Shairaz Baksh

ORCID: 0000-0002-3170-4241
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About
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Research Areas
  • Signaling Pathways in Disease
  • Biochemical and Molecular Research
  • Endoplasmic Reticulum Stress and Disease
  • NF-κB Signaling Pathways
  • Cell death mechanisms and regulation
  • Histone Deacetylase Inhibitors Research
  • Ubiquitin and proteasome pathways
  • Cytokine Signaling Pathways and Interactions
  • Peptidase Inhibition and Analysis
  • Mitochondrial Function and Pathology
  • Inflammatory mediators and NSAID effects
  • Protein Tyrosine Phosphatases
  • Cancer Immunotherapy and Biomarkers
  • Hippo pathway signaling and YAP/TAZ
  • Colorectal Cancer Treatments and Studies
  • Immunodeficiency and Autoimmune Disorders
  • Protease and Inhibitor Mechanisms
  • HER2/EGFR in Cancer Research
  • Cancer, Stress, Anesthesia, and Immune Response
  • Calpain Protease Function and Regulation
  • Adenosine and Purinergic Signaling
  • Healthcare and Environmental Waste Management
  • PARP inhibition in cancer therapy
  • ATP Synthase and ATPases Research
  • Ion channel regulation and function

Women and Children’s Health Research Institute
2016-2019

University of Alberta
1991-2019

University of Manitoba
2018

Universidad Nacional Autónoma de México
2018

Beth Israel Deaconess Hospital
2003-2005

Harvard University
2002-2005

Dana-Farber Cancer Institute
2000-2001

Pediatric Oncology Group
2000

University of Toronto
1991

The distribution of calsequestrin and calreticulin in smooth muscle non-muscle tissues was investigated. Immunoblots endoplasmic reticulum proteins probed with anti-calreticulin anti-calsequestrin antibodies revealed that only is present the rat liver reticulum. Membrane fractions isolated from uterine muscle, which are enriched sarcoplasmic reticulum, contain a protein band immunoreactive but not antibodies. presence these membrane further confirmed by 45Ca2+ overlay Stains-All techniques....

10.1016/s0021-9258(20)89624-0 article EN cc-by Journal of Biological Chemistry 1991-04-01

We report here that calreticulin interacts with protein disulfide isomerase (PDI). The PDI-calreticulin complex can be dissociated by Zn2+-iminodiacetate-substituted Sepharose-agarose chromatography, suggesting these interactions may Zn2+ dependent. Direct interaction between and PDI is also documented affinity chromatography. was the only pancreatic microsomal retained on column. Calreticulin were identified their NH2-terminal amino acid sequence analysis, mobilities in SDS-polyacrylamide...

10.1074/jbc.270.52.31338 article EN cc-by Journal of Biological Chemistry 1995-12-01

Phosphatidylinositol 3'-kinase (PI3K) is a key component of multiple signaling pathways, where it typically promotes survival, proliferation, and/or adhesion. Here, we show that in TCR signaling, the scaffolding adapter Gab2 delivers an inhibitory signal via PI3K. Overexpression T cell lines inhibits TCR-evoked activation IL-2 promoter, blocking NF-AT- and NF-kappaB-directed transcription. Inhibition abrogated by mutating p85-binding sites, treatment with PI3K inhibitors or cotransfection...

10.4049/jimmunol.165.8.4158 article EN The Journal of Immunology 2000-10-15

Fas apoptotic signaling regulates diverse physiological processes. Acute activation of triggers massive apoptosis in liver. Upon receptor stimulation, the BH3-only protein Bid is cleaved into active form, tBid. Subsequent tBid recruitment to mitochondria, which facilitated by its MTCH2 at outer mitochondrial membrane (OMM), a critical step for commitment via effector proteins Bax or Bak. MOAP-1 Bax-binding enriched OMM. Here, we show that MOAP-1-deficient mice are resistant Fas-induced...

10.1016/j.celrep.2016.05.068 article EN cc-by-nc-nd Cell Reports 2016-06-01

The Bcl-2-associated death promoter BAD is a prognostic indicator for good clinical outcome of breast cancer patients; however, whether affects biology unknown. Here we showed that increased cell growth in cells through two distinct mechanisms. Phosphorylation at S118 S99 phosphorylation, 14-3-3 binding and AKT activation to promote survival. Through second, more prominent pathway, stimulated mitochondrial oxygen consumption novel manner was downstream substrate entry into the mitochondria....

10.1038/s41388-018-0673-6 article EN cc-by Oncogene 2019-01-11

Receptor-interacting protein kinase 2 (RIP2 or RICK, herein referred to as RIPK2) is linked the pathogen pathway that activates nuclear factor <i>κ</i>-light-chain-enhancer of activated B cells (NF<i>κ</i>B) and autophagic activation. Using molecular modeling (docking) chemoinformatics analyses, we used RIPK2/ponatinib crystal structure searched in chemical databases for small molecules exerting binding interactions similar those exerted by ponatinib. The identified RIPK2 inhibitors potently...

