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BMPR1A protein, human

BMPR1A (Bone Morphogenetic Protein Receptor Type 1A) is a key regulator of cellular processes, including cell growth, differentiation, and apoptosis.
This receptor plays a crucial role in bone and cartilage development, as well as in the regulation of various signaling pathways.
Undertsanding the function and regulation of BMPR1A is essential for research on a wide range of biological and pathological processes, from skeletal disorders to cancer.
Researchers can leverage PubCompare.ai's AI-driven platform to streamline their BMPR1A-related studies, easily locating and comparing the most effective research protocols from literature, preprints, and patents.

Most cited protocols related to «BMPR1A protein, human»

Genetic Screening for Familial Hypercholesterolemia and Colorectal Cancer

Cited 13 times

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Publication 2018

APOB protein, human BMPR1A protein, human Cardiovascular Diseases Colonic Polyps Genes Genetic Diversity Genome, Human Hypercholesterolemia LDLR protein, human MLH1 protein, human MSH6 protein, human MUTYH protein, human Nucleotides Patient Acceptance of Health Care PCSK9 protein, human Pharmaceutical Preparations PMS2 protein, human Point-of-Care Systems POLD1 protein, human Reproduction SMAD4 protein, human

Generation of Ager-H2b:Venus and Pdgfrα-CreERT2 Mice

Cited 12 times

To generate Ager-H2b:Venus mice, a DNA fragment containing 8 kb upstream of the first coding exon and exons 2-7 were retrieved from a BAC clone (bMQ174, Source BioScience) and recombined into the vector pL25B upstream of a HSV-TK cassette for negative selection. A cassette encoding H2b:Venus fusion protein followed by polyA (kindly provided by Dr Anna-Katerina Hadjantonakis, Sloan Kettering Cancer Center) and a neo cassette flanked with FRT sites were recombined into the start codon. The construct was electroporated into G4 (C57BL/6Ncr×129S6/SvEvTac) hybrid ES cells. Two clones were injected into C57BL/6 blastocysts. Mice were bred to 129S4-Gt(ROSA)26Sor^tm2(FLP*)Sor/J to remove the neo cassette. Ager-H2b:Venus mice are maintained on a C57BL/6 background.
A similar strategy was used to generate the Pdgfrα-CreER^T2 ‘knock-in’ allele. A CreER^T2 poly-A cassette and a FRT-flanked neo cassette were recombined into the start codon of Pdgfrα (BAC clone: bMQ123p11, Source BioScience). The construct was electroporated into TL1 (129S6/SvEvTac) ES cells and these were injected into C57BL/6 blastocysts. The neo cassette was removed. Pdgfrα-CreER^T2 mice were maintained on a C57BL/6 background.
Sftpctm1(cre/ERT)Blh (Sftpc-CreER^T2) (Rock et al., 2011 (link)), Rosa26-CAG-lsl-tdTomato (Arenkiel et al., 2011 (link)), Rosa26-CAG-lsl-caBmpr1a (Rodriguez et al., 2010 (link)), Bmpr1a flox (Mishina et al., 2002 (link)) and Pdgfra^{tm11(EGFP)Sor} (Pdgfra-H2b:GFP) (Hamilton et al., 2003 (link)) were maintained on a C57BL/6 background. All experiments were performed according to IACUC-approved protocols.

Chung M.I., Bujnis M., Barkauskas C.E., Kobayashi Y, & Hogan B.L. (2018). Niche-mediated BMP/SMAD signaling regulates lung alveolar stem cell proliferation and differentiation. Development (Cambridge, England), 145(9), dev163014.

