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OCLN

GeneName

OCLN

Summary

OCLN, also known as occludin or hOCLN, is a 59 kDa integral membrane protein that is a critical component of tight junctions in epithelial and endothelial cells. It is primarily localised to the apical and lateral membranes of cells, where it plays a vital role in the formation and maintenance of tight junctions, which are essential for regulating paracellular permeability and maintaining the integrity of the blood-brain barrier. OCLN is involved in various cellular processes, including cell-cell junction organisation and epithelial cell migration, and is known to interact with other proteins within the protein-containing complex of tight junctions, contributing to the overall structure and function of these junctions.

Importance

OCLN is relevant to: - The maintenance of the blood-brain barrier, influencing the movement of substances between the bloodstream and the central nervous system - Epithelial integrity and barrier function, which is crucial in various tissues including the gut and skin - Wound healing processes, as it is involved in cell migration and tissue repair - Regulation of glucose transport, impacting metabolic processes and potentially influencing conditions like diabetes - Understanding diseases characterised by barrier dysfunction, such as multiple sclerosis and inflammatory bowel disease.

Top Products

For researchers investigating OCLN, we highly recommend the top-selling recombinant antibody, Anti-Occludin antibody [EPR20992] (ab216327). This well-cited product has garnered 411 citations, reflecting its strong reputation in the field. It has been validated in knockout models and is suitable for a variety of applications, including Western blotting (WB), immunohistochemistry (IHC), immunocytochemistry (ICC), flow cytometry (FC), and immunoprecipitation (IP). This versatility makes it an excellent choice for those seeking reliable detection of Occludin in their studies.

Abcam Product Citation Summary

The data indicates a significant focus on the role of OCLN (occludin) in various biological contexts, particularly in relation to tight junctions and epithelial barrier functions. Studies involving both mouse and human models highlight its importance in intestinal health, blood-brain barrier integrity, and responses to dietary factors and injuries. The use of multiple applications, primarily Western blotting and immunohistochemistry, underscores the relevance of OCLN in research on cellular interactions and disease mechanisms.

Abcam Product Citation Table

ab216327
Mouse
WB, IF
Intestinal mucosal epithelial tight junction proteins
31251471
ab216327
Pig
WB, IHC
Intestinal epithelial barrier functions
29867808
ab216327
Pig
WB
Effects of dietary Flammulina velutipes stem waste
32391146
ab216327
Mouse
WB
Blood-brain barrier integrity after subarachnoid hemorrhage
32499702
ab216327
Mouse
WB
Intestinal barrier damage
35887011
ab31721
Rat
WB
Effects of FXT on diabetic rats
24204392
ab31721
Human
IF
Tight junction protein distribution
29075202
ab31721
Human
IHC
Cell–cell interaction markers of tight junctions
28706505
ab31721
Mouse
WB
Intestinal permeability
28484281
ab31721
Mouse
WB
Barrier function in Δ/Δep2 animals
27431613
ab31721
Human
WB
Blood-brain barrier integrity in Alzheimer's disease
30801976

Domain

The C-terminal is cytoplasmic and is important for interaction with ZO-1. Sufficient for the tight junction localization. Involved in the regulation of the permeability barrier function of the tight junction (By similarity). The first extracellular loop participates in an adhesive interaction.

Function

May play a role in the formation and regulation of the tight junction (TJ) paracellular permeability barrier. It is able to induce adhesion when expressed in cells lacking tight junctions.

(Microbial infection) Acts as a coreceptor for hepatitis C virus (HCV) in hepatocytes.

Involvement in disease

Pseudo-TORCH syndrome 1

PTORCH1

An autosomal recessive neurologic disorder with characteristic clinical and neuroradiologic features that mimic intrauterine TORCH infection in the absence of evidence of infection. Affected individuals have congenital microcephaly, intracranial calcifications, and severe developmental delay.

None

The disease is caused by variants affecting the gene represented in this entry.

Post-translational modifications

Dephosphorylated by PTPRJ. The tyrosine phosphorylation on Tyr-398 and Tyr-402 reduces its ability to interact with TJP1. Phosphorylation at Ser-490 also attenuates the interaction with TJP1.

(Microbial infection) Cleaved by S.pyogenes SpeB protease; leading to its degradation (PubMed:23532847). Degradation by SpeB promotes bacterial translocation across the host epithelial barrier (PubMed:23532847).

Sequence Similarities

Belongs to the ELL/occludin family.

Tissue Specificity

Localized at tight junctions of both epithelial and endothelial cells. Highly expressed in kidney. Not detected in testis.

Cellular localization

Alternative names

Occludin, OCLN

swissprot:Q16625 omim:602876 entrezGene:100506658