectively prevents relapses, its role in acute attacks remains uncertain.MethodsWe retrospectively analyzed 38 ...
Tao Wu   +13 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

Peri-transplant eculizumab for preventing antibody-mediated rejection in kidney transplant recipients at high immunologic risk: a systematic review with design-stratified evidence synthesis

open access: yesFrontiers in Immunology
IntroductionHighly sensitized candidates, preformed donor-specific antibodies, and ABO incompatibility restrict access to kidney transplantation and increase antibody-mediated rejection (AMR) risk.
Chengze Liang   +17 more
doaj   +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

Complement C2 receptor inhibitor trispanning: a novel human complement inhibitory receptor

open access: yes, 2005
The complement system presents a powerful defense against infection and is tightly regulated to prevent damage to self by functionally equivalent soluble and membrane regulators.
Krueger, G.   +6 more
core  

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

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