10.1124/jpet.117.247163 article EN cc-by-nc Journal of Pharmacology and Experimental Therapeutics 2018-03-19
Mohammad A. Alsayegh Hanan Alshamali Mousa Khadada A Ciccolini Anne K. Ellis and 95 more Diana Quint William Powley Laurie Lee Yahya Fiteih Shairaz Baksh Harissios Vliagoftis Sebastien K. Gerega Brad Millson Katia Charland Stéphane Barakat Xichun Sun Ricardo Jimenez Susan Waserman Mark J. Fitzgerald Jacques Hébert Josiane Cognet-Sicé Kevin E. Renahan Saiful Huq Rishma Chooniedass Scott Sawyer Hans Pasterkamp Allan B. Becker Steven G. Smith Shi‐Yuan Zhang K. M. P. D. Jayasundara Claire E. Tacon Alexander Simidchiev Gilbert Nadeau Necdet B. Gunsoy Hana Müllerová Frank C. Albers Young Woong Kim Casey P. Shannon Amrit Singh Helen Neighbour Mark Larché Scott J. Tebbutt Annika Klopp Lorena Vehling Allan B. Becker Padmaja Subbarao Piush J. Mandhane Stuart E. Turvey Malcolm R. Sears Meghan B. Azad Keely Loewen Barret A. Monchka Salaheddin M. Mahmud Geert ‘t Jong Cristina Longo Gillian Bartlett Francine M. Ducharme Tibor Schuster Brenda MacGibbon Tracie A. Barnett Michelle L. North Jeff Brook Elizabeth Lee Vanessa Omana Jenny Thiele Lisa M. Steacy Greg J. Evans Miriam L. Diamond Gordon Sussman Yann Amistani Kathy Abiteboul Mark W. Tenn Chenxi Yang Christopher Carlsten Edward M. Conway Douglas P. Mack Rofina Yasmin Othman Colin Barber Chrystyna Kalicinsky Andrea E. Burke Mary Messieh Parameswaran Nair Tae‐Wook Chun Lindsay Douglas Joel Liem Lucy Duan Charlotte Miller Pascale Dupuis Lori Connors Michael Fein Joseph Shuster Hani Hadi Brooke I. Polk Nikita Raje Roxane Labrosse Philippe Bégin Louis Paradis Anne Des Roches Jonathan Lacombe‐Barrios Sanju Mishra

Background: Multiple animal antigens, spores and pollens were collected identified from the Kuwaiti atmosphere.The role for these antigens in mediating allergic rhinitis residents needs to be evaluated.Objective: To investigate causes (both indoors outdoors) of residents.Method: This is a retrospective study all positive skin tests that we obtained our Allergy clinic Mubarak Alkabeer Hospital Kuwait, during period between May 2013 December 2015, patients who presented with symptoms and/or...

10.1186/s13223-017-0192-y article EN cc-by Allergy Asthma and Clinical Immunology 2017-04-07

We describe an extractionless real-time reverse transcriptase-PCR (rRT-PCR) protocol for SARS-CoV-2 nucleic acid detection using heat as accurate cost-effective high-capacity solution to COVID-19 testing. present the effect of temperature, transport media, rRT-PCR mastermixes and gene assays on amplification limits detection. Utilizing our heated methodology, were 12.5 1 genome copy/reaction singleplex E- N1-gene assays, respectively, by utilizing E/N1 or Orf1ab/N1 multiplex assay...

10.1016/j.diagmicrobio.2021.115458 article EN cc-by-nc-nd Diagnostic Microbiology and Infectious Disease 2021-06-17

Interleukin-3 (IL-3) regulates cell growth by affecting various processes such as death, survival, and proliferation. Cues from the external environment are sensed surface receptors, complex signaling mechanisms arise within cells, leading to specific functional outcomes. In this study, we demonstrate that cytokine IL-3 induces activation of Ca(2+)-dependent phosphatase, calcineurin (Cn). Furthermore Cn dephosphorylates Gab2, resulting in c-fos We also report there is a direct interaction...

10.1074/jbc.c800087200 article EN cc-by Journal of Biological Chemistry 2008-06-28

10.1016/j.bbrc.2007.08.197 article EN Biochemical and Biophysical Research Communications 2007-09-18

Introduction. Metabolic dysfunction and chronic inflammation are robust molecular drivers of many diseases such as obesity, diabetes inflammatory bowel disease (IBD). Indeed, since is essentially a necessary component tissue repair, it stands to reason that energy for key repair mechanisms function properly. The underlying driving IBD currently attributed broad spectrum susceptible genes modulates the appearance, maintenance progression IBD. Precision medicine relies on defining patient...

10.1093/jcag/gwz006.046 article EN cc-by-nc-nd Journal of the Canadian Association of Gastroenterology 2019-03-01

Tkaczuk, Jean1; Milford, Edgar L.2; Carpenter, Charles B.2; Yu, Chao-Lan1; Baksh, Shairaz1; Burakoff, Steven J.1; McKay, Dianne B.1,2 Author Information

10.1097/00007890-200004271-01096 article EN Transplantation 2000-04-01

The tumor suppressor protein RASSF1A is epigenetically silenced in 40-50% of breast, prostate and ovarian cancers, making it an important player reproductive cancers. promotes apoptotic response following the binding necrosis factor alpha (TNFá) to receptor 1 (TNF-R1) on surface a cell. In contrast, non-catalytic adapter Grb2 binds constitutively TNF-R1, enhanced expression has been observed breast cancer cells. This suggests that there may be antagonism between leading death versus...

10.1093/biolreprod/78.s1.71 article EN Biology of Reproduction 2008-05-01

Persistent inflammation can trigger altered epigenetic, inflammatory and bioenergetics states. Inflammatory bowel disease (IBD) is a heterogeneous with an abnormal state subsequent metabolic syndrome disorder leptin alterations in the kinase, AMP-activated protein kinase (AMPK). Altered IBD has been well studied > 90% of current therapeutics are directed to inhibiting elements that drive epithelial cells colonic crypt. We hypothesize completely resolve mucosal we must (i) Inhibit mediators...

10.1093/jcag/gwz006.088 article EN cc-by-nc-nd Journal of the Canadian Association of Gastroenterology 2019-03-01
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