Anti-TGFB2 polyclonal antibody (DPABH-03686)

Rabbit anti-Human TGFB2 (aa 250-350) polyclonal antibody for WB, ICC/IF Datasheet

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Specifications


Host Species
Rabbit
Antibody Isotype
IgG
Species Reactivity
Mouse, Rat, Human
Immunogen
Synthetic peptide conjugated to KLH derived from within residues 250 - 350 of Human TGF beta 2.
Conjugate
Unconjugated

Applications


Application Notes
WB: 1μg/ml; ICC/IF: 5μg/ml.
*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
TGFB2; transforming growth factor, beta 2; LDS4; TGF-beta2; transforming growth factor beta-2; G-TSF
Entrez Gene ID
UniProt ID

Product Background


Gene summary
TGFB2 (Transforming Growth Factor Beta 2) is a Protein Coding gene. Diseases associated with TGFB2 include loeys-dietz syndrome 4 and peters anomaly. Among its related pathways are Platelet activation, signaling and aggregation and Sertoli-Sertoli Cell Junction Dynamics. GO annotations related to this gene include protein homodimerization activity and receptor binding. An important paralog of this gene is INHBB. This gene encodes a member of the transforming growth factor beta (TGFB) family of cytokines, which are multifunctional peptides that regulate proliferation, differentiation, adhesion, migration, and other functions in many cell types by transducing their signal through combinations of transmembrane type I and type II receptors (TGFBR1 and TGFBR2) and their downstream effectors, the SMAD proteins. Disruption of the TGFB/SMAD pathway has been implicated in a variety of human cancers. The encoded protein is secreted and has suppressive effects of interleukin-2 dependent T-cell growth. Translocation t(1;7)(q41;p21) between this gene and HDAC9 is associated with Peters' anomaly, a congenital defect of the anterior chamber of the eye. The knockout mice lacking this gene show perinatal mortality and a wide range of developmental, including cardiac, defects. Alternatively spliced transcript variants encoding different isoforms have been identified.
Antigen Description
TGF-beta 2 has suppressive effects on interleukin-2 dependent T-cell growth. Loeys-Dietz syndrome 4 (LDS4) [MIM:614816]: An aortic aneurysm syndrome with widespread systemic involvement. LDS4 is characterized by arterial tortuosity, aortic dissection, intracranial aneurysm and subarachnoid hemorrhage, hypertelorism, bifid uvula, pectus deformity, bicuspid aortic valve, arachnodactyly, scoliosis, foot deformities, dural ectasia, joint hyperflexibility, and thin skin with easy bruising and striae. Note=The disease is caused by mutations affecting the gene represented in this entry. Note=A chromosomal aberration involving TGFB2 is found in a family with Peters anomaly. Translocation t(1;7)(q41;p21) with HDAC9. Note=Defects in TGFB2 may be a cause of non-syndromic aortic disease (NSAD). NSAD is a frequently asymptomatic but potentially lethal disease characterized by thoracic aortic aneurysms and dissections without additional syndromic features. Transforming growth factor-beta 2 (TGF-β2) is a secreted protein known as a cytokine that performs many cellular functions and has a vital role during embryonic development (alternative names: Glioblastoma-derived T-cell suppressor factor, G-TSF, BSC-1 cell growth inhibitor, Polyergin, Cetermin). It is an extracellular glycosylated protein. It is known to suppress the effects of interleukin dependent T-cell tumors. There are two named isoforms of this protein, created by alternative splicing of the same gene. 0The function about TGFB2 antigen include beta-amyloid binding; cytokine activity; growth factor activity; protein binding.
Pathway
ATF-2 transcription factor network; Amoebiasis; Cell cycle; Chagas disease (American trypanosomiasis).

Citations


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References


Tsao, BP; Cantor, RM; et al. PARP alleles within the linked chromosomal region are associated with systemic lupus erythematosus. JOURNAL OF CLINICAL INVESTIGATION 103:1135-1140(1999).
Zuo, S; Jones, WK; et al. Paracrine Effect of Wnt11-Overexpressing Mesenchymal Stem Cells on Ischemic Injury. STEM CELLS AND DEVELOPMENT 21:598-608(2012).

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