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HCLS1 associated protein X-1

HAX-1, HS1-associated protein X-1
The protein encoded by this gene is known to associate with hematopoietic cell-specific Lyn substrate 1, a substrate of Src family tyrosine kinases. It also interacts with the product of the polycystic kidney disease 2 gene, mutations in which are associated with autosomal-dominant polycystic kidney disease, and with the F-actin-binding protein, cortactin. It was earlier thought that this gene product is mainly localized in the mitochondria, however, recent studies indicate it to be localized in the cell body. Mutations in this gene result in autosomal recessive severe congenital neutropenia, also known as Kostmann disease. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, PrP, HAD, bcl-2, G-CSF
Papers on HAX-1
Regulation of Focal Adhesion Dynamics and Cell Motility by the EB2 and Hax1 Protein Complex.
Wu et al., Chicago, United States. In J Biol Chem, Jan 2016
By quantitative proteomics, we identified mammalian HCLS1-associated protein X-1 (HAX1) as an EB2-specific interacting protein.
Game of clones: the genomic evolution of severe congenital neutropenia.
Touw, Rotterdam, Netherlands. In Hematology Am Soc Hematol Educ Program, Jan 2016
It is now well-established that mutations in HAX1 and ELANE (and more rarely in other genes) are the genetic cause of SCN.
HAX-1 regulates cyclophilin-D levels and mitochondria permeability transition pore in the heart.
Kranias et al., Cincinnati, United States. In Proc Natl Acad Sci U S A, Dec 2015
Studies in human lymphocytes suggested that the hematopoietic-substrate-1 associated protein X-1 (HAX-1) is linked to regulation of mitochondrial membrane function, but its role in controlling mPTP activity remains obscure.
HAX-1 inhibits apoptosis in prostate cancer through the suppression of caspase-9 activation.
Liu et al., Kaifeng, China. In Oncol Rep, Nov 2015
HS1 associated protein X-1 (HAX-1), a substrate of Src family tyrosine kinases, plays a critical role in cell apoptosis.
HAX-1 is overexpressed in hepatocellular carcinoma and promotes cell proliferation.
Xu et al., Shanghai, China. In Int J Clin Exp Pathol, 2014
In this study we reported HCLS1-associated protein X-1 (HAX-1) is overexpression in HCC in human HCC sample.
Disruption of the PRKCD-FBXO25-HAX-1 axis attenuates the apoptotic response and drives lymphomagenesis.
Bassermann et al., München, Germany. In Nat Med, 2014
An unbiased screen uncovered the prosurvival protein HCLS1-associated protein X-1 (HAX-1) as the bona fide substrate of FBXO25 that is targeted after apoptotic stresses.
Phospholamban interactome in cardiac contractility and survival: A new vision of an old friend.
Kranias et al., Cincinnati, United States. In J Mol Cell Cardiol, 2014
These include the inhibitor-1 (I-1) of protein phosphatase 1 (PP1), the small heat shock protein 20 (Hsp20) and the HS-1 associated protein X-1 (HAX1).
Neurological findings and genetic alterations in patients with Kostmann syndrome and HAX1 mutations.
Donadieu et al., Paris, France. In Pediatr Blood Cancer, 2014
OBJECTIVES: To describe the clinical profile and the prevalence of severe congenital neutropenia (SCN) and HAX1 mutations, so-called Kostmann syndrome, in France.
Cellular stress pathways in pediatric bone marrow failure syndromes: many roads lead to neutropenia.
Corey et al., Chicago, United States. In Pediatr Res, 2014
SCN, for example, is a genetically heterogeneous syndrome associated with mutations of ELANE, HAX1, GFI1, WAS, G6PC3, or CSF3R.
The role of CaMKII regulation of phospholamban activity in heart disease.
Kranias et al., La Plata, Argentina. In Front Pharmacol, 2013
Furthermore, the effects of PLN and its phosphorylation on cardiac function are subject to additional regulation by its interacting partners, the anti-apoptotic HAX-1 protein and Gm or the anchoring unit of protein phosphatase 1. Regulation of PLN activity by this multimeric complex becomes even more important in pathological conditions, characterized by aberrant Ca(2) (+)-cycling.
Pathogenic mechanisms and clinical implications of congenital neutropenia syndromes.
Klein et al., München, Germany. In Curr Opin Allergy Clin Immunol, 2013
Continuous careful explorations of known entities such as ELANE, GFI1, HAX1, G6PC3 deficiency and XLN help to define principles controlling differentiation and function of neutrophil granulocytes.
Interactions among HCLS1, HAX1 and LEF-1 proteins are essential for G-CSF-triggered granulopoiesis.
Welte et al., Hannover, Germany. In Nat Med, 2012
In patients with severe congenital neutropenia, inherited mutations in the gene encoding HCLS1-associated protein X-1 (HAX1) lead to profound defects in G-CSF-triggered phosphorylation of HCLS1 and subsequently to reduced autoregulation and expression of LEF-1.
Screening of binding proteins that interact with human Salvador 1 in a human fetal liver cDNA library by the yeast two-hybrid system.
Hu et al., Wuhan, China. In Mol Biol Rep, 2012
We also confirmed the interaction of HAX-1 and hSav1 in mammalian cells.
HAX-1 promotes the chemoresistance, invasion, and tumorigenicity of esophageal squamous carcinoma cells.
Dong et al., Zhengzhou, China. In Dig Dis Sci, 2012
HAX-1 promotes the proliferation, chemoresistance, invasion, and tumorigenicity of esophageal squamous cell carcinoma.
Specific alterations of the HtrA2/HAX-1 ratio in the penumbra upon focal cerebral ischemia in mice.
Langhagen et al., Germany. In Neurochem Res, 2012
Focal cerebral ischemia significantly decreased cytosolic accumulation of HAX-1, induced an upregulation of HtrA2, an upregulation of AIF and activation of caspase-3
hSav1 interacts with HAX1 and attenuates its anti-apoptotic effects in MCF-7 breast cancer cells.
Hu et al., Wuhan, China. In Int J Mol Med, 2011
hSav1 interacts with HAX1 and attenuates its protective role against apoptosis in MCF-7 breast cancer cells.
Hax1 regulates neutrophil adhesion and motility through RhoA.
Huttenlocher et al., Madison, United States. In J Cell Biol, 2011
Hax1 is a novel regulator of neutrophil uropod detachment and chemotaxis through RhoA
Genetic defects in severe congenital neutropenia: emerging insights into life and death of human neutrophil granulocytes.
Klein, Hannover, Germany. In Annu Rev Immunol, 2010
Deficiency of the mitochondrial proteins HAX1 and AK2 cause premature apoptosis of myeloid progenitor cells associated with dissipation of the mitochondrial membrane potential, whereas mutations in ELA2/ELANE and G6PC3 are associated with signs of increased endoplasmic reticulum stress.
Hax1-mediated processing of HtrA2 by Parl allows survival of lymphocytes and neurons.
Ihle et al., Memphis, United States. In Nature, 2008
a Bcl-2-family-related protein, Hax1, is required to suppress apoptosis in lymphocytes and neurons
HAX1 deficiency causes autosomal recessive severe congenital neutropenia (Kostmann disease).
Welte et al., Hannover, Germany. In Nat Genet, 2007
HAX1 is a major regulator of myeloid homeostasis and mutant proteins cause autosomal recessive severe congenital neutropenia.
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