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Human Hemostasis

$129
20 µl
$303
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Immunohistochemistry (Paraffin), Immunoprecipitation, Western Blotting

Background: VWF (Von Willebrand factor) is a multimeric plasma glycoprotein that promotes adhesion of platelets to sites of vascular injury (1). Mature circulating VWF is made up of disulfide-bonded multimers that are in a complex with factor VIII (2). VWF is stored in secretory Weibel-Palade bodies in endothelial cells (3,4). It is synthesized as a large precursor protein and undergoes extensive posttranslational modifications including dimerization in the endoplasmic reticulum followed by cleavage of the pro-peptide and multimerization in the Golgi apparatus (3,4). VWF is important in hemostasis, and genetic defects in the structure and modification of VWF can cause von Willebrand disease (VWD), the most common congenital bleeding disorder in humans (5).  Alternatively, increased levels of VWF have been shown to be involved in acute coronary thrombosis and are a clinical risk marker for atherosclerosis (6). VWF has also been shown to have a role in inflammation, functioning as an adhesive site for a variety of leukocyte subsets (7). Through siRNA experiments and the use VWF-deficient mice, it has also been shown that VWF regulates angiogenesis (8).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Monkey

Application Methods: Western Blotting

Background: Glucose-6-phosphate isomerase (GPI) is a multi-functional protein belonging to the glucose phosphate isomerase family (1,2). As an intracellular metabolic enzyme, GPI plays a pivotal role in glycolysis and gluconeogenesis by catalyzing the interconversion of D-glucose-6-phosphate and D-fructose-6-phosphate (3). GPI is also secreted, where it functions as a cytokine (referred to as Autocrine Motility Factor, AMF), acting via the E3-ubiquitin-protein ligase AMFR/gp78 (4). In normal tissues, GPI/AMF has been shown to promote both immune cell maturation and neuronal cell survival (5,6). It is also secreted in abundance by some tumor cells (7), where it has been shown to promote tumor cell migration and metastasis (8,9).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Monkey

Application Methods: Western Blotting

Background: Annexin A7/ANXA7 is a member of the annexin family of calcium/phospholipid-binding proteins, and is involved in the process of membrane fusion and exocytosis (1). Annexin A7 is a GTPase, and both GTP-binding and PKC activity are important in regulating protein function (2,3). Membrane binding of annexin A7 is calcium dependent (4). Two isoforms exist due to alternative splicing. Subcellular localization of annexin A7 has been shown to be in the cytoplasm, vesicular structures, membrane and in adrenal chromaffin granules (5,6). Nuclear localization has been shown in the developing mouse central nervous system as well as in adult mouse brain (7). Annexin A7-deficient mouse studies show that the protein has a role in insulin secretion and calcium signaling (8) as well as cardiac intracellular calcium homeostasis electrical stability (9). The gene for annexin A7 is a putative tumor suppressor (10), and alterations in the copy number have been reported in prostate cancer (11). Annexin A7 expression has also been correlated with survival in human glioblastoma patients (12), and haploinsufficiency in mice may promote genetic instability leading to tumorigenesis (13).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse

Application Methods: Immunoprecipitation, Western Blotting

Background: Friend leukemia integration 1 (FLI1) transcription factor is an ETS domain-containing transcription factor that plays an important and highly conserved role in vertebrate development, particularly hematopoiesis, where it functions to activate transcription of genes that promote erythroblast proliferation (1-4). In mice, the Fli1 locus is a common retroviral insertion site for the Friend murine leukemia virus (F-MuLV), such that a majority of F-MuLV-induced erythroleukemias are associated with aberrant Fli1 expression (5). Notably in humans, aberrant FLI1 expression has also been linked to poor prognosis in acute myeloid leukemia (6). Also in humans, a t(11;22)(q24;q12) chromosomal translocation has been described that generates a chimeric protein (EWS/FLI1) comprised of the amino-terminal transactivation domain of Ewing's sarcoma breakpoint region 1 (EWS) and the carboxy-terminal ETS domain of FLI1 (7). The EWS/FLI1 fusion protein functions as a transcriptional activator that is reportedly responsible for >85% of the known cases of pediatric Ewing’s sarcoma, an aggressive bone and soft tissue tumor (8,9).