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ULK2 Antibody (C-term)Purified Rabbit Polyclonal Antibody (Pab)

Country
United States
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Ordering Information
Catalog # Size Availability Price  
AP8105b 0.1 mg 400 ul In Stock $ 255.00 Add to cart
  • Specification
  • Citiations : 0
  • Reviews
  • Protocols
  • Backgrounds

ULK2 Antibody (C-term) - Product info

ApplicationWB
  • Applications Legend:
  • W=Western Blotting
  • IP=Immunoprecipitation
  • IHC-P=Immunohistochemistry (Paraffin)
  • IF-IC=Immunofluorescence (Immunocytochemistry)
  • F=Flow Cytometry
Primary AccessionQ8IYT8
ReactivityHuman, Mouse
Concentration0.25 mg/ml
IsotypeRabbit Ig
Calculated MW112694 Da

ULK2 Antibody (C-term) - Additional info

Gene ID 9706
Other Names
ULK2; KIAA0623; Serine/threonine-protein kinase ULK2; Unc-51-like kinase 2
Target/Specificity
This ULK2 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 620~649 amino acids from the C-terminal sequence of human ULK2.
Dilution
WB~~1:100~500
Format
Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein G column, eluted with high and low pH buffers and neutralized immediately, followed by dialysis against PBS.
Storage
Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.
Precautions
ULK2 Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures.

ULK2 Antibody (C-term) - Protein Information

Name ULK2
Synonyms KIAA0623
Function
Serine/threonine-protein kinase involved in autophagy in response to starvation. Acts upstream of phosphatidylinositol 3- kinase PIK3C3 to regulate the formation of autophagophores, the precursors of autophagosomes. Part of regulatory feedback loops in autophagy: acts both as a downstream effector and a negative regulator of mammalian target of rapamycin complex 1 (mTORC1) via interaction with RPTOR. Activated via phosphorylation by AMPK, also acts as a negative regulator of AMPK through phosphorylation of the AMPK subunits PRKAA1, PRKAB2 and PRKAG1. May phosphorylate ATG13/KIAA0652, FRS2, FRS3 and RPTOR; however such data need additional evidences. Not involved in ammonia-induced autophagy or in autophagic response of cerebellar granule neurons (CGN) to low potassium concentration. Plays a role early in neuronal differentiation and is required for granule cell axon formation: may govern axon formation via Ras-like GTPase signaling and through regulation of the Rab5-mediated endocytic pathways within developing axons
Cellular Location
Cytoplasmic vesicle membrane; Peripheral membrane protein. Note=Localizes to pre-autophagosomal membrane

ULK2 Antibody (C-term) - Related products

AM1884a: ULK2 antibody ( Ascites)

AM1884b: ULK2 Antibody

AP8105a: ULK2 Antibody (N-term)

AP8105b: ULK2 Antibody (C-term)

RI15623: ULK2 predesign siRNA

BP8105b: ULK2 Antibody (C-term) Blocking Peptide

AT4464a: ULK2 Antibody (monoclonal) (M01)

AT4465a: ULK2 Antibody (monoclonal) (M10)

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Provided below are standard protocols that you may find useful for product applications.

BACKGROUND

Macroautophagy is the major inducible pathway for the general turnover of cytoplasmic constituents in eukaryotic cells, it is also responsible for the degradation of active cytoplasmic enzymes and organelles during nutrient starvation. Macroautophagy involves the formation of double-membrane bound autophagosomes which enclose the cytoplasmic constituent targeted for degradation in a membrane bound structure, which then fuse with the lysosome (or vacuole) releasing a single-membrane bound autophagic bodies which are then degraded within the lysosome (or vacuole). Two human homologs of the yeast autophagy-specific kinase exist: ULK1(APG1) and ULK2. APG1 plays a critical role in regulating key elements of the autophagy pathway. APG1 stimulates autophagy, leading to autophagy-dependent restriction of cell growth and ultimately cell apoptosis at high levels of activity, and is a negative regulator of mTOR signaling.

REFERENCES

Yan, J., et al., Oncogene 18(43):5850-5859 (1999).