A novel protein (Fbf-1) that binds to CD95/APO-1/FAS and shows sequence similarity to trichohyalin and plectin

Schmidt, Thorsten; Karsunky, Holger; Fraß, Beate; Baum, Wiebke; Denzel, Angela; Möröy, Tarik

doi:10.1016/s0167-4781(00)00163-9

Cited by 13 publications

(12 citation statements)

References 15 publications

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“…WBP-2 was originally identified as a putative ligand that binds to the WW domain of Yes kinase-associated protein 1 (YAP1) with relatively high affinity and specificity, consisting of three proline-rich motifs known as PPXY motifs, and it acts as a coactivator of the gene transcription regulation (e.g., estrogen receptors and progesterone receptors (ER/PR) transactivation pathway) and may play important roles in diverse pathological processes, such as cancer, inherited genetic diseases, and inflammation ( Dhananjayan et al, 2006;Chan et al, 2011). Fas-binding factor 1 (FBF1) was originally identified as a cytoplasm protein that interacted with the Fas cell surface receptor (TNFRSF6) (Schmidt et al, 2000b). Fas, a member of the tumor necrosis factor receptor superfamily and a key regulator of apoptosis, plays a key role in the physiological regulation of programmed cell death, and it is involved in the pathogenesis of various malignancies and diseases of the immune system (Wajant, 2002).…”

Section: Genome-wide Association Studymentioning

confidence: 99%

Genetic associations of leukoaraiosis indicate pathophysiological mechanisms in white matter lesions etiology

Lin¹,

Huang

Tzeng

2015

Reviews in the Neurosciences

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AbstractLeukoaraiosis (LA), also called white matter lesions (WMLs) and white matter hyperintensities (WMHs), is a frequent neuroimaging finding commonly seen on magnetic resonance imaging brain scans of elderly people with prevalence ranging from 50% to 100%. Although it remains asymptomatic, LA is not considered to be benign, and it is showed to be related to a host of poor clinical outcomes and increases the risk of disability, dementia, depression, stroke, and the overall morbidity and mortality. Pathologically, LA is characterized by loss of myelin and axons, patchy demyelination, and denudation of ependyma in regions of WMH. Age and hypertension are the most importantly established risk factors for LA. However, the precise pathogenic mechanisms remain unclear. Together with the previous findings, our recent genetic results strongly supported that LA is associated with immune response and neuroinflammation. Therefore, we confidently hypothesized that LA was not only a common neuroimaging phenomenon in the elderly but also an emerging neuroinflammatory disorder in the central nervous system. This article focusing on neuroimaging classification, genetics basis, and putative molecular mechanism introduced the basic knowledge and current status of LA and put forward some of our research ideas and results from our molecular genetics research, which may pave the way for deciphering the putative pathogenic mechanism, risk factor, epigenetic index, and its application in diagnostic agents or drug target for prevention and treatment. Thus, it could provide clinicians and researchers with a specific and modern overview of LA to enable the understanding of recent progress and future directions in this illness.

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Section: Genome-wide Association Studymentioning

confidence: 99%

Genetic associations of leukoaraiosis indicate pathophysiological mechanisms in white matter lesions etiology

Lin¹,

Huang

Tzeng

2015

Reviews in the Neurosciences

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“…Proteins that show homology to trichohyalin and plectin, Journal of Cell Science 118 (5) AJM-1 (Köppen et al, 2001) and Fbf-1 (Schmidt et al, 2000) have been reported. AJM-1 is a coiled-coil protein localizing to an apical junctional domain of Caenorhabditis elegans epithelia basal to the HMR-HMP (cadherin-catenin) complex.…”

Section: Discussionmentioning

confidence: 99%

“…In the absence of AJM-1, the integrity of this domain is compromised (Köppen et al, 2001). Fbf-1 was identified to be a novel protein that bound to the cytosolic domain of the murine CD95/APO-1/FAS, a cell surface receptor mediating programmed cell death in response to various stimuli (Schmidt et al, 2000). At present, it is completely unclear whether trichoplein, AJM-1 and Fbf-1 have a common physiological function as family proteins that show homology to trichohyalin and plectin.…”

Section: Discussionmentioning

confidence: 99%

Identification of trichoplein, a novel keratin filament-binding protein

Nishizawa

Izawa

Inoko

et al. 2005

Journal of Cell Science

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Keratins 8 and 18 (K8/18) are major components of the intermediate filaments (IFs) of simple epithelia. We report here the identification of a novel protein termed trichoplein. This protein shows a low degree of sequence similarity to trichohyalin, plectin and myosin heavy chain, and is a K8/18-binding protein. Among interactions between trichoplein and various IF proteins that we tested using two-hybrid methods, trichoplein interacted significantly with K16 and K18, and to some extent with K5, K6a, K8 and K14. In in vitro co-sedimentation assays, trichoplein directly binds to K8/18, but not with vimentin, desmin, actin filaments or microtubules. An antibody raised against trichoplein specifically recognized a polypeptide with a relative molecular mass of 61 kDa in cell lysates. Trichoplein was immunoprecipitated using this antibody in a complex with K8/18 and immunostaining revealed that trichoplein colocalized with K8/18 filaments in HeLa cells. In polarized Caco-2 cells, trichoplein colocalized not only with K8/18 filaments in the apical region but also with desmoplakin, a constituent of desmosomes. In the absorptive cells of the small intestine, trichoplein colocalized with K8/18 filaments at the apical cortical region, and was also concentrated at desmosomes. Taken together, these results suggest that trichoplein is a keratin-binding protein that may be involved in the organization of the apical network of keratin filaments and desmosomes in simple epithelial cells.

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“…For example many 3'-UTRs house AUUUA motif-containing AUrich elements (AREs), 31 iron-responsive elements (IREs) 32 or adenylation control element (ACEs). 33 ARE-binding proteins (ARE-BPs) such as Fas binding factor 1 (FBF1), 34 KH-type splicing regulatory protein (KSRP), 35,36 T-cell-restricted intracellular antigen-related protein (TIAR) 37 can act in trans with these UTR AREs to suppress protein expression. Thus, we predict that the 3'-UTR of TLR4 can down-regulate TLR4 gene expression.…”

Section: Discussionmentioning

confidence: 99%

Functional variant in the 3’-untranslated region of toll-like receptor 4 is associated with nasopharyngeal carcinoma risk

Song¹,

Chen²,

Zhang³

et al. 2006

Cancer Biology & Therapy

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A novel protein (Fbf-1) that binds to CD95/APO-1/FAS and shows sequence similarity to trichohyalin and plectin

Cited by 13 publications

References 15 publications

Genetic associations of leukoaraiosis indicate pathophysiological mechanisms in white matter lesions etiology

Genetic associations of leukoaraiosis indicate pathophysiological mechanisms in white matter lesions etiology

Identification of trichoplein, a novel keratin filament-binding protein

Functional variant in the 3’-untranslated region of toll-like receptor 4 is associated with nasopharyngeal carcinoma risk

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