Results 221 to 230 of about 14,918,859 (275)

Paclitaxel induces NM2‐dependent cellular contraction through GEF‐H1 dissociation from microtubules and RhoA/ROCK activation in cancer cells

open access: yesMolecular Oncology, EarlyView.
Taxanes are widely used chemotherapeutics whose effects on cellular mechanics remain poorly understood. We show that paclitaxel induces rapid cellular contraction by promoting GEF‐H1 dissociation from microtubules and non‐muscle myosin II activation through RhoA/ROCK.
Gloria Asensio‐Juárez   +5 more
wiley   +1 more source

APOBEC3 activity and DNA polymerase‐ε deficiency are associated with distinct IDH1 R132 hotspot mutations

open access: yesMolecular Oncology, EarlyView.
Isocitrate dehydrogenase 1 (IDH1) mutations are highly recurrent in multiple human cancer types, including cholangiocarcinoma and glioma. IDH1 R132C is the most common IDH1 mutation in cholangiocarcinoma and likely arises from APOBEC3A‐ or APOBEC3B‐mediated deamination.
Kelly E. Butler   +3 more
wiley   +1 more source

Inherited and acquired factor V deficiency

open access: yesBlood Coagulation & Fibrinolysis, 2011
The clotting factor V, also known as proaccelerin or labile factor, is synthesized by the liver and possibly by the megakaryocytes. Factor V exerts a pivotal role in hemostasis, as it participates in both procoagulant and anticoagulant pathways, being an essential cofactor of the prothrombinase complex in the former case and participating in the ...
LIPPI, Giuseppe   +5 more
openaire   +4 more sources

Combined Factor V and Factor VIII Deficiency

open access: yesSeminars in Thrombosis and Hemostasis, 2009
Combined deficiency of factor V (FV) and factor VIII (FVIII) (F5F8D, or FV+FVIII) is a autosomal recessive bleeding disorder caused by mutations in genes encoding two components of the endoplasmic reticulum (ER)-Golgi intermediate compartment (ERGIC-53), that is, lectin mannose binding protein ( LMAN1) and multiple coagulation factor deficiency 2 ...
Marta, Spreafico, Flora, Peyvandi
openaire   +3 more sources

Hereditary Labile Factor (Factor V) Deficiency

JAMA, 1961
Hereditary labile factor (Factor V) deficiency is transmitted as an autosomal recessive. Only individuals who inherit the defective gene from both parents are bleeders. In the family studied, the father is Greek while the mother is Polish. The diagnosis is made by determining the prothrombin time by the one-stage method, which is completely corrected ...
I A, FRIEDMAN   +4 more
openaire   +2 more sources

Congenital Factor V Deficiency

Scandinavian Journal of Haematology, 1978
A 14‐month‐old girl suffering from a heavy bleeding tendency, caused by a severe isolated congenital factor V deficiency is described. In this study 56 family members were examined. 10 of them had a factor V level ranging 26–60% of the normal – these were classified as heterozygotes.
G, Mitterstieler, W, Müller, W, Geir
openaire   +2 more sources

The Treatment of Patients with Factor-V Deficiency

Thrombosis and Haemostasis, 1965
SummaryTwo patients with congenital factor-V deficiency and a third with a combined deficiency of factor V and factor VIII are described. Under cover of fresh frozen plasma, tooth extractions were performed on two of these patients and spontaneous bleeding arrested.It is concluded that the achievement of a blood level of factor V of 20 per cent once ...
B, Rush, H, Ellis
openaire   +2 more sources

Factor V Deficiency: A Subtle Presentation

The Indian Journal of Pediatrics, 2013
Congenital factor V deficiency (also known as labile factor or proaccelerin) is a rather uncommon [1:1000,000] inherited coagulopathy (autosomal recessive inheritance). Affected patients become symptomatic in early childhood with spontaneous or post-traumatic bleeding complications.
Mukesh Uttamchand, Sanklecha   +2 more
openaire   +2 more sources

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