Publication 2018

Alleles Blastocyst BMPR1A protein, human Clone Cells Cloning Vectors Codon, Initiator DNA, A-Form Embryonic Stem Cells Exons Hybrid Cells Institutional Animal Care and Use Committees Malignant Neoplasms Mus Platelet-Derived Growth Factor alpha Receptor Poly A Proteins RAGE receptor protein, human Rosa tdTomato

Conditional Activation of BMPR1A in Osteoblasts

Cited 10 times

Mice expressing the tamoxifen (TM)-inducible Cre fusion protein Cre-ER^™ (Danielian et al., 1998 (link); Hayashi and McMahon, 2002 (link)) under the control of a 3.2 kb mouse pro-collagen α1(I) promoter (Col1-CreER^™), which is active in osteoblasts, odontoblasts and tendon fibroblasts (Rossert et al., 1995 (link)), were generated by pronuclear injection and crossed with floxed Bmpr1a mice (Mishina et al., 2002 (link)). Mice that conditionally express a constitutively active form of Bmpr1a (caBmpr1a), which has a mutation in the GS domain of BMPR1A that results in ligand-independent activation of Smad signaling after Cre recombination, were generated using a transgenic construct similar to one previously reported (Fukuda et al., 2006 (link)) (see Fig. S4A in the supplementary material). ROSA26 Cre reporter (R26R) (Soriano, 1999 (link)) and TOPGAL (DasGupta and Fuchs, 1999 (link)) mice were obtained from Dr Philippe Soriano and the Jackson Laboratory, respectively. Tamoxifen (TM; Sigma) was dissolved in a small volume of ethanol, diluted with corn oil at a concentration of 10 mg/ml. TM (75 mg/kg) was injected intraperitoneally daily into pregnant mice (100 to 200 ml/mouse) for at least 3 days starting at E13.5.

Kamiya N., Ye L., Kobayashi T., Mochida Y., Yamauchi M., Kronenberg H.M., Feng J.Q, & Mishina Y. (2008). BMP signaling negatively regulates bone mass through sclerostin by inhibiting the canonical Wnt pathway. Development (Cambridge, England), 135(22), 3801-3811.

Publication 2008

Animals, Transgenic BMPR1A protein, human Collagen Corn oil Ethanol Fibroblasts Ligands Mice, Laboratory Mutation Odontoblasts Osteoblasts Proteins Recombination, Genetic Tamoxifen Tendons

Targeted NGS Analysis of Cancer Genes

Cited 7 times

For targeted NGS analysis, Ion AmpliSeq designer software (Life Technologies, Tokyo, Japan) was used to design primers, which consisted of 610 primer pairs in two pools covering the exons and exon–intron boundaries of 25 cancer-predisposing genes (APC, ATM, BARD1, BMPR1A, BRIP1, CDH1, CDK4, CDKN2A, CHEK2, EPCAM, MLH1, MRE11A, MSH2, MSH6, MUTYH, NBN, PALB2, PMS2, PTEN, RAD50, RAD51C, RAD51D, SMAD4, STK11, and TP53) (Walsh et al. 2011 (link); Couch et al. 2014b (link); Economopoulou et al. 2015 (link); Tung et al. 2015 (link)). Multiplex polymerase chain reaction (PCR) was performed using 50–100 ng genomic DNA with 17 cycles with a premixed primer pool using Ion AmpliSeq Library Kit 2.0, as previously described (Hirotsu et al. 2014 (link)). The PCR amplicons were treated with 2 μL FuPa reagent to partially digest primer sequences and phosphorylate the amplicons. The amplicons were ligated to adapters with the diluted barcodes of the Ion Xpress Barcode Adapters kit (Life Technologies). Adaptor-ligated amplicon libraries were purified using Agencourt AMPure XP reagents (Beckman Coulter, Tokyo, Japan). The library concentration was determined using an Ion Library Quantitation Kit (Life Technologies), then each library was diluted to 8 pM and the same amount of libraries was pooled for one sequence reaction. Next, emulsion PCR was carried out using the Ion OneTouch System and Ion PI Template OT2 200 Kit v2 (Life Technologies) according to the manufacturer’s instructions. Template-positive Ion Sphere Particles were then enriched with Dynabeads MyOne Streptavidin C1 Beads (Life Technologies) using an Ion OneTouch ES system (Life Technologies). Purified Ion Sphere particles were loaded on an Ion PI Chip v2. Massively parallel sequencing was carried out on an Ion Proton System (Life Technologies) using the Ion PI Sequencing 200 Kit v2. Sequencing was performed using 500 flow runs that generated ∼200 bp reads.

