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AB226339

Anti-SorLA/SORL1 antibody - C-terminal

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(2 Publications )

Rabbit Polyclonal SorLA/SORL1 antibody. C-terminal. Suitable for WB and reacts with Human samples. Cited in 2 publications. Immunogen corresponding to Synthetic Peptide within Human SORL1 aa 2150 to C-terminus.

View Alternative Names

C11orf32, SORL1, Sortilin-related receptor, Low-density lipoprotein receptor relative with 11 ligand-binding repeats, SorLA-1, Sorting protein-related receptor containing LDLR class A repeats, LDLR relative with 11 ligand-binding repeats, LR11, SorLA

1 Images
Western blot - Anti-SorLA/SORL1 antibody - C-terminal (AB226339)
  • WB

Supplier Data

Western blot - Anti-SorLA/SORL1 antibody - C-terminal (AB226339)

Cell lysates were prepared using NETN lysis buffer.

All lanes:

Western blot - Anti-SorLA/SORL1 antibody - C-terminal (ab226339) at 0.1 µg/mL

Lane 1:

HeLa (human epithelial cell line from cervix adenocarcinoma) whole cell lysate at 50 µg

Lane 2:

HEK-293T (human epithelial cell line from embryonic kidney transformed with large T antigen) whole cell lysate at 50 µg

Lane 3:

Jurkat (human T cell leukemia cell line from peripheral blood) whole cell lysate at 50 µg

Predicted band size: 248 kDa

true

Exposure time: 3s

Key facts

Host species

Rabbit

Clonality

Polyclonal

Isotype

IgG

Carrier free

No

Reacts with

Human

Applications

WB

applications

Immunogen

Synthetic Peptide within Human SORL1 aa 2150 to C-terminus. The exact immunogen used to generate this antibody is proprietary information.

Q92673

Reactivity data

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Properties and storage information

Form
Liquid
Purification technique
Affinity purification Immunogen
Purification notes
ab226339 was affinity purified using an epitope specific to SorLA/SORL1 immobilized on solid support.
Storage buffer
pH: 7 - 8 Preservative: 0.09% Sodium azide Constituents: Tris citrate/phosphate
Shipped at conditions
Blue Ice
Appropriate short-term storage duration
1-2 weeks
Appropriate short-term storage conditions
+4°C
Appropriate long-term storage conditions
+4°C
Aliquoting information
Upon delivery aliquot
Storage information
Avoid freeze / thaw cycle

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

SorLA also known as SORL1 or sortilin-related receptor 1 plays a mechanical role in intracellular transport processes. This multi-domain protein with a molecular weight of approximately 250 kDa assists in the trafficking of proteins between the Golgi apparatus endosomes and the cell surface. SorLA expresses most abundantly in neurons but also shows presence in other tissues like the heart and kidney. Its functional expression in these areas indicates a broad role in cellular logistics particularly in neurons where it impacts synaptic functioning.
Biological function summary

SorLA acts as a sorting receptor and contributes significantly to the regulation of protein sorting and signaling pathways within the cell. SorLA interacts with various ligands and forms complexes including lipid transport proteins and neuropeptides. The protein also plays a role in the sorting of the amyloid precursor protein (APP) assisting in the regulation of its processing and reducing the production of amyloid-beta a component significant in neurodegenerative processes.

Pathways

SorLA participates actively in the cellular pathways associated with protein trafficking and processing. It is integral to pathways involving endocytosis and the regulation of APP processing. SorLA interacts with important proteins such as APP and the low-density lipoprotein receptor-related protein 1 (LRP1). These interactions exemplify SorLA’s critical involvement in the cellular maintenance of protein homeostasis and in mitigating the production of potentially pathogenic peptides therefore interfacing with wider neurobiological functions.

SorLA’s role connects with neurodegenerative conditions with a notable focus on Alzheimer’s disease. The protein's interaction with APP processing places it in a central position in the pathology of Alzheimer’s disease as dysregulation can lead to increased amyloid-beta production and plaque formation. Additionally SorLA exhibits relevance in some cardiovascular diseases through its modulation of lipoprotein metabolism linking it with the functioning of proteins like apolipoproteins which when disrupted can contribute to the progression of atherosclerosis.

Product protocols

For this product, it's our understanding that no specific protocols are required. You can visit:

