Anti-LRRK2 antibody [N138/6] - N-terminal,Abcam,AB186334

The clone number has been updated from S138-6 to N138/6, both clone numbers name the same antibody clone.

Host

Mouse

Reactivity

Rat, Human

Application

WB, ICC/IF

Platform ID

BAB374564474

Abcam

Headquarters

Discovery Drive Cambridge Biomedical Campus Cambridge CB2 0AX UK

Contact

Tel: +44 (0)1223 696000
Fax: +44 (0)1223 215 215

Product Specifications
Scientific Background

Specifications

NameAnti-LRRK2 antibody [N138/6] - N-terminal
Cat. No.AB186334
HostMouse
IsotypeIgG1
ReactivityRat, Human
ApplicationWB, ICC/IF
ClonalityMonoclonal
Clone NumberN138/6
Concentration1 mg/mL Batch dependent concentration
ImmunogenRecombinant Fragment Protein within Human LRRK2 aa 1-500. The exact immunogen used to generate this antibody is proprietary information.
PurityAffinity purification Protein G
Appearance/FormLiquid
ShippingBlue Ice
FormulationPreservative: 0.1% Sodium azide Constituents: PBS, 50% Glycerol (glycerin, glycerine)
Storage-20°C
Regulatory StatusResearch Use Only

Scientific Background

Target data The protein expressed by the gene LRRK2 is a serine/threonine-protein kinase that phosphorylates a wide range of proteins involved in neuronal plasticity, autophagy, and vesicle trafficking. It serves as a key regulator of RAB GTPases by affecting the GTP/GDP exchange and interaction partners of RABs through phosphorylation, targeting proteins like RAB3A, RAB3B, and others. LRRK2 manages the GDP/GTP exchange for RAB8A by phosphorylating 'Thr-72', inhibiting RAB8A's interaction with GDI1/GDI2, and influencing primary ciliogenesis to enhance SHH signaling in the brain. It works with RAB29 in retromer-dependent recycling of proteins between lysosomes and the Golgi. The protein is involved in shaping neuronal morphology in the CNS, synaptic vesicle trafficking, and recruiting SEC16A to assist in ER to Golgi transport. It enhances autophagy via the CaMKK/AMPK pathway and relates to nicotinic acid adenine dinucleotide phosphate receptors and lysosomal activity. LRRK2 phosphorylates PRDX3 and APP, influencing neuron apoptosis. Independently, it inhibits MAPT degradation, fostering MAPT oligomerization. Additionally, LRRK2 possesses GTPase activity that regulates its kinase activity. This supplementary information is collated from multiple sources and compiled automatically. See full target information LRRK2

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