sCD23 plays an important role in various chronic inflammation disorders as well as allergy. sCD23 can trigger the release of TNF-alpha. Neither TACE nor MMP nor MT-MMPs involved in shedding but some non-disclosed member of the ADAM family. PMID: 15163541 [PubMed - indexed for MEDLINE] Capacity to mediate inflammatory cell function and tumor growth and metastasis a cytoplasmic variant [2] (SWISS-PROT:P01375), a cytokine
SWISS-PROT describes it well, cleavage site also mentioned in [2]. Proteinase 3 (PRTN 3) (PR-3)" (SWISS-PROT) has been reported to be in involved in TNF alpha processing (Gearing, 1995), presumed to modulating the activity of the metalloproteinase [2]
TNF-alpha Converting Enzyme (TNF-alpha convertase) (ADAM17, TACE, CSVP, CD156b antigen) (NCBI PROW) (SWISS-PROT:P78536)
From SWISS-PROT:
CC   -!- FUNCTION: CLEAVES THE MEMBRANE-BOUND PRECURSOR OF TNF-ALPHA TO ITS
CC       MATURE SOLUBLE FORM. RESPONSIBLE FOR THE PROTEOLYTIC RELEASE OF
CC       SEVERAL OTHER CELL-SURFACE PROTEINS, INCLUDING P75 TNF-RECEPTOR,
CC       INTERLEUKIN 1 RECEPTOR TYPE II, P55 TNF-RECEPTOR, TRANSFORMING
CC       GROWTH FACTOR-ALPHA, L-SELECTIN, AND THE AMYLOID PRECURSOR
CC       PROTEIN. ALSO INVOLVED IN THE ACTIVATION OF NOTCH PATHWAY (BY
CC       SIMILARITY).
CC   -!- CATALYTIC ACTIVITY: CLEAVES TNF-ALPHA AT 76-ALA-|-VAL-77.

The protein represents a link of my interest for soluble variants of membrane proteins (splice-variant with cleavage site) with the apical-basolateral sorting
Abstract: The primary structure of human kit ligand (KL) growth factor mRNA was analyzed by polymerase chain reaction (PCR) and nucleotide sequencing. Two bands from the total RNAs of a variety of human tumor cell lines were amplified by RT-PCR. Nucleotide sequences of these cloned cDNAs revealed that an 84-nucleotide stretch, corresponding to a spacer chain which contains the site for proteolytic release of the cytokine domain, was missing in the shorter clone, resulting in a transmembrane-bound form of KL. The relative intensity of the two bands in human bone marrow and tumor cells was then determined. In the bone marrow cells, THP1 and HuH7, the band for the membrane-bound type of KL was relatively more intense, whereas the reverse was the case in Daudi, K562 and HT1080 cells, suggesting that there are variations in the expression level of these two human KL mRNAs.
Abstract: Kit-ligand also known as Stem Cell factor, Mast cell growth factor or Steel factor has been implicated in the proliferation, survival and migration of embryonic melanoblasts. In addition, in the adult epidermis, melanocytes remain under the influence of kit-ligand produced by the keratinocyte environment. Consequently, changes in kit-ligand level and presentation exemplified e.g. in cutaneous mastocytosis, has shown to influence melanocyte numbers and morphology. We have recently determined the intracellular trafficking signals required for kit-ligand presentation at the basolateral membrane of epithelial cells. In order to determine the morphogenetic capacity of altered kit-ligand presentation towards responsive melanoblasts, we have established a co-culture system comprised of kit-ligand responsive melb-a cells and kidney epithelial cells (MDCK) expressing wildtype or mutant kit-ligand. In this co-culture system, melanoblast survival in the basolateral aspect of the MDCK monolayer depends on the expression of wildtype kit-ligand. In contrast, melanoblasts are "guided" to leave the epithelial monolayer in response to "apical" presentation of mutant kit-ligand missing the basolateral targeting sequence. These data will be discussed in the context of melanoma progression and kit-ligand independent survival of melanocytes in the epidermis.

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Vocabulary

 ET-1 is a soluble protein, the cleavage is 21 residues into the mature peptide, not from the N-terminus. Mice do no have alternate splicing but a C-terminal termination