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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Septin 5

CDCrel-1, SEPT5, PNUTL1, septin 5
This gene is a member of the septin gene family of nucleotide binding proteins, originally described in yeast as cell division cycle regulatory proteins. Septins are highly conserved in yeast, Drosophila, and mouse and appear to regulate cytoskeletal organization. Disruption of septin function disturbs cytokinesis and results in large multinucleate or polyploid cells. This gene is mapped to 22q11, the region frequently deleted in DiGeorge and velocardiofacial syndromes. A translocation involving the MLL gene and this gene has also been reported in patients with acute myeloid leukemia. Alternative splicing results in multiple transcript variants. The presence of a non-consensus polyA signal (AACAAT) in this gene also results in read-through transcription into the downstream neighboring gene (GP1BB; platelet glycoprotein Ib), whereby larger, non-coding transcripts are produced. [provided by RefSeq, Dec 2010] (from NCBI)
Top mentioned proteins: E3 ubiquitin ligase, Ubiquitin, CAN, SEP2, cdc10
Papers using CDCrel-1 antibodies
Immunohistochemical study of immunoglobulin light chain amyloidosis with antibodies to the immunoglobulin light chain variable region
Mizukami Yoichi et al., In Proteome Science, 2005
... The anti-Septin 5 antibody was from Abcam (Cambridge, MA) ...
Papers on CDCrel-1
Targeted multiplexed selected reaction monitoring analysis evaluates protein expression changes of molecular risk factors for major psychiatric disorders.
Bahn et al., Rotterdam, Netherlands. In Int J Neuropsychopharmacol, 2015
deletion syndrome-associated protein septin 5 to schizophrenia.
Identification of target genes using gene expression profile of granulocytes from patients with chronic myeloid leukemia treated with tyrosine kinase inhibitors.
de Souza et al., Campinas, Brazil. In Leuk Lymphoma, 2014
Among the overexpressed genes found in CML at diagnosis are SEPT5, RUNX1, MIER1, KPNA6 and FLT3, while PAN3, TOB1 and ITCH were decreased when compared to healthy volunteers.
Radiation protection from whole-body gamma irradiation (6.7 Gy): behavioural effects and brain protein-level changes by an aminothiol compound GL2011 in the Wistar rat.
Lubec et al., Vienna, Austria. In Amino Acids, 2014
Protein-level changes of peroxiredoxin-5, Mn-superoxide dismutase 2, voltage-dependent anion-selective channel protein 1, septin 5 and dopamine D2 receptor complex levels were paralleling radiation damage and protection.
Mixed lineage leukemia-septin 5 fusion transcript in de novo adult acute myeloid leukemia with t(11;22)(q23;q11.2): A case report.
Chen et al., Beijing, China. In Oncol Lett, 2014
Reverse transcription polymerase chain reaction (PCR) analysis demonstrated an MLL-septin 5 (SEPT5) fusion transcript in the patient.
MLL-SEPT5 fusion transcript in infant acute myeloid leukemia with t(11;22)(q23;q11).
Belaud-Rotureau et al., In Leuk Lymphoma, 2014
Fluorescence in situ hybridization study revealed that the 3'MLL segment was translocated onto the derivative chromosome 22 and the breakpoint on chromosome 22 was located in or near the SEPT5 gene at 22q11.21.
DNA methylation profiling in the Carolina Breast Cancer Study defines cancer subclasses differing in clinicopathologic characteristics and survival.
Millikan et al., In Breast Cancer Res, 2013
Genes relatively hypermethylated in HR+, luminal A, or p53 wild-type breast cancers included FABP3, FGF2, FZD9, GAS7, HDAC9, HOXA11, MME, PAX6, POMC, PTGS2, RASSF1, RBP1, and SCGB3A1, whereas those more highly methylated in HR-, basal-like, or p53 mutant tumors included BCR, C4B, DAB2IP, MEST, RARA, SEPT5, TFF1, THY1, and SERPINA5.
Prognostic CpG methylation biomarkers identified by methylation array in esophageal squamous cell carcinoma patients.
Wang et al., Tainan City, Taiwan. In Int J Med Sci, 2013
RESULTS: We identified a panel of nine CpG methylation probes located at promoter or exon1 region of eight genes including DDIT3, FES, FLT3, NTRK3, SEPT5, SEPT9, SOX1, and SOX17, for prognosis prediction in ESCC patients.
