Anti-SF3B2 Antibody Picoband® Fluoro647 Conjugated

Splicing factor 3B subunit 2 is a protein that in humans is encoded by the SF3B2 gene. This gene encodes subunit 2 of the splicing factor 3b protein complex. Splicing factor 3b, together with splicing factor 3a and a 12S RNA unit, forms the U2 small nuclear ribonucleoproteins complex (U2 snRNP) . The splicing factor 3b/3a complex binds pre-mRNA upstream of the intron's branch site in a sequence-independent manner and may anchor the U2 snRNP to the pre-mRNA. Splicing factor 3b is also a component of the minor U12-type spliceosome. Subunit 2 associates with pre-mRNA upstream of the branch site at the anchoring site. Subunit 2 also interacts ly with subunit 4 of the splicing factor 3b complex. Subunit 2 is a highly hydrophilic protein with a proline-rich N-terminus and a glutamate-rich stretch in the C-terminus.

Forkhead box protein F1; Forkhead-related activator 1; FREAC-1; Forkhead-related protein FKHL5; Forkhead-related transcription factor 1; FOXF1; FKHL5; FREAC1

Transcriptional regulator involved in different processes such as glucose metabolism, aerobic glycolysis, muscle cell differentiation and autophagy. Recognizes and binds the forkhead DNA sequence motif (5'-GTAAACA-3') and can both act as a transcription activator or repressor, depending on the context. Together with FOXK2, acts as a key regulator of metabolic reprogramming towards aerobic glycolysis, a process in which glucose is converted to lactate in the presence of oxygen. Acts by promoting expression of enzymes for glycolysis (such as hexokinase-2 (HK2), phosphofructokinase, pyruvate kinase (PKLR) and lactate dehydrogenase), while suppressing further oxidation of pyruvate in the mitochondria by up-regulating pyruvate dehydrogenase kinases PDK1 and PDK4. Probably plays a role in gluconeogenesis during overnight fasting, when lactate from white adipose tissue and muscle is the main substrate. Involved in mTORC1-mediated metabolic reprogramming: in response to mTORC1 signaling, translocates into the nucleus and regulates the expression of genes associated with glycolysis and downstream anabolic pathways, such as HIF1A, thereby regulating glucose metabolism. Together with FOXK2, acts as a negative regulator of autophagy in skeletal muscle: in response to starvation, enters the nucleus, binds the promoters of autophagy genes and represses their expression, preventing proteolysis of skeletal muscle proteins. Acts as a transcriptional regulator of the myogenic progenitor cell population in skeletal muscle. Binds to the upstream enhancer region (CCAC box) of myoglobin (MB) gene, regulating the myogenic progenitor cell population. Promotes muscle progenitor cell proliferation by repressing the transcriptional activity of FOXO4, thereby inhibiting myogenic differentiation. Involved in remodeling processes of adult muscles that occur in response to physiological stimuli. Required to correct temporal orchestration of molecular and cellular events necessary for muscle repair. Represses myogenic differentiation by inhibiting MEFC activity. Positively regulates Wnt/beta-catenin signaling by translocating DVL into the nucleus. Reduces virus replication, probably by binding the interferon stimulated response element (ISRE) to promote antiviral gene expression.

1. Gozani, O., Feld, R., Reed, R. Evidence that sequence-independent binding of highly conserved U2 snRNP proteins upstream of the branch site is required for assembly of spliceosomal complex A. Genes Dev. 10: 233-243, 1996. 2. Singer, S. L., Haan, E., Slee, J., Goldblatt, J. Familial hemifacial microsomia due to autosomal dominant inheritance: case reports. Aust. Dent. J. 39: 287-291, 1994. 3. Stumpf, A. M. Personal Communication. Baltimore, Md. 02/26/2022.