Rabbit Anti-Human ARHGAP11A (C-terminal) Polyclonal antibody

Name: Rabbit Anti-Human ARHGAP11A (C-terminal) Polyclonal antibody
SKU: CABT-BL317
Rating: 5 (1 reviews)

Rabbit Anti-Human ARHGAP11A (C-terminal) Polyclonal antibody for WB, IF/ICC

COA

SDS

Datasheet

Key features and details

Specificity: ARHGAP11A Antibody detects endogenous levels of total ARHGAP11A.
Host: Rabbit
Application: WB, IF/ICC
Species Reactivity: Human, Mouse

Summary

Specifications

Antibody Isotype

IgG

Species Reactivity

Human; Mouse

Immunogen

A synthesized peptide derived from human ARHGAP11A, corresponding to a region within C-terminal amino acids.

Conjugate

Unconjugated

Applications

Application Notes

WB 1:500-1:1000
IF/ICC 1:100-1:500

General Notes

This product (Catalog No. CABT-BL317) is a rabbit-derived polyclonal antibody raised against human ARHGAP11A. This antibody exhibits cross-reactivity with ARHGAP11A from mouse. It has been affinity purified by Protein A. ARHGAP11A (Rho GTPase Activating Protein 11A) is a human protein-coding gene that encodes a member of the Rho GTPase-activating proteins (RhoGAPs), which regulate the activity of Rho family small GTPases. These GTPases act as molecular switches controlling a variety of cellular processes, including cytoskeletal organization, cell migration, proliferation, and cell cycle progression. ARHGAP11A promotes the inactivation of Rho GTPases by accelerating the hydrolysis of GTP to GDP, thereby turning off Rho-mediated signaling pathways. It is expressed in multiple tissues and has been implicated in processes such as cell division and maintenance of cellular architecture. Dysregulation of ARHGAP11A expression has been associated with roles in cancer biology, particularly in influencing tumor cell proliferation and invasion through modulation of cytoskeletal dynamics and signaling pathways.
CABT-BL317 is suitable for use in WB 1 (500-1:1000), IF/ICC 1 (100-1:500) applications.
CABT-BL317 is supplied as a liquid formulation in Phosphate buffered saline, pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. For long-term storage, keep at −20 °C. For short-term use, store at 2–8 °C. Avoid repeated freeze–thaw cycles to maintain antibody integrity and performance.

Target

Entrez Gene ID

9824

UniProt ID

Q6P4F7

Citations

Have you cited CABT-BL317 in a publication? Let us know and earn a reward for your research.

Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

A single splice site mutation in human-specific ARHGAP11B causes basal progenitor amplification

SCIENCE ADVANCES

Authors: Florio, Marta; Namba, Takashi; Paeaebo, Svante; Hiller, Michael; Huttner, Wieland B.

Abstract

The gene ARHGAP11B promotes basal progenitor amplification and is implicated in neocortex expansion. It arose on the human evolutionary lineage by partial duplication of ARHGAP11A, which encodes a Rho guanosine triphosphatase-activating protein (RhoGAP). However, a lack of 55 nucleotides in ARHGAP11B mRNA leads to loss of RhoGAP activity by GAP domain truncation and addition of a human-specific carboxy-terminal amino acid sequence. We show that these 55 nucleotides are deleted bymRNA splicing due to a single C -> G substitution that creates a novel splice donor site. We reconstructed an ancestral ARHGAP11B complementary DNA without this substitution. Ancestral ARHGAP11B exhibits RhoGAP activity but has no ability to increase basal progenitors during neocortex development. Hence, a single nucleotide substitution underlies the specific properties of ARHGAP11B that likely contributed to the evolutionary expansion of the human neocortex.

Human-specific gene ARHGAP11B promotes basal progenitor amplification and neocortex expansion

SCIENCE

Authors: Florio, Marta; Albert, Mareike; Taverna, Elena; Namba, Takashi; Brandl, Holger; Lewitus, Eric; Haffner, Christiane; Sykes, Alex; Wong, Fong Kuan; Peters, Jula; Guhr, Elaine; Klemroth, Sylvia; Pruefer, Kay; Kelso, Janet; Naumann, Ronald; Nuesslein, Ina; Dahl, Andreas; Lachmann, Robert; Paeaebo, Svante; Huttner, Wieland B.

Abstract

Evolutionary expansion of the human neocortex reflects increased amplification of basal progenitors in the subventricular zone, producing more neurons during fetal corticogenesis. In this work, we analyze the transcriptomes of distinct progenitor subpopulations isolated by a cell polarity-based approach from developing mouse and human neocortex. We identify 56 genes preferentially expressed in human apical and basal radial glia that lack mouse orthologs. Among these, ARHGAP11B has the highest degree of radial glia-specific expression. ARHGAP11B arose from partial duplication of ARHGAP11A (which encodes a Rho guanosine triphosphatase-activating protein) on the human lineage after separation from the chimpanzee lineage. Expression of ARHGAP11B in embryonic mouse neocortex promotes basal progenitor generation and self-renewal and can increase cortical plate area and induce gyrification. Hence, ARHGAP11B may have contributed to evolutionary expansion of human neocortex.