Hirotsu Y., Nakagomi H., Sakamoto I., Amemiya K., Oyama T., Mochizuki H, & Omata M. (2015). Multigene panel analysis identified germline mutations of DNA repair genes in breast and ovarian cancer. Molecular Genetics & Genomic Medicine, 3(5), 459-466.

Publication 2015

Aleurites alpha-fluoro-beta-ureidopropionic acid BMPR1A protein, human CDH1 protein, human CDKN2A Gene CHEK2 protein, human DNA Chips DNA Library Emulsions Exons Gene, Cancer Genome Introns MLH1 protein, human MRE11 protein, human MSH6 protein, human Multiplex Polymerase Chain Reaction MUTYH protein, human Oligonucleotide Primers Oncogenes PALB2 protein, human PI 200 PMS2 protein, human Polymerase Chain Reaction Protons PTEN protein, human Rad50 protein, human RAD51C protein, human SMAD4 protein, human STK11 protein, human Streptavidin TACSTD1 protein, human TP53 protein, human

Immunohistochemistry and Tissue Staining Protocols

Cited 6 times

Alizarin Red and Alcian Blue staining were done according to published protocols [10 (link)]. Hematoxylin and eosin staining was performed on fixed or frozen tissue sections using Harris Modified Hematoxylin and Eosin Y Solution (Sigma, St. Louis, MO, http://www.sigmaaldrich.com), according to the manufacturer's instructions. LacZ staining was performed as previously described [18 (link)]. Immunohistochemistry: Immunostaining for different markers was done according to standard protocols. Briefly, sections and cultured cells were fixed with 4% paraformaldehyde in PBS. Nonspecific binding was blocked with 10% normal serum diluted in 1% bovine serum albumin (BSA; Jackson ImmunoResearch Laboratories, West Grove, PA, http://www.jacksonimmuno.com) and 0.25% Triton X-100 (Sigma) for 1 hour in room temperature. The sections were then incubated with primary antibodies diluted with 1% BSA + 0.25% Triton X-100 at 4°C overnight. The sections were then incubated with appropriate secondary antibodies (Cy3 or Cy2 conjugated antibodies (Jackson ImmunoResearch Laboratories) diluted with 1% BSA + 0.25% Triton X-100 or Alexa Fluor 488, Alexa Fluor 594, and Alexa 647 (1:1000, Invitrogen) in the dark at room temperature for 2 hours. Counterstaining was then performed with 4,6-diamidino-2-phenylindole (1:5000). Mouse anti-col II (CIIC1) was obtained from the Developmental Studies Hybridoma Bank (Iowa City, IA, http://dshb.biology.uiowa.edu. Mouse anti-BMP4 was purchased from Chemicon (Temecula, CA, http://www.chemicon.com), and rat anti-CD45 was purchased from BD (BD PharMingen, San Diego, http://www.bdbiosciences.com/index_us.shtml). Rabbit anti-ACVR1 (#AP7101c), rabbit anti-BMPR1A (#AP2004a), and rabbit anti-BMPR1B (#AP2005b) were purchased from Abgent (Abgent, Inc., San Diego, http://www.abgent.com) for Western blotting.

Kan L., Liu Y., McGuire T.L., Berger D.M., Awatramani R.B., Dymecki S.M, & Kessler J.A. (2009). Dysregulation of Local Stem/Progenitor Cells as a Common Cellular Mechanism for Heterotopic Ossification. Stem cells (Dayton, Ohio), 27(1), 150-156.

Publication 2009

Alcian Blue Alexa594 alexa fluor 488 Antibodies BMPR1A protein, human BMPR1B protein, human Bone Morphogenetic Protein 4 Cultured Cells Eosin Frozen Sections Hematoxylin Hybridomas Immunohistochemistry LacZ Genes Mice, House paraform Rabbits Serum Serum Albumin, Bovine Tissues Triton X-100

Most recents protocols related to «BMPR1A protein, human»

