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Recurrent de novo mutations disturbing the GTP (Montrer AK3 Protéines)/GDP binding pocket of RAB11B cause intellectual disability and a distinctive brain phenotype.
High RAB11B expression is associated with pancreatic cancer.
Rab11A (Montrer RAB11A Protéines) and Rab11B differentially regulate intracellular trafficking of PAR1 (Montrer MARK2 Protéines) through distinct endosomal sorting mechanisms
we determined a crystal structure of the PKG (Montrer PRKG1 Protéines) II LZ-Rab11b complex. The PKG (Montrer PRKG1 Protéines) II LZ domain presents a mostly nonpolar surface onto which Rab11b docks, through van (Montrer TNIP1 Protéines) der (Montrer GDF3 Protéines) Waals interactions
Upon Rab11b depletion, FGFR4 (Montrer FGFR4 Protéines) is trapped in the pericentriolar recycling compartment.
the predominant mechanism of melanin transfer is keratinocyte-induced exocytosis, mediated by Rab11b through remodeling of the melanosome membrane, followed by subsequent endocytosis by keratinocytes
Data show that the cAMP/PKA/CREB (Montrer CREB1 Protéines) signaling pathway initiates acidosis-induced V-ATPase (Montrer ATP6V1H Protéines) trafficking in salivary ducts via regulation of Rab11b expression.
These findings reveal a novel role for Rab11b in limiting, rather than promoting, the plasma membrane expression of Cav1.2 (Montrer CACNA1C Protéines) L-type Ca2 (Montrer CA2 Protéines)+ channels.
These data introduce Rab11b as a crucial regulator and Rip11 (Montrer RAB11FIP5 Protéines) as mediator of acidosis-induced V-ATPase (Montrer ATP6V1H Protéines) traffic in duct cells of submandibular gland.
propose a model where Rab11B specifically transports vesicles derived from the Golgi to the immature Inner Membrane Complex of the growing daughter parasites.
these data show an interaction between the smallGTPase Rab11b and the BK channel (Montrer KCNMA1 Protéines), which suggests that BK is shuttledthrough a slow recycling endocytic pathway.
These data indicate that Rab11b, and to a lesser extent Rab11a (Montrer RAB11A Protéines), is involved in establishing the constitutive and cAMP-stimulated Na(+) transport in mpkCCD cells.
These data indicate that Rab11b is necessary for the trafficking of cGK-II and that the cGMP/cGK-II signaling pathway is closely related to Rab11b recycling pathway.
Data show that in huntingtin-null embryonic stem cells, the levels of Rab11 on membranes and nucleotide exchange activity on Rab11 are significantly reduced compared with normal embryonic stem cells.
Study shows that both Rab11 (Montrer RAB11A Protéines) and its effector Rip11 (Montrer RAB11FIP5 Protéines) participate in insulin (Montrer INS Protéines) granule exocytosis and that Rip11 (Montrer RAB11FIP5 Protéines), as a substrate of PKA, regulates the potentiation of exocytosis by cAMP in pancreatic beta-cells.
The Ras superfamily of small GTP-binding proteins, which includes the Ras (see MIM 190020), Ral (see MIM 179550), Rho (see MIM 165390), Rap (see MIM 179520), and Rab (see MIM 179508) families, is involved in controlling a diverse set of essential cellular functions. The Rab family, including RAB11B, appears to play a critical role in regulating exocytotic and endocytotic pathways (summary by Zhu et al., 1994
ras-related protein Rab-11B
, GTP-binding protein YPT3
, RAB11B, member of RAS oncogene family