Target data

Sorting receptor that directs several proteins to their correct location within the cell (Probable). Along with AP-1 complex, involved Golgi apparatus - endosome sorting (PubMed : 17646382). Sorting receptor for APP, regulating its intracellular trafficking and processing into amyloidogenic-beta peptides. Retains APP in the trans-Golgi network, hence preventing its transit through late endosomes where amyloid beta peptides Abeta40 and Abeta42 are generated (PubMed : 16174740, PubMed : 16407538, PubMed : 17855360, PubMed : 24523320). May also sort newly produced amyloid-beta peptides to lysosomes for catabolism (PubMed : 24523320). Does not affect APP trafficking from the endoplasmic reticulum to Golgi compartments (PubMed : 17855360). Sorting receptor for the BDNF receptor NTRK2/TRKB that facilitates NTRK2 trafficking between synaptic plasma membranes, postsynaptic densities and cell soma, hence positively regulates BDNF signaling by controlling the intracellular location of its receptor (PubMed : 23977241). Sorting receptor for GDNF that promotes GDNF regulated, but not constitutive secretion (PubMed : 21994944). Sorting receptor for the GDNF-GFRA1 complex, directing it from the cell surface to endosomes. GDNF is then targeted to lysosomes and degraded, while its receptor GFRA1 recycles back to the cell membrane, resulting in a GDNF clearance pathway. The SORL1-GFRA1 complex further targets RET for endocytosis, but not for degradation, affecting GDNF-induced neurotrophic activities (PubMed : 23333276). Sorting receptor for ERBB2/HER2. Regulates ERBB2 subcellular distribution by promoting its recycling after internalization from endosomes back to the plasma membrane, hence stimulating phosphoinositide 3-kinase (PI3K)-dependent ERBB2 signaling. In ERBB2-dependent cancer cells, promotes cell proliferation (PubMed : 31138794). Sorting receptor for lipoprotein lipase LPL. Promotes LPL localization to endosomes and later to the lysosomes, leading to degradation of newly synthesized LPL (PubMed : 21385844). Potential sorting receptor for APOA5, inducing APOA5 internalization to early endosomes, then to late endosomes, wherefrom a portion is sent to lysosomes and degradation, another portion is sorted to the trans-Golgi network (PubMed : 18603531). Sorting receptor for the insulin receptor INSR. Promotes recycling of internalized INSR via the Golgi apparatus back to the cell surface, thereby preventing lysosomal INSR catabolism, increasing INSR cell surface expression and strengthening insulin signal reception in adipose tissue. Does not affect INSR internalization (PubMed : 27322061). Plays a role in renal ion homeostasis, controlling the phospho-regulation of SLC12A1/NKCC2 by STK39/SPAK kinase and PPP3CB/calcineurin A beta phosphatase, possibly through intracellular sorting of STK39 and PPP3CB (By similarity). Stimulates, via the N-terminal ectodomain, the proliferation and migration of smooth muscle cells, possibly by increasing cell surface expression of the urokinase receptor uPAR/PLAUR. This may promote extracellular matrix proteolysis and hence facilitate cell migration (PubMed : 14764453). By acting on the migration of intimal smooth muscle cells, may accelerate intimal thickening following vascular injury (PubMed : 14764453). Promotes adhesion of monocytes (PubMed : 23486467). Stimulates proliferation and migration of monocytes/macrophages (By similarity). Through its action on intimal smooth muscle cells and macrophages, may accelerate intimal thickening and macrophage foam cell formation in the process of atherosclerosis (By similarity). Regulates hypoxia-enhanced adhesion of hematopoietic stem and progenitor cells to the bone marrow stromal cells via a PLAUR-mediated pathway. This function is mediated by the N-terminal ectodomain (PubMed : 23486467). Metabolic regulator, which functions to maintain the adequate balance between lipid storage and oxidation in response to changing environmental conditions, such as temperature and diet. The N-terminal ectodomain negatively regulates adipose tissue energy expenditure, acting through the inhibition the BMP/Smad pathway (By similarity). May regulate signaling by the heterodimeric neurotrophic cytokine CLCF1-CRLF1 bound to the CNTFR receptor by promoting the endocytosis of the tripartite complex CLCF1-CRLF1-CNTFR and lysosomal degradation (PubMed : 26858303). May regulate IL6 signaling, decreasing cis signaling, possibly by interfering with IL6-binding to membrane-bound IL6R, while up-regulating trans signaling via soluble IL6R (PubMed : 28265003).
See full target information SORL1

Publications (2)

Recent publications for all applications. Explore the full list and refine your search

Alzheimer's research & therapy 17:100 PubMed40336092

2025

Soluble SorLA in CSF, a novel biomarker to explore disrupted trafficking of SorLA protein in Alzheimer disease.

Applications

Unspecified application

Species

Unspecified reactive species

Romain Castelot,Aline Zarea,David Wallon,Anne Rovelet-Lecrux,Catherine Schramm,Muriel Quillard-Muraine,Anne Beaume,Frédéric Blanc,Olivier Bousiges,Julien Dumurgier,Maïté Formaglio,Gwenael Leguyader,Sylvain Lehmann,Cecilia Marelli,Matthieu Martinet,Leonor Nogueira,Jérémie Pariente,Isabelle Quadrio,Adeline Rollin-Sillaire,Susanna Schraen,Gaël Nicolas,Magalie Lecourtois

International journal of biological sciences 19:1528-1542 PubMed37056924

2023

SIRT7 Downregulation Promotes Breast Cancer Metastasis Via LAP2α-Induced Chromosomal Instability.

Applications

Unspecified application

Species

Unspecified reactive species

Qin Huo,Siqi Chen,Jialang Zhuang,Chuntao Quan,Yue Wang,Ni Xie
View all publications

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