Locoregional and Metastatic NSCLC Relapse Treatment

If the relapse is defined as locoregional, in candidates for local treatment, the expert panel considered that 38.3% undergo a surgical procedure (lobectomy), while 80.6% receive some kind of radiotherapy (RT). Specifically, 19.0% are treated with radical RT adjuvant or neoadjuvant to surgery, 40.0% with stereotactic body radiotherapy (SBRT), and 21.7% with chemotherapy plus concomitant radiotherapy (CT–RT). Also, 35.1% of the patients receive platinum-based chemotherapy, 21.7% as CT–RT (without surgery) and 13.4% as adjuvant to surgery. Among patients receiving CT–RT, those with stage III are candidates for durvalumab maintenance (approximately 45% according to the experts panel). Figure 1 depicts the local treatments distribution considered in the model in case of locoregional relapse.Fig. 1

Local treatments in locoregional relapse. a shows the different local treatments grouped into surgery, radiotherapy, and chemotherapy, while 1b shows the distribution of these local treatments without grouping. *Adjuvant chemotherapy: 9% platinum + gemcitabine, 13% platinum + pemetrexed, 70% platinum + vinorelbine, 8% platinum + paclitaxel. **Chemo-radiotherapy: 38% platinum + vinorelbine, 31% platinum + paclitaxel, 31% platinum + etoposide

If metastases are diagnosed at the time of relapse (or the disease has progressed from a previous locoregional relapse), the patient starts a first-line (1L) of oncologic treatment depending on the histology and molecular profile of the tumor. According to the consensus reached by the expert panel through the 2 rounds of questionnaires:

96.4% of squamous histology patients (30% of the total) receive a first-line treatment, and subsequently 52.4%, 24.5% and 4.0% reached second-line (2L), third-line (3L) and fourth-line (4L), respectively.

97.1% of adenocarcinoma histology patients (70% of total) receive a 1L treatment, and subsequently 61.5%, 34.9% and 13.1% reached 2L, 3L and 4L, respectively.

The distribution of treatments in each line for the different histological subtypes and molecular profiles is shown in Fig. 2. Treatments are grouped into the following categories: platinum-based chemotherapies, chemotherapies plus VEGF inhibitors, chemotherapies with a single agent, targeted therapies with a TKI, immunotherapies as monotherapy, and chemo-immunotherapies. The detailed distribution with specific treatments is shown in Additional files 1, 2, 3, 4, 5, 6.Fig. 2

Pharmacological treatment distribution in each line of treatment after metastatic relapse. 1L: first-line; 2L: second-line; 3L: third-line; 4L; forth-line

Posology for each specific treatment was obtained from their respective summary of product characteristic [24 ]. The duration of 1L and 2L treatments was estimated from the median PFS reported in the respective clinical trials [25 (link)–47 (link)], and it was assumed that patients reaching 3L and 4L receive approximately 4.5 cycles and 3 cycles, respectively. Finally, based on the distribution of treatments for each line and the median PFS for each treatment, the weighted mean of the time spent on each treatment line was estimated.
As a result, 1L average duration was estimated in 6.3 months for patients with squamous histology and 33.6, 18.2, 19.0, 8.4 and 10.2 months for ALK + , EGFR + , ROS1 + , WT-TPS < 50% and WT-TPS > 50%patients, respectively. 2L average duration was 3.1 months for patients with squamous histology and 7.1, 7.5, 5.9, and 3.3 months for ALK + , EGFR + , ROS1 + and WT patients, respectively. For all patients, 3L and 4L length were 3.1 and 2.1 months respectively.

De Castro J., Insa A., Collado-Borrell R., Escudero-Vilaplana V., Martínez A., Fernandez E., Sullivan I., Arrabal N., Carcedo D, & Manzaneque A. (2023). Economic burden of locoregional and metastatic relapses in resectable early-stage non-small cell lung cancer in Spain. BMC Pulmonary Medicine, 23, 69.

