Hax-1: a regulator of calcium signaling and apoptosis progression with multiple roles in human disease

Simmen, Thomas

doi:10.1517/14728222.2011.561787

Cited by 34 publications

(24 citation statements)

References 93 publications

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“…However, further studies are needed to elucidate the molecular mechanisms by which HAX-1 modulates the malignant behaviors of ESCC cells. HAX-1 is known as an important inhibitor of apoptosis and is implicated in tumorigenesis [27]. Thus, we speculate that the increased proliferation and chemoresistance of ESCC cells upon HAX-1 overexpression is at least partly due to the inhibition of apoptosis by HAX-1.…”

Section: Discussionmentioning

confidence: 81%

RETRACTED ARTICLE: HAX-1 Promotes the Chemoresistance, Invasion, and Tumorigenicity of Esophageal Squamous Carcinoma Cells

et al. 2012

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Section: Discussionmentioning

confidence: 81%

RETRACTED ARTICLE: HAX-1 Promotes the Chemoresistance, Invasion, and Tumorigenicity of Esophageal Squamous Carcinoma Cells

et al. 2012

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“…Although Hax-1 binds G592R Kv3.3, its ability to trigger Arp2/3 dependent actin nucleation and to link N-type inactivation to the cytoskeleton is impaired when bound to this mutant channel. Thus, other actions of Hax-1, such as suppression of caspase activation and apoptosis signaling may also be impaired (Fadeel and Grzybowska, 2009; Simmen, 2011). Moreover, effects of cortical Kv3.3-Hax-1 interactions are likely to be abolished in disease-causing mutations that prevent trafficking of Kv3.3 to the plasma membrane (Gallego-Iradi et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Kv3.3 Channels Bind Hax-1 and Arp2/3 to Assemble a Stable Local Actin Network that Regulates Channel Gating

Zhang

Fleming

et al. 2016

Cell

105

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Mutations in the Kv3.3 potassium channel (KCNC3) cause cerebellar neurodegeneration and impair auditory processing. The cytoplasmic C-terminus of Kv3.3 contains a proline-rich domain conserved in proteins that activate actin nucleation through Arp2/3. We found that Kv3.3 recruits Arp2/3 to the plasma membrane, resulting in formation of a relatively stable cortical actin filament network resistant to cytochalasin D which inhibits fast barbed end actin assembly. These Kv3.3-associated actin structures are required to prevent very rapid N-type channel inactivation during short depolarizations of the plasma membrane. The effects of Kv3.3 on the actin cytoskeleton are mediated by the binding of the cytoplasmic C-terminus of Kv3.3 to Hax-1, an anti-apoptotic protein that regulates actin nucleation through Arp2/3. A human Kv3.3 mutation within a conserved proline-rich domain produces channels that bind Hax-1 but are impaired in recruiting Arp2/3 to the plasma membrane, resulting in growth cones with deficient actin veils in stem cell-derived neurons.

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“…HAX-1, a kind of multifunctional protein, is recently discovered [19]. It was first discovered in its interaction with HS-1 (Src kinase substrate), suggesting that HAX-1 is involved in B cell signal transduction.…”

Section: Discussionmentioning

confidence: 99%

Analysis of HAX-1 gene expression in esophageal squamous cell carcinoma

Tang

Zang

et al. 2013

Diagn Pathol

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ObjectiveTo explore the expression of HAX-1 mRNA and protein in esophageal squamous cell carcinoma (ESCC) and its relation with the prognosis of patients with ESCC.MethodsThe expression of HAX-1 mRNA and protein were detected with quantitative real-time RT-PCR and immunohistochemical method in 112 ESCC samples and 112 corresponding non-neoplastic samples. Survival curves were made with follow-up data. The relations of the prognosis with clinical and pathological characteristics were analyzed.ResultsThe expression level of HAX-1 mRNA and the strong positive rate of HAX-1 protein were significantly higher in ESCC samples (0.527 ± 0.060 and 45.54%) than that in non-neoplastic samples (0.121 ± 0.017 and 0.00%), and in ESCC samples with lymph node metastasis (0.554 ± 0.054 and 71.11%) than that in ESCC samples without lymph node metastasis (0.509 ± 0.058 and 28.36%) (all P < 0.01). HAX-1 mRNA expression level was a risk factor of lymph node metastasis in patients with ESCC (P = 0.000). There were significant differences in survival curves between lymph node metastatic group and non-metastatic group (P = 0.000), and among groups of HAX-1 protein expression +, ++and +++(,P = 0.000); but no statistical significance between male patients and female patients (P = 0.119), and between ≥60 years old patients and <60 years old patients (P = 0.705). The level of HAX-1 mRNA (P = 0.000) and protein (P = 0.005) were risk factors of survival, but lymph node metastasis (P = 0.477) was not.ConclusionThere is HAX-1 over-expression in ESCC tissue and HAX-1 mRNA level is a risk factor of lymph node metastasis. The level of HAX-1 mRNA and protein were risk factors of survival in patients with ESCC. HAX-1 may be a novel therapeutic target for ESCC treatment.Virtual slidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/5130393079296037

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Hax-1: a regulator of calcium signaling and apoptosis progression with multiple roles in human disease

Cited by 34 publications

References 93 publications

RETRACTED ARTICLE: HAX-1 Promotes the Chemoresistance, Invasion, and Tumorigenicity of Esophageal Squamous Carcinoma Cells

RETRACTED ARTICLE: HAX-1 Promotes the Chemoresistance, Invasion, and Tumorigenicity of Esophageal Squamous Carcinoma Cells

Kv3.3 Channels Bind Hax-1 and Arp2/3 to Assemble a Stable Local Actin Network that Regulates Channel Gating

Analysis of HAX-1 gene expression in esophageal squamous cell carcinoma

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