Targeted gene disruption shows that knobs enable malaria-infected red cells to cytoadhere under physiological shear stress. (Q34422119)

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2 November 2019

title

Targeted gene disruption shows that knobs enable malaria-infected red cells to cytoadhere under physiological shear stress (English)

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2 November 2019

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3

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2 November 2019

Ross Waller

4

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2 November 2019

author name string

B S Crabb

1

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2 November 2019

B M Cooke

2

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2 November 2019

S R Caruana

5

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2 November 2019

K M Davern

6

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2 November 2019

M E Wickham

7

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2 November 2019

G V Brown

8

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2 November 2019

R L Coppel

9

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2 November 2019

A F Cowman

10

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2 November 2019

language of work or name

English

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publication date

1 April 1997

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2 November 2019

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2 November 2019

volume

89

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2 November 2019

issue

2

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2 November 2019

page(s)

287-296

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A human 88-kD membrane glycoprotein (CD36) functions in vitro as a receptor for a cytoadherence ligand on Plasmodium falciparum-infected erythrocytes

2 November 2019

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Cloning the P. falciparum gene encoding PfEMP1, a malarial variant antigen and adherence receptor on the surface of parasitized human erythrocytes

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Plasmodium falciparum erythrocyte membrane protein 1 is a parasitized erythrocyte receptor for adherence to CD36, thrombospondin, and intercellular adhesion molecule 1.

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Knob-independent cytoadherence of Plasmodium falciparum to the leukocyte differentiation antigen CD36.

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Rolling and stationary cytoadhesion of red blood cells parasitized by Plasmodium falciparum: separate roles for ICAM‐1, CD36 and thrombospondin

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Characterization of a protein correlated with the production of knob-like protrusions on membranes of erythrocytes infected with Plasmodium falciparum

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7 January 2021

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7 January 2021

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