Publication 2023

ACVR1 protein, human Adenocarcinoma BMPR1A protein, human Chemotherapy, Adjuvant durvalumab EGFR protein, human Gemcitabine Immunotherapy inhibitors Neoadjuvant Therapy Neoplasms Operative Surgical Procedures Paclitaxel Patients Pharmaceutical Adjuvants Pharmacotherapy Platinum Radiotherapy Radiotherapy, Adjuvant Relapse ROS1 protein, human Stereotactic Body Radiotherapy Vascular Endothelial Growth Factors Vinorelbine

Germline Genetic Testing for Cancer

Germline genetic testing costs were covered by institutional research study funds and by foundational grants. Genetic testing was performed on the saliva sample via the clinical Color Genomics targeted panel of 30 cancer predisposition genes: APC, ATM, BAP1, BARD1, BMPR1A, BRCA1, BRCA2, BRIP1, CDH1, CDK4, CDKN2A(p14ARF), CDKN2A (p16INK4a), CHEK2, EPCAM, GREM1, MITF, MLH1, MSH2, MSH6, MUTYH, NBN, PALB2, PMS2, POLD1, POLE, PTEN, RAD51C, RAD51D, SMAD4, STK11, and TP53.

Cheng H.H., Sokolova A.O., Gulati R., Bowen D., Knerr S.A., Klemfuss N., Grivas P., Hsieh A., Lee J.K., Schweizer M.T., Yezefski T., Zhou A., Yu E.Y., Nelson P.S, & Montgomery B. (2023). Internet-Based Germline Genetic Testing for Men With Metastatic Prostate Cancer. JCO Precision Oncology, 7, e2200104.

Publication 2023

BMPR1A protein, human BRCA1 protein, human CDH1 protein, human CDKN2A Gene CHEK2 protein, human Gene, BRCA2 Gene, Cancer Germ Line GREM1 protein, human MITF protein, human MLH1 protein, human MSH6 protein, human MUTYH protein, human Oncogenes p14ARF Protein PALB2 protein, human PMS2 protein, human POLD1 protein, human PTEN protein, human RAD51C protein, human Saliva SMAD4 protein, human STK11 protein, human Susceptibility, Disease TACSTD1 protein, human TP53 protein, human

Comprehensive Genetic Cancer Screening

Genetic testing was performed in a Clinical Laboratory Improvement Amendments– and College of American Pathology–approved laboratory (Myriad Genetic Laboratories Inc, Salt Lake City, UT). The hereditary cancer panel was composed of 25-35 cancer-associated genes; the initial multigene panel test included 25 genes (APC, ATM, BARD1, BMPR1A, BRCA1, BRCA2, BRIP1, CDH1, CDK4, CHEK2, MLH2, MSH2, MSH6, MUTYH, NBN, P14ARF, P16, PALB2, PMS2, PTEN, RAD51C, RAD51D, SMAD4, STK11, and TP53). Subsequent additions to the panel test in 2016 and 2019 included GREM1, HOXB13, POLD1, POLE, AXIN2, GALNT12, MSH3, NTHL1, RNF43, and RPS20. This next-generation sequencing assay has been detailed previously.^{15 (link),16 (link)} Sequencing and large rearrangement analysis was performed for all genes evaluated except HOXB13, POLD1, and POLE, for which only sequencing is performed, and EPCAM and GREM1, in which only large rearrangement analysis is performed.
Variant classification was performed using the American College of Molecular Genetics and Genomics and Association for Molecular Pathology guidelines, as well as previously described statistical variant classification methods.^{17 (link)-20 (link)} Variants with a laboratory classification of deleterious or suspected deleterious were considered pathogenic.

Cummings S., Alfonso A., Hughes E., Kucera M., Mabey B., Singh N, & Eng C. (2023). Cancer Risk Associated With PTEN Pathogenic Variants Identified Using Multigene Hereditary Cancer Panel Testing. JCO Precision Oncology, 7, e2200415.

Publication 2023

AXIN2 protein, human Biological Assay BMPR1A protein, human BRCA1 protein, human CDH1 protein, human CHEK2 protein, human Clinical Laboratory Services Gene, BRCA2 Gene, Cancer Genes GREM1 protein, human HOXB13 protein, human Malignant Neoplasms mismatch repair protein 1, human MSH6 protein, human MUTYH protein, human NTHL1 protein, human Oncogenes PALB2 protein, human Pathogenicity PMS2 protein, human POLD1 protein, human PTEN protein, human RAD51C protein, human Reproduction RPS20 protein, human Salts SMAD4 protein, human STK11 protein, human TACSTD1 protein, human TP53 protein, human

