The phrase "auto linkage" is correct and usable in written English.
It can be used in contexts related to technology, automation, or systems that connect or link automatically without manual intervention.
Example: "The software features an auto linkage function that allows for seamless integration with other applications."
Alternatives: "automatic connection" or "automated linking".
Moreover the auto-linkage is relatively specific for each serpin.
Such preferential auto-linkages are readily explicable if they involve major domain exchanges but the surprising finding is that preferential auto-linkage also takes place even when the linkage involves only a small 6-residue peptide sequence, as with the polymerogenic serpins depicted in Fig. 1a and b.
An indication as to why self-association is so competitively successful comes from the demonstration here of a β-bonding interface in antithrombin that is constantly being exposed in blood but is immediately and preferentially blocked by a specific auto-linkage.
But protection against such promiscuous and potentially lethal linkages will be provided by the much more competitively avid formation of auto-linkages.
This toxicity will be limited however by the competitive blocking of the site by auto-linkages resulting in the progressive extension of the oligomer and its eventual sequestration.
This ability to preferentially form auto-linkages enables the early oligomer to scavenge and selectively remove molecules that may, even transitorily, change their fold.
Not only does antithrombin selectively and specifically dimerise to protect a vacated interface (Figs. 1c and 3a) but in the serpins in general, exposure of a hexapeptide β-acceptor site (Fig. 1b) is competitively filled by auto-linkages in a 50 1 preference to the natural hexapeptide (Fig. 2b).
In general, it appears that the C-termini of some of the RBRs are exclusively involved in auto-inhibitory interactions or controlling linkage specificity during ubiquitin chain assembly.
The exact pathogenesis of rheumatoid arthritis (RA) remains uncertain, but autoimmune processes are clearly relevant as evidenced by major histocompatibility complex (MHC) linkage [ 1, 2], auto-antibodies (rheumatoid factor (RF)) and other antigenic specificities [ 3].
An anti-CD38 antibody (CPK-H; MBL, Nagoya, Japan) was added to protect transduced T cells from auto-lysis through cross-linkage of the anti-CD38-CAR with intrinsic CD38, described previously.
We're also seeing more "drive by wire," systems, in which auto companies replace heavy, complex, mechanical and hydraulic linkages with electronic controls.