Possible role of a septin, SEPT1, in spreading in squamous cell carcinoma DJM-1 cells.
Nagata et al., Gifu, Japan. In Biol Chem, 2013
In DJM-1 cells, SEPT1 together with other members of SEPT2-subgroup, SEPT4 and SEPT5, was enriched in lamellipodia and the localization was dependent on the cortical actin structure.
Chronic overload of SEPT4, a parkin substrate that aggregates in Parkinson's disease, causes behavioral alterations but not neurodegeneration in mice.
Kinoshita et al., Nagoya, Japan. In Mol Brain, 2012
Parkin substrates include two septins; SEPT4/CDCrel-2 which coaggregates with α-synuclein as Lewy bodies in Parkinson's disease, and its closest homolog SEPT5/CDCrel-1/PNUTL1 whose overload with viral vector can rapidly eliminate dopamine neurons in rats.
Septins of Platyhelminths: identification, phylogeny, expression and localization among developmental stages of Schistosoma mansoni.
Brindley et al., São Carlos, Brazil. In Plos Negl Trop Dis, 2012
These orthologues were related to the SEPT5, SEPT10 and SEPT7 septins of humans, and hence we have termed the schistosome septins SmSEPT5, SmSEPT10, SmSEPT7.1 and SmSEPT7.2.
Use of viral vectors to create animal models for Parkinson's disease.
Aebischer et al., Lausanne, Switzerland. In Neurobiol Dis, 2012
To date, viral PD models comprise α-synuclein and LRRK-2-based overexpression models, as well as models that mimic parkin loss of function by overexpression of the parkin substrates Pael-R, CDCrel-1, p38/JTV or synphilin-1.
Localization of septin proteins in the mouse cochlea.
Ito et al., Kyoto, Japan. In Hear Res, 2012
Report SEPT4/5/7 expression in mouse cochlea and roles in auditory function.
Mouse Models of 22q11.2-Associated Autism Spectrum Disorder.
Boku et al., United States. In Autism Open Access, 2011
genesTbx1 and Sept5 causes distinct phenotypic sets of ASD symptoms.
Characterization of presynaptic septin complexes in mammalian hippocampal neurons.
Trimble et al., Toronto, Canada. In Biol Chem, 2011
Knockdown of SEPT5 or SEPT7 in developing hippocampal neurons impaired axon growth.
MLL-SEPTIN gene fusions in hematological malignancies.
Teixeira et al., Porto, Portugal. In Biol Chem, 2011
Five different septin genes (SEPT2, SEPT5, SEPT6, SEPT9, and SEPT11) have been identified as MLL fusion partners, giving rise to chimeric fusion proteins in which the N terminus of MLL is fused, in frame, to almost the entire open reading frame of the septin partner gene.
Ankyrin repeat-rich membrane spanning/Kidins220 protein interacts with mammalian Septin 5.
Chang et al., Seoul, South Korea. In Mol Cells, 2010
The direct interaction between ARMS/Kidins220 and Sept5 suggests a possible role of ARMS/Kidins220 as a functional link between neurotrophin receptors and septins to mediate neurotrophin-induced intracellular signaling events.
Septins regulate developmental switching from microdomain to nanodomain coupling of Ca(2+) influx to neurotransmitter release at a central synapse.
Wang et al., Toronto, Canada. In Neuron, 2010
The result of this study suggested that Septin 5 is a core molecular substrate that differentiates distinct release modalities at the central synapse.
Neuronal expression of two isoforms of mouse Septin 5.
Hisanaga et al., Tokyo, Japan. In J Neurosci Res, 2010
Here, we showed existence of two Sept5 isoforms in the mouse and studied their tissue and developmental expressions that would be helpful for exploring isoform specific function.
Septins, a novel group of GTP-binding proteins: relevance in hemostasis, neuropathology and oncogenesis.
Zieger et al., Freiburg, Germany. In Klin Padiatr, 2009
Platelets from SEPT5 knockout mice show an enhanced serotonin secretion and platelet aggregation in response to subthreshold levels of agonists.
Structural and expression changes of septins in myeloid neoplasia.
Teixeira et al., Porto, Portugal. In Crit Rev Oncog, 2008
First, some septins (SEPT2, SEPT5, SEPT6, SEPT9, and SEPT11) have been repeatedly identified as in-frame fusion partners of the MLL gene in de novo and therapy-related myeloid neoplasia, in both children and adults.
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