OCLN

This gene encodes an integral membrane protein that is required for cytokine-induced regulation of the tight junction paracellular permeability barrier. Mutations in this gene are thought to be a cause of band-like calcification with simplified gyration and polymicrogyria (BLC-PMG), an autosomal recessive neurologic disorder that is also known as pseudo-TORCH syndrome. Alternative splicing results in multiple transcript variants. A related pseudogene is present 1.5 Mb downstream on the q arm of chromosome 5. [provided by RefSeq, Apr 2011]

Occludin

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.

Bicellular tight junction assemblyManual Assertion Based On ExperimentIMP:UniProtKB
Cell-cell junction organizationManual Assertion Based On ExperimentIMP:MGI
Maintenance of blood-brain barrier1 PublicationNAS:ARUK-UCL
Negative regulation of gene expressionManual Assertion Based On ExperimentIMP:ARUK-UCL
Negative regulation of protein phosphorylationManual Assertion Based On ExperimentIMP:ARUK-UCL
Positive regulation of blood-brain barrier permeabilityManual Assertion Based On ExperimentIMP:ARUK-UCL
Positive regulation of gene expressionManual Assertion Based On ExperimentIMP:ARUK-UCL
Positive regulation of glucose importManual Assertion Based On ExperimentIMP:ARUK-UCL
Positive regulation of lamellipodium assemblyISS:ARUK-UCL
Positive regulation of microtubule polymerizationISS:ARUK-UCL
Positive regulation of wound healingISS:ARUK-UCL
Protein localization to cell leading edgeISS:ARUK-UCL
Protein-containing complex assemblyManual Assertion Based On ExperimentTAS:ProtInc
Regulation of glucose transmembrane transportManual Assertion Based On ExperimentIMP:ARUK-UCL

Cell membrane
Cell junction, tight junction

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.

Cytoplasmic: 1-66
Helical: 67-89
Extracellular: 90-135
Helical: 136-160
Cytoplasmic: 161-170
Helical: 171-195
Extracellular: 196-243
Helical: 244-265
Cytoplasmic: 266-522

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.