Редактирование: ARL4C

ADP-ribosylation factor-like protein 4C (ADP-ribosylation factor-like protein 7) (ADP-ribosylation factor-like protein LAK) [ARL7]

==Publications==

{{medline-entry
|title=[[LMX1B]] is essential for the maintenance of differentiated podocytes in adult kidneys.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23990680
|abstract=Mutations of the [[LMX1B]] gene cause nail-patella syndrome, a rare autosomal-dominant disorder affecting the development of the limbs, eyes, brain, and kidneys. The characterization of conventional Lmx1b knockout mice has shown that [[LMX1B]] regulates the development of podocyte foot processes and slit diaphragms, but studies using podocyte-specific Lmx1b knockout mice have yielded conflicting results regarding the importance of [[LMX1B]] for maintaining podocyte structures. In order to address this question, we generated inducible podocyte-specific Lmx1b knockout mice. One week of Lmx1b inactivation in adult mice resulted in proteinuria with only minimal foot process effacement. Notably, expression levels of slit diaphragm and basement membrane proteins remained stable at this time point, and basement membrane charge properties also did not change, suggesting that alternative mechanisms mediate the development of proteinuria in these mice. Cell biological and biophysical experiments with primary podocytes isolated after 1 week of Lmx1b inactivation indicated dysregulation of actin cytoskeleton organization, and time-resolved DNA microarray analysis identified the genes encoding actin cytoskeleton-associated proteins, including Abra and Arl4c, as putative [[LMX1B]] targets. Chromatin immunoprecipitation experiments in conditionally immortalized human podocytes and gel shift assays showed that [[LMX1B]] recognizes AT-rich binding sites (FLAT elements) in the promoter regions of [[ABRA]] and [[ARL4C]], and knockdown experiments in zebrafish support a model in which [[LMX1B]] and [[ABRA]] act in a common pathway during pronephros development. Our report establishes the importance of [[LMX1B]] in fully differentiated podocytes and argues that [[LMX1B]] is essential for the maintenance of an appropriately structured actin cytoskeleton in podocytes. 
|mesh-terms=* Actins
* Aging
* Animals
* Apoptosis
* Cell Differentiation
* Collagen Type IV
* Intracellular Signaling Peptides and Proteins
* LIM-Homeodomain Proteins
* Membrane Proteins
* Mice
* Mice, Inbred C57BL
* Nail-Patella Syndrome
* Oligonucleotide Array Sequence Analysis
* Podocytes
* Proteinuria
* Transcription Factors
* Zebrafish

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3810075
}}