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Data presented in our study suggests that the CAPZB gene may be a candidate gene of meat production trait and provides useful information for further studies on its roles in porcine skeletal muscle.
CAPZB, ANKRD1 (show ANKRD1 ELISA Kits), and CTBP2 (show CTBP2 ELISA Kits) are promoted as candidate genes for meat quality that provide a link between signal pathways.
A subject with micrognathia, cleft palate and hypotonia harbored a de novo, balanced chromosomal translocation that disrupts the CAPZB gene. The function of capzb was analyzed in the zebrafish model.
CAPZB is involved in tumor progression in cases of epithelioid sarcoma (EpiS), irrespective of the INI1 (show SMARCB1 ELISA Kits) expression, and may be a potential therapeutic target. The paradoxical relationship between the tumor suppressor INI1 (show SMARCB1 ELISA Kits) and the oncoprotein CAPZB in the pathogenesis of EpiS remains to be clarified
RAGE has a role in endothelial cell membrane repair and regulates F-actin remodeling and membrane resealing
Capping protein CAPZB participates in stereocilia widening in auditory hair cells by preventing newly elongating actin filaments from depolymerizing.
with strain there was significant PKCepsilon (show PRKCE ELISA Kits) translocation to the Z-disc and co-localization with CapZbeta1 or alpha-actinin (show ACTN1 ELISA Kits), which was quantified on confocal images.
Capping protein-beta knockdown decreases filopodial length, alters filopodial shape, and reduces filopodial dynamics.
Actin-capping protein is a novel regulator of microtubule stability that functions by antagonizing mDia1 activity toward actin filaments.
This study suggested that increased expression of TrkB (show NTRK2 ELISA Kits) and Capzb2 accompanies adequate brain reserve in the initial stages of AD pathology.
BAG3 (show BAG3 ELISA Kits) and Hsc70 (show HSPA8 ELISA Kits) interact with actin capping protein (show TMOD4 ELISA Kits) CapZ (show CAPZA1 ELISA Kits) to maintain myofibrillar integrity under mechanical stress.
Capping protein interacts with both actin protomers at the barbed end of the filament, and the amphipathic helix at the C-terminus of the beta-subunit binds to the hydrophobic cleft on actin.
Proper capzb dosage is important during craniofacial embryogenesis, and regulates both cell behavior and tissue morphogenesis. Loss of capzb affects cell morphology, differentiation and neural crest migration. Differentiation of both myogenic stem cells and neural crest cells requires capzb. During palate morphogenesis, defective cranial neural crest cell migration in capzb(-/-) mutants results in a cleft phenotype.
This gene encodes the beta subunit of the barbed-end actin binding protein, which belongs to the F-actin capping protein family. The capping protein is a heterodimeric actin capping protein that blocks actin filament assembly and disassembly at the fast growing (barbed) filament ends and functions in regulating actin filament dynamics as well as in stabilizing actin filament lengths in muscle and nonmuscle cells. Multiple alternatively spliced transcript variants encoding different isoforms have been found.
capping protein (actin filament) muscle Z-line, beta
, capping protein beta 1
, F-actin-capping protein subunit beta
, capZ beta
, f-actin-capping protein subunit beta
, CP beta1
, F-actin capping protein subunit beta 1
, F-actin capping protein beta subunit
, actin-capping protein Z (cap-Z) beta subunit
, beta-actinin subunit II
, capZ 36/32
, capZ B1 and B2