TGF-beta Signaling Pathway qPCR

RNA was isolated with RNeasy Mini Kit (Qiagen, Crawley, UK). The cDNA synthesis was performed using High-Capacity RNA-to-cDNA kit (Applied Biosystems, Thermo Fisher Scientific). To perform RT-qPCR, we used standard settings of the StepOne Real-Time PCR system with TaqMan Fast Advanced Master Mix and Taqman Gene Expression Assays, FAM-MGB labelled (Applied Biosystems, Thermo Fisher Scientific). The assays used were FKBP1A (Hs00356621_g1), SMAD1 (Hs00195432_m1), SMAD5 (Hs00195437_m1), SMAD4 (Hs00929647_m1), ACVR1 (Hs00153836_m1), BMPR1A (Hs01034909_g1), BMPR1B (Hs01010965_m1), BMPR2 (Hs00176148_m1) and GAPDH (Hs99999905_m1). Comparative Ct method was used to calculate the relative changes in expression with GAPDH as housekeeping gene.

Quist-Løkken I., Andersson-Rusch C., Kastnes M.H., Kolos J.M., Jatzlau J., Hella H., Olsen O.E., Sundan A., Knaus P., Hausch F, & Holien T. (2023). FKBP12 is a major regulator of ALK2 activity in multiple myeloma cells. Cell Communication and Signaling : CCS, 21, 25.

Publication 2023

Anabolism Biological Assay BMPR1A protein, human BMPR1B protein, human BMPR2 protein, human DNA, Complementary FKBP1A protein, human GAPDH protein, human Gene Expression Genes, Housekeeping SMAD4 protein, human SMAD5 protein, human

Transient knockdown of BMPs signaling genes

For transient knockdown experiments INA-6 cells were transfected using the Nucleofector device (Amaxa, Biosystems, Cologne, Germany) and Amaxa Cell Line Nucleofector Kit R (Lonza, Basel, Switzerland) as described previously [39 (link)]. We used human ON-TARGETplus SMARTpool FKBP1A (#L-009494-00-0005), ACVR1 (#L-004924-00-0005), BMPR1A (#L-004933-00-0005), SMAD1 (#L-012723-00-0005), SMAD4 (#L-003902-00-0005), SMAD5 (#L-015791-00-0005), and Non-Targeting Pool (#D-001810-10-20) siRNA (Dharmacon, Thermo Fisher Scientific). The siRNA target sequences (each pool of four) are given in Table 1.Table 1

Target sequences of siRNA

Gene name	Target sequences
FKBP1A	GAGCCAAACUGACUAUAUC, GACAGAAACAAGCCCUUUA, AAACUGGAAUGACAGGAAU, GAAAUUUGAUUCCUCCCGG
ACVR1	GAAUGGACAGUGUUGCAUA, GUCCAUAGCUAGUGGUCUU, GAAAGGCUGCUUCCAGGUU, GUACGACUAUCUUCAGCUU
BMPR1A	AAGCAGACGUCGUUACAAU, UGGACUACCUUUAUUGGUU, ACACAUGCAUAACUAAUGG, CAGCUACGCCGGACAAUAG
SMAD1	GCUCUAUUGUCUACUAUGA, GGCGGUUGCUUAUGAGGAA, CAACAAUCGUGUGGGUGAA, CAAAUGGGUUCACCUCAUA
SMAD4	GCAAUUGAAAGUUUGGUAA, CCCACAACCUUUAGACUGA, GAAUCCAUAUCACUACGAA, GUACAGAGUUACUACUUAG
SMAD5	GAUCAGAUGGGUCAAGAUA, CAACUUUCAUCAUGGCUUU, GAGCUAAAGCCGUUGGAUA, GUAGAUGGAUUCACAGAUC
Non-targeting	UGGUUUACAUGUCGACUAA, UGGUUUACAUGUUGUGUGA, UGGUUUACAUGUUUUCUGA, UGGUUUACAUGUUUUCCUA

Publication 2023

BMPR1A protein, human Cell Lines Cells FKBP1A protein, human Homo sapiens Medical Devices RNA, Small Interfering SMAD4 protein, human SMAD5 protein, human Transients

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TRIzol reagent is a monophasic solution of phenol, guanidine isothiocyanate, and other proprietary components designed for the isolation of total RNA, DNA, and proteins from a variety of biological samples. The reagent maintains the integrity of the RNA while disrupting cells and dissolving cell components.

