HAX1 deficiency causes autosomal recessive severe congenital neutropenia (Kostmann disease) (Q28280427)

Nima Rezaei

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Jan Palmblad

16

Jan Palmblad

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Bengt Fadeel

14

Bengt Fadeel

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Bodo Grimbacher

19

Bodo Grimbacher

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Alejandro A Schäffer

6

Alejandro A Schäffer

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author name string

Christoph Klein

1

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Magda Grudzien

2

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Giridharan Appaswamy

3

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Manuela Germeshausen

4

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Inga Sandrock

5

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Chozhavendan Rathinam

7

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Kaan Boztug

8

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Beate Schwinzer

9

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Georg Bohn

11

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Malin Melin

12

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Göran Carlsson

13

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Niklas Dahl

15

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Cornelia Zeidler

18

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Karl Welte

Heterogeneous expression pattern of pro- and anti-apoptotic factors in myeloid progenitor cells of patients with severe congenital neutropenia treated with granulocyte colony-stimulating factor.

20

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language of work or name

English

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publication date

January 2007

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published in

Nature Genetics

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volume

39

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issue

1

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page(s)

86-92

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cites work

1 reference

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Galpha13 stimulates cell migration through cortactin-interacting protein Hax-1.

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Severe congenital neutropenia

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Infantile genetic agranulocytosis, morbus Kostmann: presentation of six cases from the original "Kostmann family" and a review

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Mutations in ELA2, encoding neutrophil elastase, define a 21-day biological clock in cyclic haematopoiesis.

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The incidence of leukemia and mortality from sepsis in patients with severe congenital neutropenia receiving long-term G-CSF therapy

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Granulocyte colony-stimulating factor inhibits the mitochondria-dependent activation of caspase-3 in neutrophils

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Epstein-Barr virus nuclear antigen 5 interacts with HAX-1, a possible component of the B-cell receptor signalling pathway

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Interaction of Epstein-Barr virus nuclear antigen leader protein (EBNA-LP) with HS1-associated protein X-1: implication of cytoplasmic function of EBNA-LP.

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Human immunodeficiency virus type 1 Vpr interacts with antiapoptotic mitochondrial protein HAX-1

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Comparative analysis of genetically modified dendritic cells and tumor cells as therapeutic cancer vaccines

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Kostmann syndrome: severe congenital neutropenia associated with defective expression of Bcl-2, constitutive mitochondrial release of cytochrome c, and excessive apoptosis of myeloid progenitor cells

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