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      Phenotypic Plasticity and Terminal Differentiation of the Intercalated Cell: The Hensin Pathway

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          The intercalated cell of the collecting tubule exists in a spectrum of types. The alpha form secretes acid by an apical H<sup>+</sup> ATPase and a basolateral Cl:HCO<sub>3</sub> exchanger which is an alternatively spliced form of the red cell band 3 (kAE1), while the beta form secretes HCO<sub>3</sub> by having these transporters on the reverse membranes. In a clonal cell line of the beta form we found that seeding density causes this conversion. A new protein, termed hensin, was deposited in the extracellular matrix of high-density cells which on purification reversed the polarity of the transporters. Hensin also induced the expression of the microvillar protein, villin, and caused the appearance of the apical terminal web proteins, cytokeratin 19 and actin, all of which led to the development of an exuberant microvillar structure. In addition, hensin caused the beta cells to assume a columnar shape. All of these studies demonstrate that the conversion of polarity in the intercalated cell, at least in vitro, represents terminal differentiation and that hensin is the first protein in a new pathway that mediates this process. Hensin, DMBT1, CRP-ductin, and ebnerin are alternately spliced products from a single gene located on human chromosome 10q25–26, a region often deleted in several cancers, especially malignant gliomas. Hensin is expressed in many epithelial cell types, and it is possible that it plays a similarly important role in the differentiation of these epithelia as well.

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          Most cited references 9

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          The CUB domain. A widespread module in developmentally regulated proteins.

           P. Bork,  Max Beckmann (1993)
          Sequence analysis has revealed the presence of 31 copies of an extracellular domain, here called CUB, in 16 functionally diverse proteins such as the dorso-ventral patterning protein tolloid, bone morphogenetic protein 1, a family of spermadhesins, complement subcomponents Cls/Clr and the neuronal recognition molecule A5. Most of them are known to be involved in developmental processes. Our analysis of this new family includes the identification of seven previously undescribed members, the characterization of conserved features and a topology prediction of this approximately 110 residue spanning domain, which suggests an antiparallel beta-barrel similar to those in immunoglobulins.
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            DMBT1, a new member of the SRCR superfamily, on chromosome 10q25.3-26.1 is deleted in malignant brain tumours.

            Loss of sequences from human chromosome 10q has been associated with the progression of human cancer. Medulloblastoma and glioblastoma multiforme are the most common malignant brain tumours in children and adults, respectively. In glioblastoma multiforme, the most aggressive form, 80% of the tumours show loss of 10q. We have used representational difference analysis to identify a homozygous deletion at 10q25.3-26.1 in a medulloblastoma cell line and have cloned a novel gene, DMBT1, spanning this deletion. DMBT1 shows homology to the scavenger receptor cysteine-rich (SRCR) superfamily. Intragenic homozygous deletions has been detected in 2/20 medulloblastomas and in 9/39 glioblastomas multiformes. Lack of DMBT1 expression has been demonstrated in 4/5 brain-tumour cell lines. We suggest that DMBT1 is a putative tumour-suppressor gene implicated in the carcinogenesis of medulloblastoma and glibolastoma multiforme.
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              The SRCR superfamily: a family reminiscent of the Ig superfamily


                Author and article information

                Nephron Exp Nephrol
                Cardiorenal Medicine
                S. Karger AG
                April 2000
                15 March 2000
                : 8
                : 2
                : 66-71
                Departments of Medicine and Physiology, College of Physicians and Surgeons of the Columbia University, New York, N.Y., USA
                20650 Exp Nephrol 2000;8:66–71
                © 2000 S. Karger AG, Basel

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                Figures: 1, Tables: 1, References: 32, Pages: 6
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