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Anti-Cleaved-Notch 2 (D1733) Antibody

品牌：Antibodies

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規(guī)格：50μl

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Anti-Cleaved-Notch 2 (D1733) Antibody

商品詳情參考文獻相關(guān)資料

Overview

Name:	Anti-Cleaved-Notch 2 (D1733) Antibody See all Cleaved-Notch 2 primary antibodies
Description:	Rabbit polyclonal antibody to Cleaved-Notch 2 (D1733)
Specificity:	Cleaved-Notch 2 (D1733) Polyclonal Antibody detects endogenous levels of fragment of activated Notch 2 protein resulting from cleavage adjacent to D1733.
Applications:	WB, IHC, ELISA
Reactivity:	Human, Mouse, Rat
Immunogen:	Synthesized peptide derived from the Internal region of human Notch 2.
Host:	Rabbit
Clonality:	Polyclonal
Conjugate:	Unconjugated
Purification:	The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Concentration:	1mg / ml
Formulation:	Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Storage:	Store at -20?C / 1 year

Target

Function:	Functions as a receptor for membrane-bound ligands Jagged1, Jagged2 and Delta1 to regulate cell-fate determination. Upon ligand activation through the released notch intracellular domain (NICD) it forms a transcriptional activator complex with RBPJ/RBPSUH and activates genes of the enhancer of split locus. Affects the implementation of differentiation, proliferation and apoptotic programs (By similarity). Involved in bone remodeling and homeostasis. In collaboration with RELA/p65 enhances NFATc1 promoter activity and positively regulates RANKL-induced osteoclast differentiation. Positively regulates self-renewal of liver cancer cells (PubMed:25985737).
Tissue Specificity:	Expressed in the brain, heart, kidney, lung, skeletal muscle and liver. Ubiquitously expressed in the embryo.
Involvement in Disease:	Alagille syndrome 2: A form of Alagille syndrome, an autosomal dominant multisystem disorder. It is clinically defined by hepatic bile duct paucity and cholestasis in association with cardiac, skeletal, and ophthalmologic manifestations. There are characteristic facial features and less frequent clinical involvement of the renal and vascular systems. Hajdu-Cheney syndrome: A rare skeletal disorder characterized by the association of facial anomalies, acro-osteolysis, general osteoporosis, insufficient ossification of the skull, and periodontal disease (premature loss of permanent teeth). Other features include cleft palate, congenital heart defects, polycystic kidneys, orthopedic problems and anomalies of the genitalia, intestines and eyes.
Sequence Similarities:	Belongs to the NOTCH family.
Post-Translational Modification:	Synthesized in the endoplasmic reticulum as an inactive form which is proteolytically cleaved by a furin-like convertase in the trans-Golgi network before it reaches the plasma membrane to yield an active, ligand-accessible form. Cleavage results in a C-terminal fragment N(TM) and a N-terminal fragment N(EC). Following ligand binding, it is cleaved by TNF-alpha converting enzyme (TACE) to yield a membrane-associated intermediate fragment called notch extracellular truncation (NEXT). This fragment is then cleaved by presenilin dependent gamma-secretase to release a notch-derived peptide containing the intracellular domain (NICD) from the membrane (By similarity).
Cellular Location:	Cell membrane.