C1 inhibitor hinge region mutations produce dysfunction by different mechanisms (Q34245813)

31 July 2017

title

C1 inhibitor hinge region mutations produce dysfunction by different mechanisms (English)

1 reference

31 July 2017

9

J. Bissler

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18 September 2022

author name string

Davis AE 3rd

1

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31 July 2017

A. E. Davis

1

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18 September 2022

K. Aulak

2

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18 September 2022

R. B. Parad

3

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18 September 2022

H. P. Stecklein

4

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18 September 2022

E. Eldering

5

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18 September 2022

C. E. Hack

6

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18 September 2022

J. Kramer

7

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18 September 2022

R. C. Strunk

8

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18 September 2022

F. S. Rosen

10

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18 September 2022

language of work or name

English

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publication date

1 August 1992

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31 July 2017

1 reference

31 July 2017

volume

1

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31 July 2017

issue

5

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31 July 2017

page(s)

354-358

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The structural basis for neutrophil inactivation of C1 inhibitor.

31 July 2017

cites work

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Hormone binding globulins undergo serpin conformational change in inflammation

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Crystal structure of ovalbumin as a model for the reactive centre of serpins

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Dysfunctional C1-inhibitor(At), isolated from a type II hereditary-angio-oedema plasma, contains a P1 'reactive centre' (Arg444----His) mutation

21 January 2018

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A functional abnormal antithrombin III (AT III) deficiency: AT III Charleville

21 January 2018

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Synthesis of the second component of complement by long-term primary cultures of human monocytes

21 January 2018

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Structural basis of latency in plasminogen activator inhibitor-1

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Mobile reactive centre of serpins and the control of thrombosis

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On the size of the active site in proteases. I. Papain

21 January 2018

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7 January 2021

Plakalbumin, alpha 1-antitrypsin, antithrombin and the mechanism of inflammatory thrombosis

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7 January 2021

Human alpha 1-proteinase inhibitor. Crystal structure analysis of two crystal modifications, molecular model and preliminary analysis of the implications for function

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7 January 2021

Antithrombin Cambridge, 384 Ala to Pro: a new variant identified using the polymerase chain reaction

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7 January 2021

Molecular characterization of antithrombin III (ATIII) variants using polymerase chain reaction. Identification of the ATIII Charleville as an Ala 384 Pro mutation

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7 January 2021

Type II hereditary angioneurotic edema that may result from a single nucleotide change in the codon for alanine-436 in the C1 inhibitor gene

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7 January 2021

Antithrombin Vicenza, Ala 384 to Pro (GCA to CCA) mutation, transforming the inhibitor into a substrate

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7 January 2021

Plasma levels of C1- inhibitor complexes and cleaved C1- inhibitor in patients with hereditary angioneurotic edema.

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7 January 2021

Genetically determined heterogeneity of the C1 esterase inhibitor in patients with hereditary angioneurotic edema

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7 January 2021

Variability in purified dysfunctional C1(-)-inhibitor proteins from patients with hereditary angioneurotic edema. Functional and analytical gel studies

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7 January 2021

Human C1 inhibitor: improved isolation and preliminary structural characterization

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7 January 2021

Cleavage of Structural Proteins during the Assembly of the Head of Bacteriophage T4

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7 January 2021

Isolation of biologically active ribonucleic acid from sources enriched in ribonuclease

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7 January 2021

Human C1 inhibitor: primary structure, cDNA cloning, and chromosomal localization

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7 January 2021

DNA sequencing with chain-terminating inhibitors

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7 January 2021

High efficiency polyoma DNA transfection of chloroquine treated cells

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7 January 2021

Alpha 2-antiplasmin Enschede: alanine insertion and abolition of plasmin inhibitory activity

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7 January 2021

Dysfunctional C1 inhibitor Ta: deletion of Lys-251 results in acquisition of an N-glycosylation site

1 reference

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7 January 2021

A molecular basis for the two locus model of human complement component C4

1 reference

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7 January 2021

Substitution of a single amino acid (aspartic acid for histidine) converts the functional activity of human complement C4B to C4A

1 reference

https://api.crossref.org/works/10.1038%2FNG0892-354

7 January 2021

A common neoepitope is created when the reactive center of C1-inhibitor is cleaved by plasma kallikrein, activated factor XII fragment, C1 esterase, or neutrophil elastase

1 reference

https://api.crossref.org/works/10.1038%2FNG0892-354

7 January 2021

Identifiers

DOI

10.1038/NG0892-354

1 reference

Dimensions Publication ID

31 July 2017

1015684306

0 references

1 reference