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Bmpr1a by Abcam

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BMPR1A is a cell surface receptor that belongs to the bone morphogenetic protein receptor family. It is involved in the regulation of various cellular processes, including cell growth, differentiation, and apoptosis. BMPR1A plays a crucial role in the transduction of bone morphogenetic protein signals.

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P-Smad1/5/8 is a laboratory reagent used to detect phosphorylated Smad1, Smad5, and Smad8 proteins. These Smad proteins are key mediators of the BMP signaling pathway. This product can be used in techniques such as Western blotting to analyze the activation status of the BMP signaling cascade.

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Anti bmpr1a by Abcam

Anti-Bmpr1a is a primary antibody that recognizes the Bone Morphogenetic Protein Receptor Type 1A (BMPR1A). BMPR1A is a transmembrane serine/threonine kinase that is part of the TGF-beta superfamily receptor complex.

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β-actin is a cytoskeletal protein that is ubiquitously expressed in eukaryotic cells. It is a component of the microfilament system and plays a crucial role in various cellular processes, such as cell motility, maintenance of cell shape, and intracellular trafficking.

What is the BMPR1A protein and what are its key functions in the human body?

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Are there different variations or types of the BMPR1A protein that researchers should be aware of?

Yes, there are different variations or isoforms of the BMPR1A protein that researchers should be aware of. The BMPR1A gene can undergo alternative splicing, resulting in the production of multiple BMPR1A protein variants. These variants may have slightly different structures and functions, which can impact their roles in various biological processes and pathological conditions. Understanding the different BMPR1A protein types and their specific applications is crucial for designing targeted research studies and therapeutic interventions.

What are some common usage challenges or considerations when working with the BMPR1A protein, human?

One of the main challenges when working with the BMPR1A protein, human, is ensuring the reproducibility and accuracy of your research protocls. The BMPR1A protein is involved in complex signaling pathways and cellular processes, and small variations in experimental conditions can lead to vastly different results. Researchers must carefully optimize their protocols and validate their findings to ensure the reliability of their BMPR1A-related studies. Additionally, the BMPR1A protein's role in a wide range of biological and pathological processes means that researchers must have a deep understanding of its context-specific functions to draw meaningful conclusions from their experiments.

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More about "BMPR1A protein, human"

BMPR1A (Bone Morphogenetic Protein Receptor Type 1A) is a crucial regulator of cellular processes, including cell growth, differentiation, and apoptosis.
This receptor plays a vital role in bone and cartilage development, as well as in the regulation of various signaling pathways.
Understanding the function and regulation of BMPR1A is essential for research on a wide range of biological and pathological processes, from skeletal disorders to cancer.
Researchers can leverage PubCompare.ai's AI-driven platform to streamline their BMPR1A-related studies.
The platform helps researchers easily locate and compare the most effective research protocols from literature, preprints, and patents, using intelligent AI analysis.
This can help optimize workflows and get the best results for BMPR1A protein research.
When studying BMPR1A, researchers may utilize techniques like TRIzol reagent for RNA extraction, the High-Capacity cDNA Reverse Transcription Kit for cDNA synthesis, and the HiSeq 2000 platform for gene expression analysis.
Antibodies like Anti-Bmpr1a can also be used to study the protein's expression and localization.
Complementary techniques like RNeasy Mini Kit for RNA purification and analysis of downstream signaling molecules like P-Smad1/5/8 and BMP4 can provide a comprehensive understanding of the BMPR1A pathway.
Leveraging PubCompare.ai's AI-powered insights can help researchers streamline their BMPR1A studies, leading to more efficient and effective research outcomes.
The platform's ability to identify and compare the most relevant protocols from a vast pool of literature, preprints, and patents can save researchers time and effort, allowing them to focus on advancing their studies on this crucial protein.