Anti-SLC44A1 monoclonal antibody [FITC] (CABT-46878MH)

Mouse anti-Human SLC44A1 monoclonal antibody for FC

Additional Formats Available

Specifications


Host Species
Mouse
Antibody Isotype
IgG2b
Clone
VIM-15b
Species Reactivity
Human
Immunogen
MV4-11 acute monocyte leukaemia cells.
Conjugate
FITC

Applications


Application Notes
Flow Cyt: Neat - 1/5;
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.

Target


Alternative Names
SLC44A1; solute carrier family 44 (choline transporter), member 1; CD92; CTL1; CDW92; CHTL1
Entrez Gene ID
UniProt ID
Q8WWI5

Product Background


Pathway
Choline metabolism in cancer; Glycerophospholipid biosynthesis; Metabolism; Metabolism of lipids and lipoproteins; Phospholipid metabolism; SLC-mediated transmembrane transport; Synthesis of PC; Transmembrane transport of small molecules;

Citations


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Mouse IgG2b Isotype Control [FITC] DAGIC979 FC Mouse PDF Inquiry

References


Mechanism of choline deficiency and membrane alteration in postural orthostatic tachycardia syndrome primary skin fibroblasts

FASEB JOURNAL

Authors: Schenkel, Laila C.; Singh, Ratnesh K.; Michel, Vera; Zeisel, Steven H.; da Costa, Kerry-Ann; Johnson, Amy R.; Mudd, Harvey S.; Bakovic, Marica

Fibroblasts from a patient with postural orthostatic tachycardia syndrome (POTS), who presented with low plasma choline and betaine, were studied to determine the metabolic characteristics of the choline deficiency. Choline is required for the synthesis of the phospholipid phosphatidylcholine (PC) and for betaine, an important osmoregulator. Here, choline transport, lipid homeostasis, and mitochondria function were analyzed in skin fibroblasts from POTS and compared with control cells. The choline transporter-like protein 1/solute carrier 44A1 (CTL1/SLC44A1) and mRNA expression were 2-3 times lower in POTS fibroblasts, and choline uptake was reduced 60% (P < 0.05). Disturbances of membrane homeostasis were observed by reduced ratios between PC:phosphatidylethanolamine and sphingomyelin:cholesterol, as well as by modified phospholipid fatty acid composition. Choline deficiency also impaired mitochondria function, which was observed by a reduction in oxygen consumption, mitochondrial potential, and glycolytic activity. When POTS cells were treated with choline, transporter was up-regulated, and uptake of choline increased, offering an option for patient treatment. The characteristics of the POTS fibroblasts described here represent a first model of choline and CTL1/SLC44A1 deficiency, in which choline transport, membrane homeostasis, and mitochondrial function are impaired.Schenkel, L. C., Singh, R. K., Michel, V., Zeisel, S. H., da Costa, K.-A., Johnson, A. R., Mudd, H. S., Bakovic, M. Mechanism of choline deficiency and membrane alteration in postural orthostatic tachycardia syndrome primary skin fibroblasts.

EWSR1-PATZ1 gene fusion may define a new glioneuronal tumor entity

BRAIN PATHOLOGY

Authors: Siegfried, Aurore; Rousseau, Audrey; Maurage, Claude-Alain; Pericart, Sarah; Nicaise, Yvan; Escudie, Frederic; Grand, David; Delrieul, Alix; Gomez-Brouchet, Anne; Le Guellec, Sophie; Franchet, Camille; Boetto, Sergio; Vinchon, Matthieu; Sol, Jean-Christophe; Roux, Franck-Emmanuel; Rigau, Valerie; Bertozzi, Anne-Isabelle; Jones, David T. W.; Figarella-Branger, Dominique; Uro-Coste, Emmanuelle

We investigated the challenging diagnostic case of a ventricular cystic glioneuronal tumor with papillary features, by RNA sequencing using the Illumina TruSight RNA Fusion panel. We did not retrieve the SLC44A1-PRKCA fusion gene specific for papillary glioneuronal tumor, but an EWSR1-PATZ1 fusion transcript. RT-PCR followed by Sanger sequencing confirmed the EWSR1-PATZ1 fusion. It matched with canonic EWSR1 fusion oncogene, juxtaposing the entire N-terminal transcriptional activation domain of EWSR1 gene and the C-terminal DNA binding domain of a transcription factor gene, PATZ1. PATZ1 protein belongs to the BTB-ZF (broad-complex, tramtrack and bric-a-brac -zinc finger) family. It directly regulates Pou5f1 and Nanog and is essential to maintaining stemness by inhibiting neural differentiation. EWSR1-PATZ1 fusion is a rare event in tumors: it was only reported in six round cell sarcomas and in three gliomas of three exclusively molecular studies. The first reported glioma was a BRAF(V600E) negative ganglioglioma, the second a BRAF(V600E) negative glioneuronal tumor, not otherwise specified and the third, very recently reported, a high grade glioma, not otherwise specified. In our study, forty BRAF(V600E) negative gangliogliomas were screened by FISH using EWSR1 break-apart probes. We performed methylation profiling for the index case and for seven out of the ten FISH positive cases. The index case clustered apart from other pediatric low grade glioneuronal entities, and specifically from the well-defined ganglioglioma methylation group. An additional pediatric intraventricular ganglioglioma clustered slightly more closely with ganglioglioma, but showed differences from the main ganglioglioma group and similarities with the index case. Both cases harbored copy number variations at the PATZ1 locus. EWSR1-PATZ1 gene fusion might define a new type of glioneuronal tumors, distinct from gangliogliomas.

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